Structural highlights
Disease
[SART3_HUMAN] Defects in SART3 are the cause of disseminated superficial actinic porokeratosis type 1 (DSAP1) [MIM:175900]. DSAP1 is an autosomal dominant disorder, characterized by multiple superficial keratotic lesions surrounded by a slightly raised keratotic border, developing during the third or fourth decade of life on sun-exposed areas of skin.[1]
Function
[SART3_HUMAN] Regulates Tat transactivation activity through direct interaction. May be a cellular factor for HIV-1 gene expression and viral replication.[2]
Evolutionary Conservation
Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.
References
- ↑ Zhang ZH, Niu ZM, Yuan WT, Zhao JJ, Jiang FX, Zhang J, Chai B, Cui F, Chen W, Lian CH, Xiang LH, Xu SJ, Liu WD, Zheng ZZ, Huang W. A mutation in SART3 gene in a Chinese pedigree with disseminated superficial actinic porokeratosis. Br J Dermatol. 2005 Apr;152(4):658-63. PMID:15840095 doi:10.1111/j.1365-2133.2005.06443.x
- ↑ Liu Y, Li J, Kim BO, Pace BS, He JJ. HIV-1 Tat protein-mediated transactivation of the HIV-1 long terminal repeat promoter is potentiated by a novel nuclear Tat-interacting protein of 110 kDa, Tip110. J Biol Chem. 2002 Jun 28;277(26):23854-63. Epub 2002 Apr 16. PMID:11959860 doi:10.1074/jbc.M200773200
