CPSF3: Difference between revisions

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*{{cite journal  | vauthors=Jin J, Smith FD, Stark C |title=Proteomic, functional, and domain-based analysis of in vivo 14-3-3 binding proteins involved in cytoskeletal regulation and cellular organization. |journal=Curr. Biol. |volume=14 |issue= 16 |pages= 1436–50 |year= 2004 |pmid= 15324660 |doi= 10.1016/j.cub.2004.07.051 |display-authors=etal}}
*{{cite journal  | vauthors=Jin J, Smith FD, Stark C |title=Proteomic, functional, and domain-based analysis of in vivo 14-3-3 binding proteins involved in cytoskeletal regulation and cellular organization. |journal=Curr. Biol. |volume=14 |issue= 16 |pages= 1436–50 |year= 2004 |pmid= 15324660 |doi= 10.1016/j.cub.2004.07.051 |display-authors=etal}}
*{{cite journal  | vauthors=Gerhard DS, Wagner L, Feingold EA |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504  | pmc=528928 |display-authors=etal}}
*{{cite journal  | vauthors=Gerhard DS, Wagner L, Feingold EA |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504  | pmc=528928 |display-authors=etal}}
*{{cite journal  | vauthors=Mandel CR, Kaneko S, Zhang H |title=Polyadenylation factor CPSF-73 is the pre-mRNA 3'-end-processing endonuclease. |journal=Nature |volume=444 |issue= 7121 |pages= 953–6 |year= 2007 |pmid= 17128255 |doi= 10.1038/nature05363 |display-authors=etal}}
*{{cite journal  | vauthors=Mandel CR, Kaneko S, Zhang H |title=Polyadenylation factor CPSF-73 is the pre-mRNA 3'-end-processing endonuclease. |journal=Nature |volume=444 |issue= 7121 |pages= 953–6 |year= 2007 |pmid= 17128255 |doi= 10.1038/nature05363 |display-authors=etal|pmc=3866582 }}
*{{cite journal  | vauthors=de la Vega L, Sánchez-Duffhues G, Fresno M |title=The 73 kDa subunit of the CPSF complex binds to the HIV-1 LTR promoter and functions as a negative regulatory factor that is inhibited by the HIV-1 Tat protein. |journal=J. Mol. Biol. |volume=372 |issue= 2 |pages= 317–30 |year= 2007 |pmid= 17669424 |doi= 10.1016/j.jmb.2007.06.075 |display-authors=etal}}
*{{cite journal  | vauthors=de la Vega L, Sánchez-Duffhues G, Fresno M |title=The 73 kDa subunit of the CPSF complex binds to the HIV-1 LTR promoter and functions as a negative regulatory factor that is inhibited by the HIV-1 Tat protein. |journal=J. Mol. Biol. |volume=372 |issue= 2 |pages= 317–30 |year= 2007 |pmid= 17669424 |doi= 10.1016/j.jmb.2007.06.075 |display-authors=etal}}
}}
}}

Latest revision as of 01:22, 12 May 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Cleavage and polyadenylation specificity factor subunit 3 is a protein that in humans is encoded by the CPSF3 gene.[1][2]


Model organisms

Model organisms have been used in the study of CPSF3 function. A conditional knockout mouse line called Cpsf3tm1b(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute.[3] Male and female animals underwent a standardized phenotypic screen[4] to determine the effects of deletion.[5][6][7][8] Additional screens performed: - In-depth immunological phenotyping[9]

References

  1. Jenny A, Minvielle-Sebastia L, Preker PJ, Keller W (Dec 1996). "Sequence similarity between the 73-kilodalton protein of mammalian CPSF and a subunit of yeast polyadenylation factor I". Science. 274 (5292): 1514–7. doi:10.1126/science.274.5292.1514. PMID 8929409.
  2. "Entrez Gene: CPSF3 cleavage and polyadenylation specific factor 3, 73kDa".
  3. Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  4. 4.0 4.1 "International Mouse Phenotyping Consortium".
  5. Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  6. Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  7. Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  8. White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Sanger Institute Mouse Genetics Project, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell. 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMC 3717207. PMID 23870131.
  9. 9.0 9.1 "Infection and Immunity Immunophenotyping (3i) Consortium".

External links

Further reading