PAWR

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PAWR
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases PAWR, Pawr, 2310001G03Rik, PAR4, Par-4, pro-apoptotic WT1 regulator
External IDs MGI: 2149961 HomoloGene: 1940 GeneCards: PAWR
RNA expression pattern
PBB GE PAWR 214237 x at fs.png

PBB GE PAWR 204004 at fs.png

PBB GE PAWR 204005 s at fs.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_002583

NM_054056

RefSeq (protein)

NP_002574

NP_473397.1
NP_473397

Location (UCSC) Chr 12: 79.57 – 79.69 Mb Chr 10: 108.33 – 108.41 Mb
PubMed search [1] [2]
Wikidata
View/Edit Human View/Edit Mouse

PRKC, apoptosis, WT1, regulator, also known as PAWR or Prostate apoptosis response-4 (Par-4), is a human gene coding for a tumor-suppressor protein that induces apoptosis in cancer cells, but not in normal cells.

Function[edit]

The tumor suppressor WT1 represses and activates transcription. The protein encoded by this gene is a WT1-interacting protein that itself functions as a transcriptional repressor. It contains a putative leucine zipper domain which interacts with the zinc finger DNA binding domain of WT1. This protein is specifically upregulated during apoptosis of prostate cells.[3] The active domain of the Par-4 protein has been found to confer cancer resistance in transgenic mice without compromising normal viability or aging, and may have therapeutic significance.[4]

Interactions[edit]

PAWR has been shown to interact with:

References[edit]

  1. ^ "Human PubMed Reference:". 
  2. ^ "Mouse PubMed Reference:". 
  3. ^ "Entrez Gene: PAWR PRKC, apoptosis, WT1, regulator". 
  4. ^ Zhao Y, Burikhanov R, Qiu S, Lele SM, Jennings CD, Bondada S, Spear B, Rangnekar VM (Oct 2007). "Cancer resistance in transgenic mice expressing the SAC module of Par-4". Cancer Research. 67 (19): 9276–85. doi:10.1158/0008-5472.CAN-07-2124. PMID 17909035. 
  5. ^ Guo Q, Xie J (Feb 2004). "AATF inhibits aberrant production of amyloid beta peptide 1-42 by interacting directly with Par-4". The Journal of Biological Chemistry. 279 (6): 4596–603. doi:10.1074/jbc.M309811200. PMID 14627703. 
  6. ^ Kawai T, Akira S, Reed JC (Sep 2003). "ZIP kinase triggers apoptosis from nuclear PML oncogenic domains". Molecular and Cellular Biology. 23 (17): 6174–86. doi:10.1128/mcb.23.17.6174-6186.2003. PMC 180930Freely accessible. PMID 12917339. 
  7. ^ Díaz-Meco MT, Municio MM, Frutos S, Sanchez P, Lozano J, Sanz L, Moscat J (Sep 1996). "The product of par-4, a gene induced during apoptosis, interacts selectively with the atypical isoforms of protein kinase C". Cell. 86 (5): 777–86. doi:10.1016/s0092-8674(00)80152-x. PMID 8797824. 
  8. ^ Xie J, Guo Q (Jul 2004). "Par-4 inhibits choline uptake by interacting with CHT1 and reducing its incorporation on the plasma membrane". The Journal of Biological Chemistry. 279 (27): 28266–75. doi:10.1074/jbc.M401495200. PMID 15090548. 
  9. ^ Roussigne M, Cayrol C, Clouaire T, Amalric F, Girard JP (Apr 2003). "THAP1 is a nuclear proapoptotic factor that links prostate-apoptosis-response-4 (Par-4) to PML nuclear bodies". Oncogene. 22 (16): 2432–42. doi:10.1038/sj.onc.1206271. PMID 12717420. 
  10. ^ Johnstone RW, See RH, Sells SF, Wang J, Muthukkumar S, Englert C, Haber DA, Licht JD, Sugrue SP, Roberts T, Rangnekar VM, Shi Y (Dec 1996). "A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1". Molecular and Cellular Biology. 16 (12): 6945–56. doi:10.1128/mcb.16.12.6945. PMC 231698Freely accessible. PMID 8943350. 

Further reading[edit]