ATMIN (ATM interactor) is a transcription factor that plays dual roles in DNA damage response and transcriptional regulation. Primary function: ATMIN serves as an essential cofactor for ATM kinase activation, particularly in response to replication stress and methylating DNA damage 1. ATMIN and ATM protein stability are mutually dependent, with ATMIN binding ATM through a carboxy-terminal motif; notably, ATMIN functions complement those of NBS1 in signal-dependent ATM activation, with ATMIN required for chloroquine and hypotonic stress responses but not ionizing radiation-induced signaling 1. Mechanism: As a transcriptional activator, ATMIN binds the DYNLL1 promoter and activates its transcription 2. DYNLL1, ATMIN's primary target, regulates DNA end resection by binding MRE11 and limiting nucleolytic degradation, thereby influencing homologous recombination and genomic stability 3. In hypoxic conditions, ATMIN expression is repressed through p53 and HIF-1α-dependent mechanisms, reducing DYNLL1 expression and impairing base excision repair 4. Disease relevance: ATMIN functions as a haploinsufficient tumor suppressor in lung adenocarcinoma; its loss near the FRA16D fragile site correlates with poor survival 5. Additionally, ATMIN is synthetically viable with BRCA1/2 loss 6. In nasopharyngeal carcinoma, high ATMIN expression (stabilized by USP10 deubiquitination) promotes chemoresistance through LCK activation 7. Clinical significance: ATMIN's role in both DNA damage responses and transcriptional regulation positions it as a potential therapeutic target in BRCA-deficient and chemoresistant cancers.