PABPC4

Polyadenylate-binding protein 4 (PABPC4) is a protein that in humans is encoded by the PABPC4 gene.[5][6]

PABPC4
Identifiers
AliasesPABPC4, APP-1, APP1, PABP4, iPABP, poly(A) binding protein cytoplasmic 4
External IDsOMIM: 603407 MGI: 2385206 HomoloGene: 37855 GeneCards: PABPC4
Orthologs
SpeciesHumanMouse
Entrez

8761

230721

Ensembl

ENSG00000090621

ENSMUSG00000011257

UniProt

Q13310

n/a

RefSeq (mRNA)

NM_003819
NM_001135653
NM_001135654

NM_130881
NM_148917
NM_001356377

RefSeq (protein)

NP_001129125
NP_001129126
NP_003810

n/a

Location (UCSC)Chr 1: 39.56 – 39.58 MbChr 4: 123.16 – 123.19 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

Poly(A)-binding proteins (PABPs) bind to the poly(A) tail present at the 3-prime ends of most eukaryotic mRNAs. PABPC4 or IPABP (inducible PABP) was isolated as an activation-induced T-cell mRNA encoding a protein. Activation of T cells increased PABPC4 mRNA levels in T cells approximately 5-fold. PABPC4 contains 4 RNA-binding domains and proline-rich C terminus. PABPC4 is localized primarily to the cytoplasm. It is suggested that PABPC4 might be necessary for regulation of stability of labile mRNA species in activated T cells. PABPC4 was also identified as an antigen, APP1 (activated-platelet protein-1), expressed on thrombin-activated rabbit platelets. PABPC4 may also be involved in the regulation of protein translation in platelets and megakaryocytes or may participate in the binding or stabilization of polyadenylates in platelet dense granules.[6]

Model organisms

Model organisms have been used in the study of PABPC4 function. A conditional knockout mouse line, called Pabpc4tm1a(KOMP)Wtsi[10][11] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[12][13][14]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[8][15] Twenty tests were carried out on mutant mice and one significant abnormality was observed: female homozygous mutants displayed impaired glucose tolerance.[8]

Interactions

PABPC4 has been shown to interact with PHLDA1.[16]

References

  1. GRCh38: Ensembl release 89: ENSG00000090621 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000011257 - Ensembl, May 2017
  3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. Féral C, Mattéi MG, Pawlak A, Guellaën G (Nov 1999). "Chromosomal localization of three human poly(A)-binding protein genes and four related pseudogenes". Hum Genet. 105 (4): 347–53. doi:10.1007/s004390051113. PMC 1865476. PMID 10543404.
  6. "Entrez Gene: PABPC4 poly(A) binding protein, cytoplasmic 4 (inducible form)".
  7. "Glucose tolerance test data for Pabpc4". Wellcome Trust Sanger Institute.
  8. 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. S2CID 85911512.
  9. Mouse Resources Portal, Wellcome Trust Sanger Institute.
  10. "International Knockout Mouse Consortium".
  11. "Mouse Genome Informatics".
  12. 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 (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  13. Dolgin E (2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  14. Collins FS, Rossant J, Wurst W (2007). "A Mouse for All Reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. S2CID 18872015.
  15. van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.
  16. Hinz T, Flindt S, Marx A, Janssen O, Kabelitz D (May 2001). "Inhibition of protein synthesis by the T cell receptor-inducible human TDAG51 gene product". Cell. Signal. 13 (5): 345–52. doi:10.1016/S0898-6568(01)00141-3. PMID 11369516.

Further reading

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