Involvement of actin filament in the generation of Ca²⁺mobilizing messengers in glucose-induced Ca²⁺signaling in pancreatic β-cells

Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) and Endolysosomal Two-pore Channels Modulate Membrane Excitability and Stimulus-Secretion Coupling in Mouse Pancreatic β Cells

“…NAADP-induced Ca 2+ release in MIN6 cells can be disrupted by the lysomotropic agent glycyl- l -phenylalanine-β-naphthylamide (GPN) or bafilomycin, which disrupts acidic store Ca 2+ storage implicating lysosomally related organelles as the principal target for NAADP in these cells ( 19 , 20 , 23 ). In the pancreatic β cell line MIN6, and primary mouse β cells, glucose increases NAADP synthesis and hence intracellular levels ( 18 , 20 , 22 ), consistent with its role as an intracellular messenger. NAADP introduced into mouse pancreatic β cells via a patch pipette was found to evoke a series of oscillatory plasma membrane currents, which were blocked by the NAADP antagonist Ned-19 ( 21 ) and were abolished in pancreatic β cells prepared from Tpcn2 −/− mice ( 29 ).…”

“…Glucose ( 18 ) and glucagon like-peptide 1 ( 18 , 20 ) have both been reported to increase β cell NAADP levels, effects that may be partially dependent on the ADP-ribosyl cyclase, CD38 ( 20 , 22 ). At present, ADP-ribosyl cyclases, including CD38, are the only characterized enzymes that have been demonstrated to catalyze the synthesis of NAADP, using NADP and nicotinic acid as substrates by a base-exchange mechanism ( 46 , 47 ).…”

An immunohistochemical, enzymatic, and behavioral study of CD157/BST-1 as a neuroregulator

“…However, in the nervous system, CD157 may play a role in neuronal migration during neural stem cell proliferation and neurogenesis. It has been shown that CD157 binds with members of the integrin family [50]. Furthermore, integrin β3 and the serotonin transporter interact to modulate serotonin uptake in the mouse brain [51].…”

β Cell Store-Operated Ion Channels

“…An indirect mechanism for actin as a regulator of SOCE comes from its ability to regulate cluster of differentiation 38 (CD38), also known as cyclic ADP-ribose hydrolase or cyclic ADP-ribose cyclase (Shawl et al 2012). Glucose stimulation of β-cells induces the internalization of CD38, and this internalization is an essential step for cyclic ADP-ribose (cADPR) production.…”

“…Glucose stimulation of β-cells induces the internalization of CD38, and this internalization is an essential step for cyclic ADP-ribose (cADPR) production. Inhibition of actin depolymerization prevents CD38 internalization and cADPR production (Shawl et al 2012). This role of actin depolymerization to permit cADPR production will influence the activation of RYR and release of intracellular Ca 2+ stores and thus could play a role in SOCE activation.…”