| First Author | Belkacemi A | Year | 2018 |
| Journal | Cell Rep | Volume | 22 |
| Issue | 5 | Pages | 1339-1349 |
| PubMed ID | 29386119 | Mgi Jnum | J:270713 |
| Mgi Id | MGI:6278654 | Doi | 10.1016/j.celrep.2018.01.010 |
| Citation | Belkacemi A, et al. (2018) IP3 Receptor-Dependent Cytoplasmic Ca(2+) Signals Are Tightly Controlled by Cavbeta3. Cell Rep 22(5):1339-1349 |
| abstractText | Voltage-gated calcium channels (Cavs) are major Ca(2+) entry pathways in excitable cells. Their beta subunits facilitate membrane trafficking of the channel's ion-conducting alpha1 pore and modulate its gating properties. We report that one beta subunit, beta3, reduces Ca(2+) release following stimulation of phospholipase C-coupled receptors and inositol 1,4,5-trisphosphate (IP3) formation. This effect requires the SH3-HOOK domain of Cavbeta3, includes physical beta3/IP3 receptor interaction, and prevails when agonist-induced IP3 formation is bypassed by photolysis of caged IP3. In agreement with beta3 acting as a brake on Ca(2+) release, fibroblast migration is enhanced in vitro, and in vivo, closure of skin wounds is accelerated in the absence of beta3. To mediate specific physiological responses and to prevent Ca(2+) toxicity, cytoplasmic Ca(2+) signals must be tightly controlled. The described function of beta3, unrelated to its function as a Cav subunit, adds to this tight control. |
