C7orf27 Inhibitors

BRCA1-associated ATM activator 1 (BRAT1), encoded by the gene BRAT1, plays a crucial role in the cellular response to DNA damage, particularly in the activation of the ATM (ataxia-telangiectasia mutated) kinase, which is pivotal for cellular stress responses, including the DNA damage response (DDR). The protein is involved in the maintenance of genomic stability, a key element in the prevention of oncogenic transformations. BRAT1 functions as a part of a complex signaling network that detects and responds to DNA damage by activating a cascade of phosphorylation events. Upon sensing DNA strand breaks, BRAT1 helps facilitate the recruitment and activation of ATM, which in turn phosphorylates a variety of substrates involved in cell cycle regulation, DNA repair, and apoptosis. This activation is essential for initiating repair processes and for halting cell cycle progression to prevent the replication of damaged DNA.

Furthermore, BRAT1 is linked with the regulation of apoptosis through its interaction with p53, a tumor suppressor protein that induces cell cycle arrest or apoptosis in response to genotoxic stress. By participating in these pathways, BRAT1 contributes to the suppression of tumor development and the preservation of cellular integrity. Loss of function mutations or deficiencies in BRAT1 have been associated with various phenotypes, including neurodevelopmental disorders and increased susceptibility to cancer. BRAT1 dysfunction may lead to impaired activation of ATM, resulting in ineffective DNA repair and accumulation of genomic instability, which is a hallmark of cancer cells.In summary, BRAT1 is a protein that acts as a key regulator of the ATM kinase in the DDR pathway. Its role in orchestrating the response to DNA damage and maintaining genomic stability is crucial for protecting cells from malignant transformation and for normal cellular function.