a single-pass membrane protein of the endoplasmic reticulum that regulates autophagy. Has also been reported to localize to the mitochondrion outer membrane. Antagonizes ATG6-mediated cellular autophagy. Participates in the interaction of BCL2 with BECN1 and is required for BCL2-mediated depression of endoplasmic reticulum Ca2+ stores during autophagy. Contributes to BIK-initiated autophagy, while it is not involved in BIK-dependent activation of caspases. Involved in life span control, probably via its function as regulator of autophagy. Directly interacts with BCL2; the interaction is disrupted by BIK interaction with BCL2. It has been reported to mainly localizes to the mitochondrion outer membrane. Defects in CISD2 are the cause of Wolfram syndrome 2 (WFS2), is a rare autosomal recessive disorder characterized by optic atrophy and diabetes mellitus. Other symptoms include the presence of profound upper gastrointestinal ulceration, significant bleeding tendency, defective platelet aggregation with collagen and various neurological symptoms. Initially thought to be a zinc-finger protein, it was later shown to bind 1 2Fe-2S cluster instead. Note: This description may include information from UniProtKB.
Protein type: Autophagy; Endoplasmic reticulum; Membrane protein, integral
Cellular Component: endoplasmic reticulum membrane; mitochondrial outer membrane; protein complex; endoplasmic reticulum; integral to membrane
Molecular Function: 2 iron, 2 sulfur cluster binding; protein binding; protein homodimerization activity; metal ion binding
Biological Process: mitochondrion degradation; multicellular organismal aging; regulation of autophagy
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.