Structural highlights
Function
[ALKB7_HUMAN] Probable dioxygenase required to induce programmed necrosis in response to DNA damage caused by cytotoxic alkylating agents. Acts by triggering the collapse of mitochondrial membrane potential and loss of mitochondrial function that leads to energy depletion and cell death [1]. ALKBH7-mediated necrosis is probably required to prevent the accumulation of cells with DNA damage. Does not display DNA demethylase activity. Involved in fatty acid metabolism.[2]
Publication Abstract from PubMed
ALKBH7 is the mitochondrial AlkB family member that is required for alkylation- and oxidation-induced programmed necrosis. In contrast to the protective role of other AlkB family members after suffering alkylation-induced DNA damage, ALKBH7 triggers the collapse of mitochondrial membrane potential and promotes cell death[1]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
References
- ↑ 1.0 1.1 Solberg A, Robertson AB, Aronsen JM, Rognmo O, Sjaastad I, Wisloff U, Klungland A. Deletion of mouse Alkbh7 leads to obesity. J Mol Cell Biol. 2013 Jun;5(3):194-203. doi: 10.1093/jmcb/mjt012. Epub 2013 Apr, 8. PMID:23572141 doi:http://dx.doi.org/10.1093/jmcb/mjt012
- ↑ Fu D, Jordan JJ, Samson LD. Human ALKBH7 is required for alkylation and oxidation-induced programmed necrosis. Genes Dev. 2013 May 15;27(10):1089-100. doi: 10.1101/gad.215533.113. Epub 2013, May 10. PMID:23666923 doi:http://dx.doi.org/10.1101/gad.215533.113
