ATM interactor protein (ATMIN)

ATM interactor protein (ATMIN) is a zinc finger-containing regulatory protein that acts as an essential cofactor for the checkpoint kinase ATM (axia telangiectasia mutated), orchestrating a subset of ATM-dependent DNA damage response pathways[1][2]. Unlike NBS1, which mediates ATM activation after DNA double-strand breaks, ATMIN specifically regulates ATM activation in response to non-DSB stresses such as replication stress, hypotonic stress, and DNA replication inhibitors, thereby defining an NBS1-independent ATM signaling route[1][2]. ATMIN directly interacts with ATM and both proteins mutually stabilize each other[1]. ATMIN is required to recruit DNA damage effectors such as 53BP1 at sites of replication-induced lesions and to enable phosphorylation of key ATM targets (KAP1, p53, SMC1) after such stress[2]. Loss of ATMIN impairs the cell’s ability to respond to replication stress and leads to chromosomal instability[2]. It is also known by several aliases including ASCIZ, indicating its function as a Chk2-interacting zinc finger protein and its role in ATM/ATR-related pathways, but current evidence supports its primary role as a regulatory factor rather than as a traditional drug target such as a receptor, enzyme, or transporter[1][2].

Other names

ASCIZKIAA0431ZNF822ATM/ATR-substrate Chk2-interacting zinc finger proteinzinc finger protein 822ATM/ATR-substrate CHEK2-interacting zinc finger proteinATM INteracting protein