Publications by authors named "Harivadan Bhagat"
Article Synopsis
- Chemokines trigger calcium signaling and movement in dendritic cells, but the specific molecular mechanisms were not fully understood.
- Researchers discovered that the TRPM2 channel, alongside IP(3)-mediated Ca(2+) release and store-operated Ca(2+) entry, plays a critical role in regulating Ca(2+) in dendritic cells.
- TRPM2-deficient dendritic cells show faulty maturation and impaired ability to migrate towards chemokine signals, underscoring the importance of TRPM2 in calcium signaling and chemotaxis, and revealing ADP-ribose as an important messenger in this process.
The ectoenzyme CD38 catalyzes the production of cyclic ADP-ribose (cADPR) and ADP-ribose (ADPR) from its substrate, NAD(+). Both products of the CD38 enzyme reaction play important roles in signal transduction, as cADPR regulates calcium release from intracellular stores and ADPR controls cation entry through the plasma membrane channel TRPM2. We previously demonstrated that CD38 and the cADPR generated by CD38 regulate calcium signaling in leukocytes stimulated with some, but not all, chemokines and controls leukocyte migration to inflammatory sites.
View Article and Find Full Text PDFTRPM channels, calcium and redox sensors during innate immune responses.
Semin Cell Dev Biol
December 2006
Melastatin-related TRPM ion channels have emerged as novel therapeutic targets due to their potential ability to modulate the function and fate of immune cells during inflammation, innate, and adaptive immunity. Four family members, TRPM1, TRPM2, TRPM4 and TRPM7 have a strong presence in the immune system. TRPM channels regulate ion-homeostasis by sensing cellular redox status and cytoplasmic calcium levels.
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