This old version of Proteopedia is provided for student assignments while the new version is undergoing repairs. Content and edits done in this old version of Proteopedia after March 1, 2026 will eventually be lost when it is retired in about June of 2026.
Apply for new accounts at the new Proteopedia. Your logins will work in both the old and new versions.
3v6a
From Proteopedia
Contents |
Helical repeat structure of apoptosis inhibitor 5 reveals protein-protein interaction modules
Template:ABSTRACT PUBMED 22334682
Function
[API5_HUMAN] Antiapoptotic factor that may have a role in protein assembly. Negatively regulates ACIN1. By binding to ACIN1, it suppresses ACIN1 cleavage from CASP3 and ACIN1-mediated DNA fragmentation. Also known to efficiently suppress E2F1-induced apoptosis. Its depletion enhances the cytotoxic action of the chemotherapeutic drugs.[1] [2] [3]
About this Structure
3v6a is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.
Reference
- Han BG, Kim KH, Lee SJ, Jeong KC, Cho JW, Noh KH, Kim TW, Kim SJ, Yoon HJ, Suh SW, Lee S, Lee BI. Helical repeat structure of apoptosis inhibitor 5 reveals protein-protein interaction modules. J Biol Chem. 2012 Mar 30;287(14):10727-37. doi: 10.1074/jbc.M111.317594. Epub, 2012 Feb 12. PMID:22334682 doi:10.1074/jbc.M111.317594
- ↑ Kim JW, Cho HS, Kim JH, Hur SY, Kim TE, Lee JM, Kim IK, Namkoong SE. AAC-11 overexpression induces invasion and protects cervical cancer cells from apoptosis. Lab Invest. 2000 Apr;80(4):587-94. PMID:10780674
- ↑ Morris EJ, Michaud WA, Ji JY, Moon NS, Rocco JW, Dyson NJ. Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivo. PLoS Genet. 2006 Nov 17;2(11):e196. PMID:17112319 doi:06-PLGE-RA-0285R2
- ↑ Rigou P, Piddubnyak V, Faye A, Rain JC, Michel L, Calvo F, Poyet JL. The antiapoptotic protein AAC-11 interacts with and regulates Acinus-mediated DNA fragmentation. EMBO J. 2009 Jun 3;28(11):1576-88. doi: 10.1038/emboj.2009.106. Epub 2009 Apr 23. PMID:19387494 doi:10.1038/emboj.2009.106
