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Poly(A) binding protein, cytoplasmic 4 (inducible form)
Protein PABPC4 PDB 1cvj.png
PDB rendering based on 1cvj.
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols PABPC4 ; APP-1; APP1; PABP4; iPABP
External IDs OMIM603407 MGI2385206 HomoloGene37855 ChEMBL: 5333 GeneCards: PABPC4 Gene
RNA expression pattern
PBB GE PABPC4 201064 s at tn.png
More reference expression data
Species Human Mouse
Entrez 8761 230721
Ensembl ENSG00000090621 ENSMUSG00000011257
UniProt Q13310 Q6PHQ9
RefSeq (mRNA) NM_001135653 NM_130881
RefSeq (protein) NP_001129125 NP_570951
Location (UCSC) Chr 1:
40.03 – 40.04 Mb
Chr 4:
123.26 – 123.3 Mb
PubMed search [1] [2]

Polyadenylate-binding protein 4 is a protein that in humans is encoded by the PABPC4 gene.[1][2]


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.[2]

Model organisms[edit]

Model organisms have been used in the study of PABPC4 function. A conditional knockout mouse line, called Pabpc4tm1a(KOMP)Wtsi[6][7] 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.[8][9][10]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[4][11] Twenty tests were carried out on mutant mice and one significant abnormality was observed: female homozygous mutants displayed impaired glucose tolerance.[4]


PABPC4 has been shown to interact with PHLDA1.[12]


  1. ^ 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. 
  2. ^ a b "Entrez Gene: PABPC4 poly(A) binding protein, cytoplasmic 4 (inducible form)". 
  3. ^ "Glucose tolerance test data for Pabpc4". Wellcome Trust Sanger Institute. 
  4. ^ 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. 
  5. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  6. ^ "International Knockout Mouse Consortium". 
  7. ^ "Mouse Genome Informatics". 
  8. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V et al. (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. 
  9. ^ Dolgin E (2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  10. ^ 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. 
  11. ^ 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. 
  12. ^ 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]