Anti-NUCB1 antibody [EPR7953]

Supplementary info

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

Activity summary

The protein NUCB1 also known as Nucleobindin-1 functions mechanically as a calcium-binding protein. It has approximately a mass of 55 kDa and belongs to a group of calcium-binding proteins containing EF-hand motifs. NUCB1 expresses in a variety of tissues notably the nervous system and endocrine tissues. The protein comprises several functional domains including a signal peptide helix-loop-helix motif and nuclear localization signal.

Biological function summary

NUCB1 participates in the regulation of cellular calcium homeostasis and signaling pathways. It is not a part of a multi-protein complex but it acts as a molecular chaperone influencing the stability and function of other proteins within the cell. NUCB1 also plays a role in secretory pathways within the cell which is relevant to its expression in endocrine tissues. Its regulatory functions in calcium signaling are critical for cellular activities such as secretion and cell division.

Pathways

NUCB1 interacts with cellular signaling mechanisms particularly those related to intracellular calcium dynamics. It is involved in pathways like the calcium signaling pathway and the insulin signaling pathway. Within these pathways NUCB1 associates with proteins such as calmodulin which also binds calcium and contributes to signal transduction. The protein modulates activities within these pathways affecting how cells respond to external signals.

Associated diseases and disorders

NUCB1 exhibits associations with certain conditions linked to disturbed calcium regulation. One such disorder is Alzheimer's disease where alterations in calcium signaling play a role in disease progression. The protein furthermore relates to type 2 diabetes involving its role in the insulin signaling pathway. In these contexts NUCB1 connects to other proteins such as amyloid precursor protein in Alzheimer's disease highlighting disruptions in calcium homeostasis mechanisms.