Structural highlights
Disease
[KI21A_HUMAN] Congenital fibrosis of extraocular muscles. The disease is caused by mutations affecting the gene represented in this entry.
Function
[KANK2_HUMAN] Involved in transcription regulation by sequestering nuclear receptor coactivators, such as NCOA1, NCOA2 and NCOA3, in the cytoplasm; the function is deregulated by phosphorylation. May be involved in the control of cytoskeleton formation by regulating actin polymerization. Involved in regulation of caspase-independent apoptosis; proposed to sequester AIFM1 in mitochondria and apoptotic stimuli lead to its proteasomal degradation allowing the release of AIFM1 to the nucleus. May be involved in promotion of cell proliferation.[1] [2] [KI21A_HUMAN] Microtubule-binding motor protein probably involved in neuronal axonal transport. In vitro, has a plus-end directed motor activity (By similarity).
References
- ↑ Zhang Y, Zhang H, Liang J, Yu W, Shang Y. SIP, a novel ankyrin repeat containing protein, sequesters steroid receptor coactivators in the cytoplasm. EMBO J. 2007 Jun 6;26(11):2645-57. Epub 2007 May 3. PMID:17476305 doi:http://dx.doi.org/10.1038/sj.emboj.7601710
- ↑ Wang D, Liang J, Zhang Y, Gui B, Wang F, Yi X, Sun L, Yao Z, Shang Y. Steroid receptor coactivator-interacting protein (SIP) inhibits caspase-independent apoptosis by preventing apoptosis-inducing factor (AIF) from being released from mitochondria. J Biol Chem. 2012 Apr 13;287(16):12612-21. doi: 10.1074/jbc.M111.334151. Epub, 2012 Feb 27. PMID:22371500 doi:http://dx.doi.org/10.1074/jbc.M111.334151