NOL3/ARC Recombinant Rabbit mAb (S-4660-38)

NOL3 (Nucleolar Protein 3), also known as ARC (Apoptosis Repressor with CARD Domain), is a multifunctional anti-apoptotic protein with dual subcellular localization. Through its N-terminal CARD domain, it can simultaneously block both extrinsic and intrinsic apoptotic signaling pathways through multiple mechanisms. On one hand, NOL3 interferes with the assembly of the death-inducing signaling complex by binding to FAS and FADD, or restricts the activation of Caspase-8 by binding to it, thereby inhibiting the extrinsic apoptotic pathway; on the other hand, it can directly bind and inactivate the pro-apoptotic protein BAX, preventing its translocation from the cytoplasm to the mitochondria, thereby inhibiting mitochondrial outer membrane permeabilization and cytochrome c release, effectively blocking the intrinsic apoptotic pathway. Furthermore, NOL3 can bind to p53 to inhibit its tetramerization and transcriptional function, and through phosphorylation modifications it regulates its binding to Caspase-8 to exert calcium-buffering effects, maintaining cell survival at multiple levels. In terms of tissue distribution, NOL3 is highly expressed in heart and skeletal muscle. Under pathological conditions, its protein level is rapidly degraded via the ubiquitin-proteasome pathway during myocardial ischemia-reperfusion, making it a critical regulatory node in myocardial injury; meanwhile, NOL3 is overexpressed in various epithelial-derived tumors (such as breast cancer and renal cancer), closely associated with chemoresistance and radioresistance; and its gene mutations have been confirmed to be associated with neurological disorders such as familial cortical myoclonus.