question_text: what stage of the cell cycle does p53 work

text: Gene[edit]

text: In humans, the TP53 gene is located on the short arm of chromosome 17 (17p13.1).[7][8][9][10] The gene spans 20 kb, with a non-coding exon 1 and a very long first intron of 10 kb. The coding sequence contains five regions showing a high degree of conservation in vertebrates, predominantly in exons 2, 5, 6, 7 and 8, but the sequences found in invertebrates show only distant resemblance to mammalian TP53.[14] TP53 orthologs[15] have been identified in most mammals for which complete genome data are available.

text: In humans, a common polymorphism involves the substitution of an arginine for a proline at codon position 72. Many studies have investigated a genetic link between this variation and cancer susceptibility; however, the results have been controversial. For instance, a meta-analysis from 2009 failed to show a link for cervical cancer.[16] A 2011 study found that the TP53 proline mutation did have a profound effect on pancreatic cancer risk among males.[17] A study of Arab women found that proline homozygosity at TP53 codon 72 is associated with a decreased risk for breast cancer.[18] One study suggested that TP53 codon 72 polymorphisms, MDM2 SNP309, and A2164G may collectively be associated with non-oropharyngeal cancer susceptibility and that MDM2 SNP309 in combination with TP53 codon 72 may accelerate the development of non-oropharyngeal cancer in women.[19] A 2011 study found that TP53 codon 72 polymorphism was associated with an increased risk of lung cancer.[20]

text: Meta-analyses from 2011 found no significant associations between TP53 codon 72 polymorphisms and both colorectal cancer risk[21] and endometrial cancer risk.[22] A 2011 study of a Brazilian birth cohort found an association between the non mutant arginine TP53 and individuals without a family history of cancer.[23] Another 2011 study found that the p53 homozygous (Pro/Pro) genotype was associated with a significantly increased risk for renal cell carcinoma.[24]

text: Structure[edit]

text:
an acidic N-terminus transcription-activation domain (TAD), also known as activation domain 1 (AD1), which activates transcription factors. The N-terminus contains two complementary transcriptional activation domains, with a major one at residues 1–42 and a minor one at residues 55–75, specifically involved in the regulation of several pro-apoptotic genes.[25]
activation domain 2 (AD2) important for apoptotic activity: residues 43-63.
proline rich domain important for the apoptotic activity of p53 by nuclear exportation via MAPK: residues 64-92.
central DNA-binding core domain (DBD). Contains one zinc atom and several arginine amino acids: residues 102-292. This region is responsible for binding the p53 co-repressor LMO3.[26]
nuclear localization signaling domain, residues 316-325.
homo-oligomerisation domain (OD): residues 307-355. Tetramerization is essential for the activity of p53 in vivo.
C-terminal involved in downregulation of DNA binding of the central domain: residues 356-393.[27]

tag: ol

text: A tandem of nine-amino-acid transactivation domains (9aaTAD) was identified in the AD1 and AD2 regions of transcription factor p53.[28] KO mutations and position for p53 interaction with TFIID are listed below:[29] The competence of the p53 transactivation domains 9aaTAD to activate transcription as small peptides was reported.[30]

text: 9aaTADs mediate p53 interaction with general coactivators – TAF9, CBP/p300 (all four domains KIX, TAZ1, TAZ2 and IBiD), GCN5 and PC4, regulatory protein MDM2 and replication protein A (RPA).[28]

text: Mutations that deactivate p53 in cancer usually occur in the DBD. Most of these mutations destroy the ability of the protein to bind to its target DNA sequences, and thus prevents transcriptional activation of these genes. As such, mutations in the DBD are recessive loss-of-function mutations. Molecules of p53 with mutations in the OD dimerise with wild-type p53, and prevent them from activating transcription. Therefore, OD mutations have a dominant negative effect on the function of p53.

text: Wild-type p53 is a labile protein, comprising folded and unstructured regions that function in a synergistic manner.[31]

text: Function[edit]

text: p53 has many mechanisms of anticancer function and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms:

text:
It can activate DNA repair proteins when DNA has sustained damage. Thus, it may be an important factor in aging.[32]
It can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition (if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle).
It can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable.
It is essential for the senescence response to short telomeres.

text: Activated p53 binds DNA and activates expression of several genes including microRNA miR-34a,[33] WAF1/CIP1 encoding for p21 and hundreds of other down-stream genes. p21 (WAF1) binds to the G1-S/CDK (CDK4/CDK6, CDK2, and CDK1) complexes (molecules important for the G1/S transition in the cell cycle) inhibiting their activity.

text: When p21(WAF1) is complexed with CDK2, the cell cannot continue to the next stage of cell division. A mutant p53 will no longer bind DNA in an effective way, and, as a consequence, the p21 protein will not be available to act as the "stop signal" for cell division.[34] Studies of human embryonic stem cells (hESCs) commonly describe the nonfunctional p53-p21 axis of the G1/S checkpoint pathway with subsequent relevance for cell cycle regulation and the DNA damage response (DDR). Importantly, p21 mRNA is clearly present and upregulated after the DDR in hESCs, but p21 protein is not detectable. In this cell type, p53 activates numerous microRNAs (like miR-302a, miR-302b, miR-302c, and miR-302d) that directly inhibit the p21 expression in hESCs.[35]

text: Research has also linked the p53 and RB1 pathways, via p14ARF, raising the possibility that the pathways may regulate each other.[36]

text: p53 by regulating LIF has been shown to facilitate implantation in the mouse model and possibly in humans.[37]

text: p53 expression can be stimulated by UV light, which also causes DNA damage. In this case, p53 can initiate events leading to tanning.[38][39]

text: The p21 protein binds directly to cyclin-CDK complexes that drive forward the cell cycle and inhibits their kinase activity thereby causing cell cycle arrest to allow repair to take place. p21 can also mediate growth arrest associated with differentiation and a more permanent growth arrest associated with cellular senescence. The p21 gene contains several p53 response elements that mediate direct binding of the p53 protein, resulting in transcriptional activation of the gene encoding the p21 protein.

text: Stem cells[edit]

text: Levels of p53 play an important role in the maintenance of stem cells throughout development and the rest of human life.

text: Embryonic stem cells[edit]

text: p53 is maintained at low inactive levels in human embryonic stem cells (hESCs).[40] This is because activation of p53 leads to rapid differentiation of hESCs.[41] Studies have shown that knocking out p53 delays differentiation and that adding p53 causes spontaneous differentiation, showing how p53 promotes differentiation of hESCs and plays a key role in cell cycle as a differentiation regulator. When p53 becomes stabilized and activated in hESCs, it increases p21 to establish a longer G1. This typically leads to abolition of S-phase entry, which stops the cell cycle in G1, leading to differentiation. p53 also activates miR-34a and miR-145, which then repress the hESCs pluripotency factors, further instigating differentiation.[40]

text: Studies of human embryonic stem cells (hESCs) commonly describe the nonfunctional p53-p21 axis of the G1/S checkpoint pathway. This has subsequent relevance for cell cycle regulation and the DNA damage response (DDR). Importantly, p21 mRNA is clearly present and upregulated after the DDR in hESCs, but p21 protein is not detectable. In this cell type, p53 activates numerous microRNAs (like miR-302a, miR-302b, miR-302c, and miR-302d) that directly inhibit the p21 expression in hESCs.[35]

text: Adult stem cells[edit]

text: In adult stem cells, p53 regulation is important for maintenance of stemness in adult stem cell niches. Mechanical signals such as hypoxia affect levels of p53 in these niche cells through the hypoxia inducible factors, HIF-1α and HIF-2α. While HIF-1α stabilizes p53, HIF-2α suppresses it.[42] Suppression of p53 plays important roles in cancer stem cell phenotype, induced pluripotent stem cells and other stem cell roles and behaviors, such as blastema formation. Cells with decreased levels of p53 have been shown to reprogram into stem cells with a much greater efficiency that normal cells.[43][44] Papers suggest that the lack of cell cycle arrest and apoptosis gives more cells the chance to be reprogrammed. Decreased levels of p53 were also shown to be a crucial aspect of blastema formation in the legs of salamanders.[45] p53 regulation is very important in acting as a barrier between stem cells and a differentiated stem cell state, as well as a barrier between stem cells being functional and being cancerous.[46]

text: Regulation[edit]

text: p53 becomes activated in response to myriad stressors, including but not limited to DNA damage (induced by either UV, IR, or chemical agents such as hydrogen peroxide), oxidative stress,[47] osmotic shock, ribonucleotide depletion, and deregulated oncogene expression. This activation is marked by two major events. First, the half-life of the p53 protein is increased drastically, leading to a quick accumulation of p53 in stressed cells. Second, a conformational change forces p53 to be activated as a transcription regulator in these cells. The critical event leading to the activation of p53 is the phosphorylation of its N-terminal domain. The N-terminal transcriptional activation domain contains a large number of phosphorylation sites and can be considered as the primary target for protein kinases transducing stress signals.

text: The protein kinases that are known to target this transcriptional activation domain of p53 can be roughly divided into two groups. A first group of protein kinases belongs to the MAPK family (JNK1-3, ERK1-2, p38 MAPK), which is known to respond to several types of stress, such as membrane damage, oxidative stress, osmotic shock, heat shock, etc. A second group of protein kinases (ATR, ATM, CHK1 and CHK2, DNA-PK, CAK, TP53RK) is implicated in the genome integrity checkpoint, a molecular cascade that detects and responds to several forms of DNA damage caused by genotoxic stress. Oncogenes also stimulate p53 activation, mediated by the protein p14ARF.

text: In unstressed cells, p53 levels are kept low through a continuous degradation of p53. A protein called Mdm2 (also called HDM2 in humans), binds to p53, preventing its action and transports it from the nucleus to the cytosol. Also Mdm2 acts as ubiquitin ligase and covalently attaches ubiquitin to p53 and thus marks p53 for degradation by the proteasome. However, ubiquitylation of p53 is reversible.

text: MI-63 binds to MDM2 making the action of p53 again possible in situations were p53's function has become inhibited.[48]

text: A ubiquitin specific protease, USP7 (or HAUSP), can cleave ubiquitin off p53, thereby protecting it from proteasome-dependent degradation via the ubiquitin ligase pathway. This is one means by which p53 is stabilized in response to oncogenic insults. USP42 has also been shown to deubiquitinate p53 and may be required for the ability of p53 to respond to stress.[49]

text: Recent research has shown that HAUSP is mainly localized in the nucleus, though a fraction of it can be found in the cytoplasm and mitochondria. Overexpression of HAUSP results in p53 stabilization. However, depletion of HAUSP does not result to a decrease in p53 levels but rather increases p53 levels due to the fact that HAUSP binds and deubiquitinates Mdm2. It has been shown that HAUSP is a better binding partner to Mdm2 than p53 in unstressed cells.

text: USP10 however has been shown to be located in the cytoplasm in unstressed cells and deubiquitinates cytoplasmic p53, reversing Mdm2 ubiquitination. Following DNA damage, USP10 translocates to the nucleus and contributes to p53 stability. Also USP10 does not interact with Mdm2.[50]

text: Phosphorylation of the N-terminal end of p53 by the above-mentioned protein kinases disrupts Mdm2-binding. Other proteins, such as Pin1, are then recruited to p53 and induce a conformational change in p53, which prevents Mdm2-binding even more. Phosphorylation also allows for binding of transcriptional coactivators, like p300 and PCAF, which then acetylate the carboxy-terminal end of p53, exposing the DNA binding domain of p53, allowing it to activate or repress specific genes. Deacetylase enzymes, such as Sirt1 and Sirt7, can deacetylate p53, leading to an inhibition of apoptosis.[51] Some oncogenes can also stimulate the transcription of proteins that bind to MDM2 and inhibit its activity.

text: Role in disease[edit]

text: If the TP53 gene is damaged, tumor suppression is severely compromised. People who inherit only one functional copy of the TP53 gene will most likely develop tumors in early adulthood, a disorder known as Li-Fraumeni syndrome.

text: The TP53 gene can also be modified by mutagens (chemicals, radiation, or viruses), increasing the likelihood for uncontrolled cell division. More than 50 percent of human tumors contain a mutation or deletion of the TP53 gene.[52] Loss of p53 creates genomic instability that most often results in an aneuploidy phenotype.[53]

text: Increasing the amount of p53 may seem a solution for treatment of tumors or prevention of their spreading. This, however, is not a usable method of treatment, since it can cause premature aging.[54] Restoring endogenous normal p53 function holds some promise. Research has shown that this restoration can lead to regression of certain cancer cells without damaging other cells in the process. The ways by which tumor regression occurs depends mainly on the tumor type. For example, restoration of endogenous p53 function in lymphomas may induce apoptosis, while cell growth may be reduced to normal levels. Thus, pharmacological reactivation of p53 presents itself as a viable cancer treatment option.[55][56] The first commercial gene therapy, Gendicine, was approved in China in 2003 for the treatment of head and neck squamous cell carcinoma. It delivers a functional copy of the p53 gene using an engineered adenovirus.[57]

text: Certain pathogens can also affect the p53 protein that the TP53 gene expresses. One such example, human papillomavirus (HPV), encodes a protein, E6, which binds to the p53 protein and inactivates it. This mechanism, in synergy with the inactivation of the cell cycle regulator pRb by the HPV protein E7, allows for repeated cell division manifested clinically as warts. Certain HPV types, in particular types 16 and 18, can also lead to progression from a benign wart to low or high-grade cervical dysplasia, which are reversible forms of precancerous lesions. Persistent infection of the cervix over the years can cause irreversible changes leading to carcinoma in situ and eventually invasive cervical cancer. This results from the effects of HPV genes, particularly those encoding E6 and E7, which are the two viral oncoproteins that are preferentially retained and expressed in cervical cancers by integration of the viral DNA into the host genome.[58]

text: The p53 protein is continually produced and degraded in cells of healthy people, resulting in damped oscillation. The degradation of the p53 protein is associated with binding of MDM2. In a negative feedback loop, MDM2 itself is induced by the p53 protein. Mutant p53 proteins often fail to induce MDM2, causing p53 to accumulate at very high levels. Moreover, the mutant p53 protein itself can inhibit normal p53 protein levels. In some cases, single missense mutations in p53 have been shown to disrupt p53 stability and function.[59]

text: Suppression of p53 in human breast cancer cells is shown to lead to increased CXCR5 chemokine receptor gene expression and activated cell migration in response to chemokine CXCL13.[60]

text: One study found that p53 and Myc proteins were key to the survival of Chronic Myeloid Leukaemia (CML) cells. Targeting p53 and Myc proteins with drugs gave positive results on mice with CML.[61][62]

text: Experimental analysis of p53 mutations[edit]

text: Most p53 mutations are detected by DNA sequencing. However, it is known that single missense mutations can have a large spectrum from rather mild to very severe functional affects.[59]

text: The large spectrum of cancer phenotypes due to mutations in the TP53 gene is also supported by the fact that different isoforms of p53 proteins have different cellular mechanisms for prevention against cancer. Mutations in TP53 can give rise to different isoforms, preventing their overall functionality in different cellular mechanisms and thereby extending the cancer phenotype from mild to severe. Recents studies show that p53 isoforms are differentially expressed in different human tissues, and the loss-of-function or gain-of-function mutations within the isoforms can cause tissue-specific cancer or provides cancer stem cell potential in different tissues.[11][63][64][65] TP53 mutation also hits energy metabolism and increases glycolysis in breast cancer cells.[66]

text: The dynamics of p53 proteins, along with its antagonist Mdm2, indicate that the levels of p53, in units of concentration, oscillate as a function of time. This "damped" oscillation is both clinically documented [67] and mathematically modelled.[68][69] Mathematical models also indicate that the p53 concentration oscillates much faster once teratogens, such as double-stranded breaks (DSB) or UV radiation, are introduced to the system. This supports and models the current understanding of p53 dynamics, where DNA damage induces p53 activation (see p53 regulation for more information). Current models can also be useful for modelling the mutations in p53 isoforms and their effects on p53 oscillation, thereby promoting de novo tissue-specific pharmacological drug discovery.

text: Discovery[edit]

text: p53 was identified in 1979 by Lionel Crawford, David P. Lane, Arnold Levine, and Lloyd Old, working at Imperial Cancer Research Fund (UK) Princeton University/UMDNJ (Cancer Institute of New Jersey), and Memorial Sloan-Kettering Cancer Center, respectively. It had been hypothesized to exist before as the target of the SV40 virus, a strain that induced development of tumors. The TP53 gene from the mouse was first cloned by Peter Chumakov of the Russian Academy of Sciences in 1982,[70] and independently in 1983 by Moshe Oren in collaboration with David Givol (Weizmann Institute of Science).[71][72] The human TP53 gene was cloned in 1984[7] and the full length clone in 1985.[73]

text: It was initially presumed to be an oncogene due to the use of mutated cDNA following purification of tumor cell mRNA. Its role as a tumor suppressor gene was revealed in 1989 by Bert Vogelstein at the Johns Hopkins School of Medicine and Arnold Levine at Princeton University.[74][75]

text: Warren Maltzman, of the Waksman Institute of Rutgers University first demonstrated that TP53 was responsive to DNA damage in the form of ultraviolet radiation.[76] In a series of publications in 1991–92, Michael Kastan of Johns Hopkins University, reported that TP53 was a critical part of a signal transduction pathway that helped cells respond to DNA damage.[77]

text: In 1993, p53 was voted molecule of the year by Science magazine.[78]

text: Isoforms[edit]

text: As with 95% of human genes, TP53 encodes more than one protein. In 2005 several isoforms were discovered and until now, 12 human p53 isoforms were identified (p53α, p53β, p53γ, ∆40p53α, ∆40p53β, ∆40p53γ, ∆133p53α, ∆133p53β, ∆133p53γ, ∆160p53α, ∆160p53β, ∆160p53γ). Furthermore, p53 isoforms are expressed in a tissue dependent manner and p53α is never expressed alone.[11]

text: The full length p53 isoform proteins can be subdivided into different protein domains. Starting from the N-terminus, there are first the amino-terminal transactivation domains (TAD 1, TAD 2), which are needed to induce a subset of p53 target genes. This domain is followed by the Proline rich domain (PXXP), whereby the motif PXXP is repeated (P is a Proline and X can be any amino acid). It is required among others for p53 mediated apoptosis.[79] Some isoforms lack the Proline rich domain, such as Δ133p53β,γ and Δ160p53α,β,γ; hence some isoforms of p53 are not mediating apoptosis, emphasizing the diversifying roles of the TP53 gene.[63] Afterwards there is the DNA binding domain (DBD), which enables the proteins to sequence specific binding. The carboxyl terminal domain completes the protein. It includes the nuclear localization signal (NLS), the nuclear export signal (NES) and the oligomerisation domain (OD). The NLS and NES are responsible for the subcellular regulation of p53. Through the OD, p53 can form a tetramer and then bind to DNA. Among the isoforms, some domains can be missing, but all of them share most of the highly conserved DNA-binding domain.

text: The isoforms are formed by different mechanisms. The beta and the gamma isoforms are generated by multiple splicing of intron 9, which leads to a different C-terminus. Furthermore, the usage of an internal promoter in intron 4 causes the ∆133 and ∆160 isoforms, which lack the TAD domain and a part of the DBD. Moreover, alternative initiation of translation at codon 40 or 160 bear the ∆40p53 and ∆160p53 isoforms.[11]

text: Due to the isoformic nature of p53 proteins, there have been several sources of evidence showing that mutations within the TP53 gene giving rise to mutated isoforms are causative agents of various cancer phenotypes, from mild to severe, due to single mutation in the TP53 gene (refer to section Experimental analysis of p53 mutations for more details).

text: Interactions[edit]

text: p53 has been shown to interact with:

text:
AIMP2,[80]
ANKRD2,[81]
APTX,[82]
ATM,[83][84][85][86][87]
ATR,[83][84]
ATF3,[88][89]
AURKA,[90]
BAK1,[91]
BARD1,[92]
BLM,[93][94][95][96]
BRCA1,[92][97][98][99][100]
BRCA2,[92][101]
BRCC3,[92]
BRE,[92]
CEBPZ,[102]
CDC14A,[103]
Cdk1,[104][105]
CFLAR,[106]
CHEK1,[93][107][108]
CCNG1,[109]
CREBBP,[110][111][112]
CREB1,[112]
Cyclin H,[113]
CDK7,[113][114]
DNA-PKcs,[84][107][115]
E4F1,[116][117]
EFEMP2,[118]
EIF2AK2,[119]
ELL,[120]
EP300,[111][121][122][123]
ERCC6,[124][125]
GNL3,[126]
GPS2,[127]
GSK3B,[128]
HSP90AA1,[129][130][131]
HIF1A,[132][133][134][135]
HIPK1,[136]
HIPK2,[137][138]
HMGB1,[139][140]
HSPA9,[141]
Huntingtin,[142]
ING1,[143][144]
ING4,[145][146]
ING5,[145]
IκBα,[147]
KPNB1,[129]
LMO3,[26]
Mdm2,[110][148][149][150]
MDM4,[151][152]
MED1,[153][154]
MAPK9,[155][156]
MNAT1,[114]
NDN,[157]
NCL,[158]
NUMB,[159]
NF-κB,[160]
P16,[116][150][161]
PARC,[162]
PARP1,[82][163]
PIAS1,[118][164]
CDC14B,[103]
PIN1,[165][166]
PLAGL1,[167]
PLK3,[168][169]
PRKRA,[170]
PHB,[171]
PML,[148][172][173]
PSME3,[174]
PTEN,[149]
PTK2,[175]
PTTG1,[176]
RAD51,[92][177][178]
RCHY1,[179][180]
RELA,[160]
Reprimo[181]
RPA1,[182][183]
RPL11,[161]
S100B,[184]
SUMO1,[185][186]
SMARCA4,[187]
SMARCB1,[187]
SMN1,[188]
STAT3,[160]
TBP,[189][190]
TFAP2A,[191]
TFDP1,[192]
TIGAR,[193]
TOP1,[194][195]
TOP2A,[196]
TP53BP1,[93][197][198][199][200][201][202]
TP53BP2,[202][203]
TOP2B,[196]
TP53INP1,[204][205]
TSG101,[206]
UBE2A,[207]
UBE2I,[118][185][208][209]
UBC,[80][174][186][210][211][212][213][214]
USP7,[215]
WRN,[96][216]
WWOX,[217]
XPB,[124]
YBX1,[81][218]
YPEL3,[219]
YWHAZ,[220]
Zif268,[221]
ZNF148.[222]
SIRT1.[223]

text: Peto's paradox[edit]

text: Peto's paradox is the observation, due to Richard Peto, that at the species level, the incidence of cancer does not appear to correlate with the number of cells in an organism.[224] For example, the incidence of cancer in humans is much higher than the incidence of cancer in whales.[225] This is despite the fact that a whale has many more cells than a human. If the probability of carcinogenesis were constant across cells, one would expect whales to have a higher incidence of cancer than humans. The same is true of elephants. In October 2015, two independent studies showed that elephants have 20 copies of a tumor suppressor gene TP53 in their genome, where humans and other mammals have only one, thus providing a possible solution to the paradox.[226]


document_title: Miss Marple (TV series)

question_text: where was miss marple with joan hickson filmed

root

text: Miss Marple (TV series)

text: Background[edit]

text: Agatha Christie had never been very happy with most filmed adaptations of her works, and according to her grandson Mathew Pritchard, who handled her estate after her death, she "did not care much for television", either. Producer Pat Sandys of LWT first approached Pritchard and the Christie estate with a researched, detailed plan to film the novels Why Didn't They Ask Evans? and The Seven Dials Mystery in the early 1980s. Although indifferently treated by critics, the projects were popular with audiences and led to the filming of a number of short stories and the Tommy and Tuppence Beresford stories including The Secret Adversary and in the subsequent series Agatha Christie's Partners in Crime. With the success of that series, the BBC received approval to produce the stories of one of Christie's most famous detectives.[1]

tag: p

text: At the time the BBC was granted the screen rights to all 12 Marple novels, the rights to three already co-existed. The Mirror Crack'd From Side to Side had already been filmed and theatrically released in 1980 with Angela Lansbury in the role, and the same production company was in the process of filming A Caribbean Mystery and They Do It With Mirrors with Helen Hayes for television broadcast. Thus these three titles were the last to be dramatized under the BBC's agreement.

text: The adaptations are mainly true to the original novels. Joan Hickson, who played Miss Marple, was an octogenarian herself during most of the series' production. Decades before, she had appeared in a minor role in Murder, She Said, in which Margaret Rutherford played Miss Marple. Hickson had also appeared in a stage adaptation of the novel Appointment with Death in 1946, after which Christie sent Hickson a note that read, "I hope one day you will play my dear Miss Marple."[2]

text: Characters[edit]

text: Regular characters[edit]

text: In addition to Miss Marple, there are two semi-regular characters in the series. The first is Inspector (later Superintendent) Slack, played by David Horovitch; the second is Constable (later Sergeant) Lake, played by Ian Brimble. Slack and Lake appear in five episodes: "The Body in the Library", "The Murder at the Vicarage", "4.50 From Paddington", "They Do It with Mirrors" and "The Mirror Crack'd from Side to Side". They are the official detectives and both (particularly Slack) originally dislike and are exasperated by Miss Marple, her interference and her methods, but they eventually come to respect (and indeed, in the case of Lake, like) her.

text:
Inspector/Superintendent Slack (David Horovitch) – Slack is the senior officer in charge of many cases. He has been described as a man who has never striven more to contradict his name. Miss Marple describes him as having the same personality as that of a diesel engine, most unappealing, but efficient. When Slack first met Miss Marple, her strange personality and her quirky methods caused him to think she was batty, and thus took no notice of her. Slack especially disliked the fact that his superiors think highly of Miss Marple and consult her for advice (although he later ends up doing the same). Usually, Slack passes over Miss Marple's beliefs and dislikes her interfering, although he later comes to value her advice. In his final appearance, it is revealed that Slack has been promoted to Superintendent and appears to have grown wiser, even telling an officer to consult Miss Marple. In "They Do It with Mirrors" it is revealed that Slack has a secret passion for magic tricks, and secretly practices. Slack is featured in the novels The Murder at the Vicarage and The Body in the Library.
Constable/Sergeant Lake (Ian Brimble) – Lake is Slack's colleague and often works with him. He is also very bemused by Miss Marple, her quirky ways, her unusual methods and her claims of solving the cases based on trivial stories from her past. However, the difference was whilst Miss Marple annoyed Slack, Lake found her quite funny. By the time of They Do It With Mirrors, Lake is on friendly terms with Miss Marple and also reveals he has a young son called Adam. When Slack is promoted, Lake gets more roles in the art of criminal investigation but stays a Sergeant. Lake is featured in the novel They Do It with Mirrors.

tag: ul

text: Recurring characters[edit]

text: There are other recurring characters in Miss Marple. John Castle appears as Inspector Dermot Eric Craddock in "A Murder Is Announced" and "The Mirror Crack'd from Side to Side". Craddock was unknown to Miss Marple in the former story, but had become her nephew by the latter. Gwen Watford appears as Mrs Dolly Bantry in "The Body in the Library" and "The Mirror Crack'd from Side to Side". Barbara Hicks appears as Miss Amanda Hartnell in "The Murder at the Vicarage" and "The Mirror Crack'd from Side to Side". Christopher Good appears as Christopher Hawes in "The Murder at the Vicarage" and '"The Mirror Crack'd from Side to Side". Rhoda Lewis is village shopkeeper and postmistress Mrs Brogan in "A Pocketful of Rye", "4.50 from Paddington" and "The Mirror Crack'd from Side to Side".

text: Episodes[edit]

text:
#
Title
Airdate
Guest cast and synopsis
IMDb link

1
"The Body in the Library"
26, 27, 28 December 1984
Gwen Watford, Moray Watson, Trudie Styler, Jess Conrad, Ciaran Madden, Keith Drinkel, Debbie Arnold, Frederick Jaeger, Valentine Dyall, Raymond Francis, David Horovitch, Ian Brimble, Anthony Smee, Andrew Cruickshank, Hugh Walters, Arthur Bostrom, Martyn Read, Stephen Churchett, Astra Sheridan, John Moffatt
[3]

Set in June 1951, Miss Marple assists her neighbours the Bantrys when a lovely young girl is found dead in their library. The girl is traced to a seaside resort and the desperate family of a wealthy old man.

2
"The Moving Finger"
21, 22 February 1985
Michael Culver, Elizabeth Counsell, Richard Pearson, Sabina Franklyn, Andrew Bicknell, Hilary Mason, Dilys Hamlett, Deborah Appleby, John Arnatt, Sandra Payne, Martin Fisk, Imogen Bickford-Smith, Geoffrey Davion, Roger Ostime, Victor Maddern, Gordon Rollings, Patsy Smart, Gerald Sim
[4]

Poison pen letters are being sent to everyone in town. It seems like a vulgar joke until a letter is found next to a suicide victim. The village vicar's wife happens to be a personal friend of Miss Marple and asks her to come and discover the culprit. Then another body is found, this time clearly murder.

3
"A Murder Is Announced"
28 February, 1, 2 March 1985
Ursula Howells, Renée Asherson, Joan Sims, John Castle, Sylvia Syms, Ralph Michael, Paola Dionisotti, Samantha Bond, Simon Shepherd, Nicola King, Matthew Solon, Mary Kerridge, Vivienne Moore, David Collings, Elaine Ives-Cameron, Joyce Carey, Kevin Whately, Liz Crowther
[5]

Set on Friday October 5, 1951, when rationing was still ongoing in Britain. A party game goes wrong and a young Swiss man is dead. Friends and neighbours start to turn on each other, and Inspector Craddock is stumped. Fortunately, Miss Marple is in town visiting her niece and helps solve the crime.

4
"A Pocketful of Rye"
7, 8 March 1985
Peter Davison, Timothy West, Stacy Dorning, Annette Badland, Fabia Drake, Clive Merrison, Rachel Bell, Selina Cadell, Tom Wilkinson, Frances Low, Susan Gilmore, Frank Mills, Louis Mahoney, Rhoda Lewis, Charles Pemberton
[6]

Set in October 1949. The members of a wealthy banking family start dropping like flies, and Miss Marple is reminded of the old nursery rhyme Sing a Song of Sixpence and vows to find the villainous "blackbird" behind the crimes.

5
"The Murder at the Vicarage"
25 December 1986
Paul Eddington, Cheryl Campbell, Robert Lang, Polly Adams, Tara MacGowran, James Hazeldine, Jack Galloway, Rosalie Crutchley, Norma West, Christopher Good, Rachel Weaver
[7]

Set in spring of 1954 or 1955. Death is only steps from Miss Marple when odious magistrate Colonel Protheroe is murdered in her idyllic village of St. Mary Mead—in the Vicar's study, no less.

6
"Sleeping Murder"
11, 18 January 1987
Geraldine Alexander, John Moulder-Brown, Jean Anderson, Terrence Hardiman, Frederick Treves, John Bennett, Geraldine Newman, Jack Watson, Jean Heywood, Amanda Boxer, John Ringham, David McAlister, Kenneth Cope, Gary Watson, Donald Burton, Sheila Raynor, Peter Spraggon
[8]

A young wife, Gwenda, believes her house is haunted. With Miss Marple's guidance, she comes to realize she witnessed the murder of her stepmother there 20 years ago, as a child. Despite Miss Marple's advice to let sleeping murder lie, the newlyweds decide to investigate the crime, in the process putting Gwenda's own life at risk.

7
"At Bertram's Hotel"
25 January; 1 February 1987
Caroline Blakiston, Joan Greenwood, George Baker, James Cossins, Helena Michell, Irene Sutcliffe, Preston Lockwood, Edward Burnham, Donald Burton, Peter Baldwin
[9]

Set shortly after May 1956, when Elvis Presley's Heartbreak Hotel was released in Britain. False identities, larceny, and a crime ring are only the tip of the tentacle when Miss Marple stays in a posh London hotel (modeled after Brown's Hotel) where nothing is what it seems. Murder naturally follows, leading to a thrilling chase after the culprit.

8
"Nemesis"
8, 15 February 1987
Margaret Tyzack, John Horsley, Anna Cropper, Valerie Lush, Helen Cherry, Peter Tilbury, Liz Fraser, Bruce Payne, Joanna Hole, Jane Booker, Alison Skilbeck, Frank Gatliff, Peter Copley, Roger Hammond, David Blake Kelly, Cy Town
[10]

Set in August 1955. Miss Marple is sent on a mission from beyond the grave to clear a dead man's son. Vowing to find out the truth, she links him to a dead girl, Verity Hunt, and a family of weird sisters. She discovers love, as well as hate, can be a reason for murder.

9
"4.50 from Paddington"
25 December 1987
Maurice Denham, Joanna David, Jill Meager, Andrew Burt, Jean Boht, John Hallam, Mona Bruce, Rhoda Lewis, Richard Ashley, David Beames, David Waller, Will Tacey
[11]

Set (beginning) on October 4, 1957, when the Soviet Union launched Sputnik. Miss Marple's friend witnesses a murder in a railway carriage running parallel to her own, so Miss Marple engages a resourceful young woman to investigate. The search leads to a decrepit estate, where they suspect the body was dumped. But the seemingly innocent family who live there have secrets of their own.

10
"A Caribbean Mystery"
25 December 1989
Donald Pleasence, Sophie Ward, Adrian Lukis, T. P. McKenna, Frank Middlemass, Sue Lloyd, Robert Swan, Michael Feast, Sheila Ruskin, Joseph Mydell, Barbara Barnes, Valerie Buchanan
[12]

Set (beginning) on 8 February 1951. While holidaying in Barbados (the Caribbean island of St. Honoré in the original novel), Miss Marple hears a lot of stories by a dotty Major who tells tall tales of knowing a murderer. But when the Major turns up dead, the wild beauty of the island can't hide the trail of a manipulative and ruthless killer.

11
"They Do It with Mirrors"
29 December 1991
Jean Simmons, Joss Ackland, Faith Brook, Holly Aird, Christopher Villiers, Brenda Cowling
[13]

At an estate turned reformatory school, Miss Marple visits her old school chum Carrie Louise. When Carrie Louise's dear stepson is killed, the discontent family is only the beginning as there are literally hundreds of suspects!

12
"The Mirror Crack'd from Side to Side"
27 December 1992
Claire Bloom, Barry Newman, Gwen Watford, John Castle, Elizabeth Garvie, Judy Cornwell, Glynis Barber, Christopher Hancock, Rose Keegan, Anna Niland, Ian Brimble, Amanda Elwes, Christopher Good, Rhoda Lewis, Jon Croft, Margaret Courtenay
[14]

Set in the summer of 1959. Hollywood comes to St. Mary Mead when faded movie star Marina Gregg takes up residence for a local film shoot. But when she narrowly escapes an attempt on her life and a local woman dies instead, Miss Marple sorts the gossip rag chatter from the facts to uncover a tragedy.

tag: table

text: Production[edit]

text: BBC producer Guy Slater cast Joan Hickson as Miss Marple. The series was filmed beginning in 1983 in areas including Norfolk, Devon, Oxfordshire and Barbados. The town of Nether Wallop, Hampshire doubled as Miss Marple's home village of St. Mary Mead. Slater was replaced by producer George Gallaccio starting with the fourth film. "The Murder at the Vicarage" is set in 1954, "Nemesis" is set in 1955 or 1956, "At Bertram's Hotel" in 1956, and "4.50 from Paddington" is set in 1957.

text: Hickson vowed not to do another film after 1989's "A Caribbean Mystery", but was persuaded to return for the final two films in 1991 and 1992. "A Caribbean Mystery" was shot on location at the Coral Reef Hotel in Barbados, where Christie had stayed in her visit to the country, and which had been the inspiration for the setting of the novel. Owners Budge and Cynthia O'Hara, who still owned the hotel 30 years later, were the inspirations for the characters in the novel and were able to share a treasure trove of Christie memorabilia with the cast.[2]

text: The evocative theme tune for the TV series was composed by Ken Howard and Alan Blaikley. The series opening titles featured paintings of seemingly pleasant village life, darkened by suspicious looking characters and the shot of a murder victim behind a cricket sight screen. Gossipy women were made to look like they were hiding secrets, whilst the vicar appeared to be hiding in the shadows. Initially, these paintings were black and white. In later episodes, new, colour drawings replaced these, though they still depicted suspicious looking villagers in the surroundings.

text: Adaptations of the books A Caribbean Mystery (1964) and Nemesis (1971) were filmed out of order. "Nemesis" was produced in February 1987 and "A Caribbean Mystery" in December 1989. The significance of this is the character Jason Rafiel, who is introduced in A Caribbean Mystery and in Nemesis has died and made a request of Miss Marple to solve a years-old mystery. Because the two episodes were filmed out of order, viewers of "Nemesis" are clueless as to what part Jason Rafiel played in Miss Marple's life until they watch "A Caribbean Mystery". Rafiel was portrayed by Frank Gatliff in "Nemesis", and by Donald Pleasence in "A Caribbean Mystery".

text: The character of Inspector Craddock presents another inconsistency in the series. The character is clearly unknown to Miss Marple in "A Murder is Announced" but in his second and final appearance in "The Mirror Crack'd from Side to Side", Craddock is Miss Marple's nephew.

text: Reception[edit]

text: The first episode was enthusiastically received by critics. The Times said "once hooked, you won't be able to turn off", and The Sun said it was a series "with pulling power and real class". For episode two, "The Moving Finger", The Daily Telegraph stated "Once again Guy Slater's production is built around the brilliant performance of Joan Hickson, behind whose faded blue eyes and spinsterish sibilants, the wheels of detective intelligence can be seen positively whirring around. The enterprise is impeccably cast, beautifully ordered, lovingly photographed." Reviews for subsequent films were equally positive.[2]

text: Alan McKee, of the Museum of Broadcast Communications, reviews the series as "a good example of a 'heritage' production", popular in the 1980s. It combines new Victorianism in moral standards and a sanitised version of England's past. Mostly set in a rural past, English architecture and country mansion houses are featured. Like many BBC programmes, production values are impeccable and costumes, houses and decor, cars, hairstyles and make-up could all be described as "sumptuous".[15]

text: McKee also praises the series for "being as faithful as possible to the source material. Miss Marple does not chase the villains herself as Margaret Rutherford does in her film series, nor are the titles of the books altered to make them more sensational."[15]

text: As for Hickson personally, she is frequently described as the "definitive" Miss Marple as Christie would have pictured her, and Hickson personally credited in large part the bestowal of an OBE award to the role, as Queen Elizabeth II was a fan of the series and Hickson's performance.[2]

text: Other countries[edit]

text: All 12 episodes were shown in the United States on the PBS Mystery! series. Miss Marple was also seen in over 30 countries, including Spain, the former Soviet Union and China.

text: Home media[edit]

text: Miss Marple was first released in DVD in the UK (Region 2) in 2000. A complete box set of all 12 stories was released in 2005 by 2 Entertain Video. In North America (Region 1), episodes were first released in 2001.

text: In summer 2009 the Sunday edition of the Greek newspaper Kathimerini was offering to its readers DVDs (one per week) of the series.

text: In January 2010, the Daily Mail offered six DVDs (from 2 Entertain Video) each with a complete episode from series. The episodes in the DVD giveaway offer were "The Murder at the Vicarage", "Sleeping Murder", "At Bertram's Hotel", "Nemesis", "A Caribbean Mystery", and "They Do It with Mirrors".

text: To mark the 30th anniversary of the series, BBC Home Entertainment fully remastered the series for release on DVD and, for the first time, on Blu-ray Disc.[16] The series was released in three volumes. Miss Marple: Volume One, released on 28 October 2014, included the episodes "The Body in the Library", "A Murder Is Announced", "The Moving Finger," and "Murder at the Vicarage" and the first part of the three-part documentary special, "A Very British Murder, Part 1: A New Taste for Blood".[17] Miss Marple: Volume Two, released on 31 March 2015, included the episodes "They Do It with Mirrors", "The Mirror Crack’d from Side to Side", "4.50 from Paddington", and "A Pocketful of Rye" along with the bonus material "A Very British Murder, Part 2: Detection Most Ingenious".[18] Miss Marple: Volume Three, released on 9 June 2015, included the episodes "A Caribbean Mystery", "At Bertram’s Hotel", " Sleeping Murder", and "Nemesis" along with the bonus material "A Very British Murder, Part 3: The Golden Age".[19]


document_title: List of Los Angeles Chargers seasons

question_text: when was the last time chargers made playoffs

text: List of Los Angeles Chargers seasons

text:
This article is part of series of

Los Angeles Chargers history

Los Angeles Chargers (1960)

San Diego Chargers (1961–2016)

Los Angeles Chargers (2017–present)

List of seasons

v
t
e

text: The Los Angeles Chargers are a professional American football franchise based in the Greater Los Angeles Area. The Chargers compete in the National Football League (NFL) as a member club of the league's American Football Conference (AFC) West division. The club was founded in 1959 by Barron Hilton and played the 1960 season in Los Angeles as part of the American Football League (AFL). In the next season, the Chargers moved to San Diego.[1] In 2017, the Chargers relocated back to the Los Angeles area.

text: The franchise has experienced three major periods of success. The first was from 1960 to 1965, when the Chargers were AFL West champions five times and AFL champions once. The second was from 1978 to 1982, when the Chargers had winning seasons (seasons with more wins than losses) in each of these years, and won three consecutive division championships for the second time in franchise history. The most recent accomplishments range from 2004 to 2009, with the franchise reaching the playoffs five times in six years. Their only Super Bowl appearance was in 1994.

text: The Chargers have experienced three notable periods of decline. Between 1970 and 1977, the Chargers never won more games than they lost as part of a 13-year period without playing in the postseason, including four consecutive years last in their division from 1972 to 1975, in which year they bottomed out before two late wins avoided the NFL's first 0–14 season. From 1983 to 1991, they never placed higher than third in their division and did not make the playoffs. From 1996 to 2003, the team had no winning seasons, and had their worst season ever, winning only one of 16 games in 2000.[2]

text: The Chargers have been division champions nine times including 2009, all of them in the AFC West. They have been conference champions six times, but only once since the AFL-NFL merger in 1970. As of the end of the 2010 season, the Chargers had played 787 regular and post-season games in 51 seasons, and have appeared in the post-season 16 times.[2]

text: Seasons

text:
AFL Champions (1960–1969)
Conference Champions
Division Champions
Wild Card Berth

text:
Season
Team
League
Conference
Division
Regular season
Postseason results
Awards
Head coaches

Finish
Wins
Losses
Ties

Los Angeles Chargers

1960
1960
AFL

West
1st
10
4
0
Lost AFL Championship (at Oilers) 16–24

Sid Gillman

San Diego Chargers

1961
1961
AFL

West
1st
12
2
0
Lost AFL Championship (Oilers) 3–10

Sid Gillman

1962
1962
AFL

West
3rd
4
10
0

Earl Faison (ASG MVP)
Sid Gillman

1963
1963
AFL

West
1st
11
3
0
Won AFL Championship (1) (Patriots) 51–10
Lance Alworth (MVP)
Keith Lincoln (ASG MVP)
Sid Gillman

1964
1964
AFL

West
1st
8
5
1
Lost AFL Championship (at Bills) 7–20
Keith Lincoln (ASG MVP)
Sid Gillman

1965
1965
AFL

West
1st
9
2
3
Lost AFL Championship (Bills) 0–23
Frank Buncom (ASG MVP)
Sid Gillman

1966
1966
AFL

West
3rd
7
6
1

Sid Gillman

1967
1967
AFL

West
3rd
8
5
1

Speedy Duncan (ASG MVP)
Sid Gillman

1968
1968
AFL

West
3rd
9
5
0

Sid Gillman

1969
1969
AFL

West
3rd
8
6
0

John Hadl (ASG MVP)
Charlie Waller

1970[A]
1970
NFL
AFC
West
3rd
5
6
3

Charlie Waller

1971
1971
NFL
AFC
West
3rd
6
8
0

Harland Svare (2–2)
Sid Gillman (4–6)

1972
1972
NFL
AFC
West
4th
4
9
1

Harland Svare

1973
1973
NFL
AFC
West
4th
2
11
1

Harland Svare (1–6–1)
Ron Waller (1–5)

1974
1974
NFL
AFC
West
3rd
5
9
0

Don Woods (OROY)
Tommy Prothro

1975
1975
NFL
AFC
West
4th
2
12
0

Tommy Prothro

1976
1976
NFL
AFC
West
3rd
6
8
0

Tommy Prothro

1977
1977
NFL
AFC
West
3rd
7
7
0

Tommy Prothro

1978
1978[B]
NFL
AFC
West
3rd
9
7
0

Tommy Prothro (1–3)
Don Coryell (8–4)

1979
1979
NFL
AFC
West
1st
12
4
0
Lost Divisional Playoffs (Oilers) 14–17

Don Coryell

1980
1980
NFL
AFC
West
1st[C]
11
5
0
Won Divisional Playoffs (Bills) 20–14
Lost AFC Championship (Raiders) 27–34

Don Coryell

1981
1981
NFL
AFC
West
1st[D]
10
6
0
Won Divisional Playoffs (at Dolphins) 41–38 (OT)[E]
Lost AFC Championship (at Bengals)[F] 7–27
Kellen Winslow (PB MVP)
Don Coryell

1982[G]
1982
NFL
AFC

6th
6
3
0
Won First-Round Playoffs (at Steelers) 31–28
Lost Second-Round Playoffs (at Dolphins) 13–34
Dan Fouts (OPOY,
PB MVP)
Don Coryell

1983
1983
NFL
AFC
West
5th
6
10
0

Don Coryell

1984
1984
NFL
AFC
West
5th
7
9
0

Don Coryell

1985
1985
NFL
AFC
West
3rd
8
8
0

Don Coryell

1986
1986
NFL
AFC
West
5th
4
12
0

Leslie O'Neal (DROY)
Don Coryell (1–7)
Al Saunders (3–5)

1987[H]
1987
NFL
AFC
West
3rd
8
7
0

Dan Henning

1988
1988
NFL
AFC
West
4th
6
10
0

Dan Henning

1989
1989
NFL
AFC
West
5th
6
10
0

Dan Henning

1990
1990
NFL
AFC
West
4th
6
10
0

Bobby Ross

1991
1991
NFL
AFC
West
5th
4
12
0

Bobby Ross

1992
1992
NFL
AFC
West
1st
11
5
0
Won Wild Card Playoffs (Chiefs) 17–0
Lost Divisional Playoffs (at Dolphins) 0–31

Bobby Ross

1993
1993
NFL
AFC
West
4th
8
8
0

Bobby Ross

1994
1994
NFL
AFC
West
1st
11
5
0
Won Divisional Playoffs (Dolphins) 22–21
Won AFC Championship (at Steelers) 17–13
Lost Super Bowl XXIX (vs. 49ers) 26–49

Bobby Ross

1995
1995
NFL
AFC
West
2nd
9
7
0
Lost Wild Card Playoffs (Colts) 20–35

Bobby Ross

1996
1996
NFL
AFC
West
3rd
8
8
0

Bobby Ross

1997
1997
NFL
AFC
West
5th
4
12
0

Kevin Gilbride

1998
1998
NFL
AFC
West
5th
5
11
0

Kevin Gilbride (2–4)
June Jones (3–7)

1999
1999
NFL
AFC
West
4th
8
8
0

Mike Riley

2000
2000
NFL
AFC
West
5th
1
15
0

Mike Riley

2001
2001
NFL
AFC
West
5th
5
11
0

Mike Riley

2002
2002
NFL
AFC
West
3rd
8
8
0

Marty Schottenheimer

2003
2003
NFL
AFC
West
4th
4
12
0

Marty Schottenheimer

2004
2004
NFL
AFC
West
1st
12
4
0
Lost Wild Card Playoffs (Jets) 17–20 (OT)
Marty Schottenheimer (COY)
Drew Brees (CBPOY)
Marty Schottenheimer

2005
2005
NFL
AFC
West
3rd
9
7
0

Shawne Merriman (DROY)
Marty Schottenheimer

2006
2006
NFL
AFC
West
1st
14
2
0
Lost Divisional Playoffs (Patriots) 21–24
LaDainian Tomlinson (MVP, OPOY)
Marty Schottenheimer

2007
2007
NFL
AFC
West
1st
11
5
0
Won Wild Card Playoffs (Titans) 17–6
Won Divisional Playoffs (at Colts) 28–24
Lost AFC Championship (at Patriots) 12–21

Norv Turner

2008
2008
NFL
AFC
West
1st
8
8
0
Won Wild Card Playoffs (Colts) 23–17 (OT)
Lost Divisional Playoffs (at Steelers) 24–35

Norv Turner

2009
2009
NFL
AFC
West
1st
13
3
0
Lost Divisional Playoffs (Jets) 14–17

Norv Turner

2010
2010
NFL
AFC
West
2nd
9
7
0

Norv Turner

2011
2011
NFL
AFC
West
2nd
8
8
0

Norv Turner

2012
2012
NFL
AFC
West
2nd
7
9
0

Norv Turner

2013
2013
NFL
AFC
West
3rd
9
7
0
Won Wild Card Playoffs (at Bengals) 27–10
Lost Divisional Playoffs (at Broncos) 17–24
Philip Rivers (CBPOY)
Mike McCoy

2014
2014
NFL
AFC
West
3rd
9
7
0

Mike McCoy

2015
2015
NFL
AFC
West
4th
4
12
0

Mike McCoy

2016
2016
NFL
AFC
West
4th
5
11
0

Joey Bosa (DROY)
Mike McCoy

Los Angeles Chargers

2017
2017
NFL
AFC
West
2nd
9
7
0

Keenan Allen (CBPOY)
Anthony Lynn

Total
435
438
11
(1960–2017, Regular season only)

11
17
—
(1960–2017, Post-season games only)

446
455
11
(1960–2017, Total for all games; 1 AFL Championship, 3 NFL Titles)

text: Footnotes

text:
A As a result of the AFL-NFL merger, the league was broken into two conferences; the AFL teams moved into the American Football Conference.
B This season included the Holy Roller game.
C The Chargers finished ahead of Oakland in the AFC West based on better net points in division games.
D The Chargers finished ahead of the Denver Broncos based on better divisional record.
E This game is known as The Epic in Miami.
F This game was known as the Freezer Bowl.
G The 1982 season was shortened by a strike, so the league was divided up into two conferences instead of its normal divisional alignment.
H The strike of 1987 reduced the regular season schedule from 16 to 15 games.


document_title: Impeachment in the United States

question_text: what power does the senate have in impeachment

text: Impeachment in the United States

text: Federal impeachment[edit]

text: House of Representatives[edit]

text: Impeachment proceedings may be commenced by a member of the House of Representatives on her or his own initiative, either by presenting a list of the charges under oath, or by asking for referral to the appropriate committee. The impeachment process may be initiated by non-members. For example, when the Judicial Conference of the United States suggests a federal judge be impeached, a charge of actions constituting grounds for impeachment may come from a special prosecutor, the President, or state or territorial legislature, grand jury, or by petition.

text: The type of impeachment resolution determines the committee to which it is referred. A resolution impeaching a particular individual is typically referred to the House Committee on the Judiciary. A resolution to authorize an investigation regarding impeachable conduct is referred to the House Committee on Rules, and then to the Judiciary Committee. The House Committee on the Judiciary, by majority vote, will determine whether grounds for impeachment exist. If the Committee finds grounds for impeachment, it will set forth specific allegations of misconduct in one or more articles of impeachment. The Impeachment Resolution, or Article(s) of Impeachment, are then reported to the full House with the committee's recommendations.

text: The House debates the resolution and may at the conclusion consider the resolution as a whole or vote on each article of impeachment individually. A simple majority of those present and voting is required for each article or the resolution as a whole to pass. If the House votes to impeach, managers (typically referred to as "House managers", with a "lead House manager") are selected to present the case to the Senate. Recently, managers have been selected by resolution, while historically the House would occasionally elect the managers or pass a resolution allowing the appointment of managers at the discretion of the Speaker of the United States House of Representatives. These managers are roughly the equivalent of the prosecution/district attorney in a standard criminal trial.

text: Also, the House will adopt a resolution in order to notify the Senate of its action. After receiving the notice, the Senate will adopt an order notifying the House that it is ready to receive the managers. The House managers then appear before the bar of the Senate and exhibit the articles of impeachment. After the reading of the charges, the managers return and make a verbal report to the House.

text: Senate[edit]

text: The proceedings unfold in the form of a trial, with each side having the right to call witnesses and perform cross-examinations. The House members, who are given the collective title of managers during the course of the trial, present the prosecution case, and the impeached official has the right to mount a defense with his own attorneys as well. Senators must also take an oath or affirmation that they will perform their duties honestly and with due diligence. After hearing the charges, the Senate usually deliberates in private. The U.S. Constitution requires a two-thirds majority for conviction.

text: The Senate enters judgment on its decision, whether that be to convict or acquit, and a copy of the judgment is filed with the Secretary of State.[4] Upon conviction in the Senate, the official is automatically removed from office and may also be barred from holding future office.[5] The removed official is also liable to criminal prosecution. The President may not grant a pardon in the impeachment case, but may in any resulting criminal case.

text: Beginning in the 1980s with Harry E. Claiborne, the Senate began using "Impeachment Trial Committees" pursuant to Senate Rule XI.[6] These committees presided over the evidentiary phase of the trials, hearing the evidence and supervising the examination and cross-examination of witnesses. The committees would then compile the evidentiary record and present it to the Senate; all senators would then have the opportunity to review the evidence before the chamber voted to convict or acquit. The purpose of the committees was to streamline impeachment trials, which otherwise would have taken up a great deal of the chamber's time. Defendants challenged the use of these committees, claiming them to be a violation of their fair trial rights as well as the Senate's constitutional mandate, as a body, to have "sole power to try all impeachments." Several impeached judges sought court intervention in their impeachment proceedings on these grounds, but the courts refused to become involved due to the Constitution's granting of impeachment and removal power solely to the legislative branch, making it a political question.

text: History[edit]

text: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2016) (Learn how and when to remove this template message)

text: In the United Kingdom, impeachment was a procedure whereby a member of the House of Commons could accuse someone of a crime. If the Commons voted for the impeachment, a trial would then be held in the House of Lords. Unlike a bill of attainder, a law declaring a person guilty of a crime, impeachments did not require royal assent, so they could be used to remove troublesome officers of the Crown even if the monarch was trying to protect them.

text: The monarch, however, was above the law and could not be impeached, or indeed judged guilty of any crime. When King Charles I was tried before the Rump Parliament of the New Model Army in 1649 he denied that they had any right to legally indict him, their king, whose power was given by God and the laws of the country, saying: "no earthly power can justly call me (who is your King) in question as a delinquent … no learned lawyer will affirm that an impeachment can lie against the King." While the House of Commons pronounced him guilty and ordered his execution anyway, the jurisdictional issue tainted the proceedings.

text: With this example in mind, the delegates to the Philadelphia Convention chose to include an impeachment procedure in Article II, Section 4 of the Constitution which could be applied to any government official; they explicitly mentioned the President to ensure there would be no ambiguity. Opinions differed, however, as to the reasons Congress should be able to initiate an impeachment. Initial drafts listed only treason and bribery, but George Mason favored impeachment for "maladministration" (incompetence). James Madison argued that impeachment should only be for criminal behavior, arguing that a maladministration standard would effectively mean that the President would serve at the pleasure of the Senate.[7] Thus the delegates adopted a compromise version allowing impeachment for "treason, bribery and other high crimes and misdemeanors."

text: The precise meaning of the phrase "high crimes and misdemeanors" is somewhat ambiguous; some scholars, such as Kevin Gutzman, argue that it can encompass even non-criminal abuses of power. Whatever its theoretical scope, however, Congress traditionally regards impeachment as a power to use only in extreme cases. The House of Representatives has actually initiated impeachment proceedings 62 times since 1789.[citation needed] Two cases did not come to trial because the individuals had left office.

text: Actual impeachments of 19 federal officers have taken place. Of these, 15 were federal judges: thirteen district court judges, one court of appeals judge (who also sat on the Commerce Court), and one Supreme Court Associate Justice. Of the other four, two were Presidents, one was a Cabinet secretary, and one was a U.S. Senator. Of the 19 impeached officials, eight were convicted. One, former judge Alcee Hastings, was elected as a member of the United States House of Representatives after being removed from office.

text: The 1797 impeachment of Senator William Blount of Tennessee stalled on the grounds that the Senate lacked jurisdiction over him. No other member of Congress has ever been impeached. The Constitution does give authority to the Senate and House, so that each body may expel its own members. (see List of United States senators expelled or censured and List of United States Representatives expelled, censured, or reprimanded). Expulsion removes the individual from functioning as a representative or senator because of their misbehavior, but unlike impeachment, expulsion cannot result in barring an individual from holding future office.

text: Federal officials impeached[edit]

text:
#
Date of Impeachment
Accused
Office
Accusation(s)
Result[Note 1]
References

1
July 7, 1797

William Blount

United States Senator (Tennessee)
Conspiring to assist Britain in capturing Spanish territory
Senate refused to accept impeachment of a Senator by the House of Representatives, instead expelling him from the Senate on their own authority[8][Note 2]
[9]

2
March 2, 1803

John Pickering

Judge (District of New Hampshire)
Drunkenness and unlawful rulings
Removed on March 12, 1804[8][10]
[9][10]

3
March 12, 1804

Samuel Chase

Associate Justice (Supreme Court of the United States)
Political bias and arbitrary rulings, promoting a partisan political agenda on the bench [11]
Acquitted on March 1, 1805
[8][10]

4
April 24, 1830

James H. Peck

Judge (District of Missouri)
Abuse of power[12]
Acquitted on January 31, 1831[8][10]
[9][10]

5
May 6, 1862

West Hughes Humphreys

Judge (Eastern, Middle, and Western Districts of Tennessee)
Supporting the Confederacy
Removed and disqualified on June 26, 1862[9][8][10]
[9][10]

6
February 24, 1868

Andrew Johnson

President of the United States
Violating the Tenure of Office Act
Acquitted on May 26, 1868[8]
[9]

7
February 28, 1873

Mark W. Delahay

Judge (District of Kansas)
Drunkenness
Resigned on December 12, 1873[10][13]
[10][13]

8
March 2, 1876

William W. Belknap

United States Secretary of War
Graft/corruption
Acquitted after his resignation on August 1, 1876.[8]
[9]

9
December 13, 1904

Charles Swayne

Judge (Northern District of Florida)
Failure to live in his district, abuse of power[14]
Acquitted on February 27, 1905[8][10]
[9][10]

10
July 11, 1912

Robert Wodrow Archbald

Associate Justice (United States Commerce Court)
Judge (Third Circuit Court of Appeals)
Improper acceptance of gifts from litigants and attorneys
Removed and disqualified on January 13, 1913[9][8][10]
[9][10]

11
April 1, 1926

George W. English

Judge (Eastern District of Illinois)
Abuse of power
Resigned on November 4, 1926,[9][8] proceedings dismissed on December 13, 1926[9][10]
[9][10]

12
February 24, 1933

Harold Louderback

Judge (Northern District of California)
Corruption
Acquitted on May 24, 1933[8][10]
[9][10]

13
March 2, 1936

Halsted L. Ritter

Judge (Southern District of Florida)
Champerty/corruption, tax evasion, practicing law while a judge
Removed on April 17, 1936[8][10]
[9][10]

14
July 22, 1986

Harry E. Claiborne

Judge (District of Nevada)
Tax evasion
Removed on October 9, 1986[8][10]
[9][10]

15
August 3, 1988

Alcee Hastings

Judge (Southern District of Florida)
Accepting a bribe, and committing perjury during the resulting investigation
Removed on October 20, 1989[8][10]
[9][10]

16
May 10, 1989

Walter Nixon

Chief Judge (Southern District of Mississippi)
Perjury
Removed on November 3, 1989[8][10][Note 3]
[9][10]

17
December 19, 1998

Bill Clinton

President of the United States
Perjury and obstruction of justice
Acquitted on February 12, 1999[8]
[9]

18
June 19, 2009

Samuel B. Kent

Judge (Southern District of Texas)
Sexual assault, and obstruction of justice during the resulting investigation
Resigned on June 30, 2009,[10][15] proceedings dismissed on July 22, 2009[8][10][16]
[10][17]

19
March 11, 2010

Thomas Porteous

Judge (Eastern District of Louisiana)
Making false financial disclosures
Removed and disqualified on December 8, 2010[8][10][18]
[10][19]

text: Demands for impeachment[edit]

text: While the actual impeachment of a federal public official is a rare event, demands for impeachment, especially of presidents, are common,[20][21] going back to the administration of George Washington in the mid-1790s. In fact, most of the 63 resolutions mentioned above were in response to presidential actions.

text: While almost all of them were for the most part frivolous and were buried as soon as they were introduced, several did have their intended effect. Treasury Secretary Andrew Mellon[22] and Supreme Court Justice Abe Fortas both resigned in response to the threat of impeachment hearings, and, most famously, President Richard Nixon resigned from office after the House Judiciary Committee had already reported articles of impeachment to the floor.

text: Impeachment in the states[edit]

text: State legislatures can impeach state officials, including governors. The court for the trial of impeachments may differ somewhat from the federal model—in New York, for instance, the Assembly (lower house) impeaches, and the State Senate tries the case, but the members of the seven-judge New York State Court of Appeals (the state's highest, constitutional court) sit with the senators as jurors as well.[23] Impeachment and removal of governors has happened occasionally throughout the history of the United States, usually for corruption charges. A total of at least eleven U.S. state governors have faced an impeachment trial; a twelfth, Governor Lee Cruce of Oklahoma, escaped impeachment conviction by a single vote in 1912. Several others, most recently Connecticut's John G. Rowland, have resigned rather than face impeachment, when events seemed to make it inevitable.[24] The most recent impeachment of a state governor occurred on January 14, 2009, when the Illinois House of Representatives voted 117-1 to impeach Rod Blagojevich on corruption charges;[25] he was subsequently removed from office and barred from holding future office by the Illinois Senate on January 29. He was the eighth U.S. state governor to be removed from office.

text: The procedure for impeachment, or removal, of local officials varies widely. For instance, in New York a mayor is removed directly by the governor "upon being heard" on charges—the law makes no further specification of what charges are necessary or what the governor must find in order to remove a mayor.

text: State and territorial officials impeached[edit]

text:
Date
Accused
Office
Result

1804

William W. Irvin

Associate Judge, Fairfield County, Ohio Court of Common Pleas
Removed

1832

Theophilus W. Smith

Associate Justice, Illinois Supreme Court
Acquitted[26]

February 26, 1862

Charles L. Robinson

Governor of Kansas
Acquitted[27]

February 26, 1862

John Winter Robinson

Secretary of State of Kansas
Removed on June 12, 1862[28]

February 26, 1862

George S. Hillyer

Kansas State auditor
Removed on June 16, 1862[28]

1871

William Woods Holden

Governor of North Carolina
Removed

1871

David Butler

Governor of Nebraska
Removed[27]

February 1872

Harrison Reed

Governor of Florida
Acquitted[29]

1872

Henry C. Warmoth

Governor of Louisiana
"suspended from office," though trial was not held[30]

1876

Adelbert Ames

Governor of Mississippi
Resigned[27]

1888

James W. Tate

Kentucky State Treasurer
Removed

1901

David M. Furches

Chief Justice, North Carolina Supreme Court
Acquitted[31]

1901

Robert M. Douglas

Associate Justice, North Carolina Supreme Court
Acquitted[31]

August 13, 1913[32]

William Sulzer

Governor of New York
Removed on October 17, 1913[33]

July 1917

James E. Ferguson

Governor of Texas
Removed[34]

October 23, 1923

John C. Walton

Governor of Oklahoma
Removed

January 21, 1929

Henry S. Johnston

Governor of Oklahoma
Removed

April 6, 1929[35]

Huey P. Long

Governor of Louisiana
Acquitted

May 1958[36]

Raulston Schoolfield

Judge, Hamilton County, Tennessee Criminal Court
Removed on July 11, 1958[37]

March 14, 1984[38]

Paul Douglas

Nebraska Attorney General
Acquitted by the Nebraska Supreme Court on May 4, 1984[39]

February 6, 1988[40]

Evan Mecham

Governor of Arizona
Removed on April 4, 1988[41]

March 30, 1989[42]

A. James Manchin

West Virginia State treasurer
Resigned on July 9, 1989 before trial started[43]

January 25, 1991[44]

Ward "Butch" Burnette

Kentucky Commissioner of Agriculture
Resigned on February 6, 1991 before trial started[45]

May 24, 1994[46]

Rolf Larsen

Associate Justice, Pennsylvania Supreme Court
Removed on October 4, 1994, and declared ineligible to hold public office in Pennsylvania[47]

October 6, 1994[48]

Judith Moriarty

Secretary of State of Missouri
Removed by the Missouri Supreme Court on December 12, 1994[49]

November 11, 2004[50]

Kathy Augustine

Nevada State Controller
Censured on December 4, 2004, not removed from office[51]

April 11, 2006[52]

David Hergert

Member of the University of Nebraska Board of Regents
Removed by the Nebraska Supreme Court on July 7, 2006[53]

January 8, 2009 (first vote)[54]

Rod Blagojevich

Governor of Illinois
95th General Assembly ended

January 14, 2009 (second vote)[55]
Removed on January 29, 2009, and declared ineligible to hold public office in Illinois[56]

February 11, 2013[57]

Benigno Fitial

Governor of the Northern Mariana Islands
Resigned on February 20, 2013