PABPC4

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PABPC4
Protein PABPC4 PDB 1cvj.png
Identifiers
Aliases PABPC4, APP-1, APP1, PABP4, iPABP, poly(A) binding protein cytoplasmic 4
External IDs MGI: 2385206 HomoloGene: 37855 GeneCards: PABPC4
RNA expression pattern
PBB GE PABPC4 201064 s at fs.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_003819
NM_001135653
NM_001135654

NM_130881
NM_148917

RefSeq (protein)

NP_001129125
NP_001129126
NP_003810

n/a

Location (UCSC) Chr 1: 39.56 – 39.58 Mb Chr 4: 123.26 – 123.3 Mb
PubMed search [1] [2]
Wikidata
View/Edit Human View/Edit Mouse

Polyadenylate-binding protein 4 (PABPC4) is a protein that in humans is encoded by the PABPC4 gene.[3][4]

Function[edit]

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.[4]

Model organisms[edit]

Model organisms have been used in the study of PABPC4 function. A conditional knockout mouse line, called Pabpc4tm1a(KOMP)Wtsi[8][9] 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.[10][11][12]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[6][13] Twenty tests were carried out on mutant mice and one significant abnormality was observed: female homozygous mutants displayed impaired glucose tolerance.[6]

Interactions[edit]

PABPC4 has been shown to interact with PHLDA1.[14]

References[edit]

  1. ^ "Human PubMed Reference:". 
  2. ^ "Mouse PubMed Reference:". 
  3. ^ 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 1865476Freely accessible. PMID 10543404. 
  4. ^ a b "Entrez Gene: PABPC4 poly(A) binding protein, cytoplasmic 4 (inducible form)". 
  5. ^ "Glucose tolerance test data for Pabpc4". Wellcome Trust Sanger Institute. 
  6. ^ a b c 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. 
  7. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  8. ^ "International Knockout Mouse Consortium". 
  9. ^ "Mouse Genome Informatics". 
  10. ^ 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 3572410Freely accessible. PMID 21677750. 
  11. ^ Dolgin E (2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  12. ^ 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. 
  13. ^ 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 3218837Freely accessible. PMID 21722353. 
  14. ^ 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[edit]