Ca2+
Studies (4)
Wallerian Degeneration Is Executed by an NMN-SARM1-Dependent Late Ca2+ Influx but Only Modestly Influenced by Mitochondria
Nicotinamide mononucleotide (NMN) accumulation in the extra cellular environment contributes to the breakdown of axons (nerve fibers).
Nicotinic Acid is a Common Regulator of Heat-Sensing TRPV1-4 Ion Channels
NA activates the capsaicin receptor TRPV1 by lowering the activation threshold for heat, causing channel activation at physiological body temperature. Conversely it inhibits TRPV4 by raising activation temp to above body temp, ~41 celsius. Overall, the effects on TRPV1 and TRPV3 are potentiating while those on TRPV2 and TRPV4 are inhibitory. Little is known about the detailed structures of TRPV2-4. The TRPV receptors play a role in the flushing response.
TRPV4 Stimulation Induced Melatonin Secretion by Increasing Arylalkymine N-acetyltransferase (AANAT) Protein Level
The role of TRPV4 channel present in human ciliary body epithelial cells in AANAT production was studied. AANAT, Aralkylamine N-acetyltransferase seems to be the key enzyme involved in producing melatonin from serotonin. In rodents, transcriptional activation of aanat gene is the classical mechanism to induce melatonin biosynthesis. TRPV4 is present in the human ciliary body and ciliary body epithelial cells. Activating TRPV4 channel increases the expression of AANAT, which elevates the concentration of NAS and melatonin
Small Molecule Antagonists of NAADP-Induced Ca2+ Release in T-Lymphocytes Suggest Potential Therapeutic Agents for Autoimmune Disease
Ca2+ is one of the major ways that cells communicate and is involved in the regulation of many important cellular processes from proliferation to apoptosis. Ca2+ regulation is involved in many autoimmune conditions and nicotinic acid (niacin) and is key to this signaling.