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) |
|---|---|
| Pages (from-to) | 739-750 |
| Number of pages | 12 |
| Journal | Molecular Cell |
| Volume | 9 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jan 1 2002 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
Cite this
Calmodulin regulates Ca2+-dependent feedback inhibition of store-operated Ca2+ influx by interaction with a site in the C terminus of TrpC1. / Singh, Brij B; Liu, Xibao; Tang, Jisen; Zhu, Michael X.; Ambudkar, Indu S.
In: Molecular Cell, Vol. 9, No. 4, 01.01.2002, p. 739-750.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Calmodulin regulates Ca2+-dependent feedback inhibition of store-operated Ca2+ influx by interaction with a site in the C terminus of TrpC1
AU - Singh, Brij B
AU - Liu, Xibao
AU - Tang, Jisen
AU - Zhu, Michael X.
AU - Ambudkar, Indu S.
PY - 2002/1/1
Y1 - 2002/1/1
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0036238275&partnerID=8YFLogxK
U2 - 10.1016/S1097-2765(02)00506-3
DO - 10.1016/S1097-2765(02)00506-3
M3 - Article
C2 - 11983166
AN - SCOPUS:0036238275
VL - 9
SP - 739
EP - 750
JO - Molecular Cell
JF - Molecular Cell
SN - 1097-2765
IS - 4
ER -