Anti-NOL3 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Nucleolar protein 3 (NOL3) also known as ARC (apoptosis repressor with caspase recruitment domain) is a multifunctional protein involved in apoptosis regulation and cellular stress responses. It has a molecular mass of approximately 26 kDa. NOL3 is expressed in various tissues but it displays high levels in the heart skeletal muscles and neurons. Its expression suggests a protective role in these tissues where it interacts with various cellular components to prevent apoptosis.

Biological function summary

NOL3 contributes significantly to cell survival and apoptosis inhibition by interacting with pro-apoptotic proteins to block their function. It acts as a safeguard against external stressors that can trigger cell death. As part of its role in apoptosis regulation NOL3 engages in complex formation with other proteins to modulate apoptotic pathways. For instance it binds directly to caspases preventing their activation and further propagation of cell death signals.

Pathways

NOL3 plays a critical role in the apoptosis and stress response pathways. It participates in the intrinsic apoptosis pathway by inhibiting the activation of key apoptotic enzymes while also interacting with proteins such as Bcl-2 and Bax to further regulate cell survival. The involvement of NOL3 in stress response pathways highlights its function in promoting cellular resilience in challenging conditions often functioning together with heat shock proteins that assist in protein folding and stress recovery.

Associated diseases and disorders

NOL3 has been implicated in neurodegenerative diseases and cardiac dysfunction. In particular its dysregulation is associated with conditions like Alzheimer's disease where it might influence neural cell survival. Furthermore NOL3 interacts with amyloid precursor protein (APP) which has a role in Alzheimer's pathology. In the context of cardiac diseases altered NOL3 expression may influence cardiac hypertrophy and heart failure potentially interacting with proteins such as caspase-8 in these processes.