Abstract
The mechanism involved in [Ca2+]i-dependent feedback inhibition of store-operated Ca2+ entry (SOCE) is not yet known. Expression of Ca2+-insensitive calmodulin (Mut-CaM) but not wild-type CaM increased SOCE and decreased its Ca2+-dependent inactivation. Expression of TrpC1 lacking C terminus aa 664-793 (TrpC1ΔC) also attenuated Ca2+-dependent inactivation of SOCE. CaM interacted with endogenous and expressed TrpC1 and with GST-TrpC1 C terminus but not with TrpC1ΔC. Two CaM binding domains, aa 715-749 and aa 758-793, were identified. Expression of TrpC1Δ758-793 but not TrpC1Δ715-749 mimicked the effects of TrpC1ΔC and Mut-CaM on SOCE. These data demonstrate that CaM mediates Ca2+-dependent feedback inhibition of SOCE via binding to a domain in the C terminus of TrpC1. These findings reveal an integral role for TrpC1 in the regulation of SOCE.
Original language | English (US) |
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Pages (from-to) | 739-750 |
Number of pages | 12 |
Journal | Molecular Cell |
Volume | 9 |
Issue number | 4 |
DOIs | |
State | Published - 2002 |
Externally published | Yes |
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology