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Regulation of Store-Operated $Ca^{2+}$ Entry by SARAF
| Content Provider | MDPI |
|---|---|
| Author | Dagan, Inbal Palty, Raz |
| Copyright Year | 2021 |
| Description | Calcium $(Ca^{2+}$) signaling plays a dichotomous role in cellular biology, controlling cell survival and proliferation on the one hand and cellular toxicity and cell death on the other. Store-operated $Ca^{2+}$ entry (SOCE) by CRAC channels represents a major pathway for $Ca^{2+}$ entry in non-excitable cells. The CRAC channel has two key components, the endoplasmic reticulum $Ca^{2+}$ sensor stromal interaction molecule (STIM) and the plasma-membrane $Ca^{2+}$ channel Orai. Physical coupling between STIM and Orai opens the CRAC channel and the resulting $Ca^{2+}$ flux is regulated by a negative feedback mechanism of slow $Ca^{2+}$ dependent inactivation (SCDI). The identification of the SOCE-associated regulatory factor (SARAF) and investigations of its role in SCDI have led to new functional and molecular insights into how SOCE is controlled. In this review, we provide an overview of the functional and molecular mechanisms underlying SCDI and discuss how the interaction between SARAF, STIM1, and Orai1 shapes $Ca^{2+}$ signaling in cells. |
| Starting Page | 1887 |
| e-ISSN | 20734409 |
| DOI | 10.3390/cells10081887 |
| Journal | Cells |
| Issue Number | 8 |
| Volume Number | 10 |
| Language | English |
| Publisher | MDPI |
| Publisher Date | 2021-07-26 |
| Access Restriction | Open |
| Subject Keyword | Cells Cell Biology Store Operated Calcium Entry (soce) Stim1 Saraf Orai1 Crac Channel Slow Calcium Dependent Inactivation (cdi) |
| Content Type | Text |
| Resource Type | Article |
