Expression of a long variant of CRACR2A that belongs to the Rab GTPase protein family in endothelial cells.

Expression of a long variant of CRACR2A that belongs to the Rab GTPase protein family in endothelial cells.
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DOI:
10.1016/j.bbrc.2014.11.095
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发表时间:
2015-01-02
影响因子:
3.1
通讯作者:
Beech, David J.
Beech, David J.
中科院分区:
生物学4区
文献类型:
--
作者:
Wilson, Lesley A.;McKeown, Lynn;Tumova, Sarka;Li, Jing;Beech, David J.

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Knockdown of CRACR2A lacks effect on CRAC channels in endothelial cells. Knockdown of CRACR2A depletes a protein twice the mass of CRACR2A. A long variant of CRACR2A, CRACR2A-L, occurs in endothelial cells. CRACR2A-L is a previously unrecognised EF-hand-containing Rab GTPase. CRACR2A-L has a positive role in endothelial tube formation. CRACR2A protein is described in T cells as an EF-hand-containing modulator of calcium-release-activated calcium (CRAC) channels. Here we sought relevance to calcium entry of endothelial cells. Unexpectedly, short interfering RNA designed to deplete CRACR2A had no effect on CRAC channels in endothelial cells but reduced the abundance of a protein with about twice the mass of CRACR2A. Reference to gene sequence data indicated the potential for a variant transcript encoding a C-terminal Rab GTPase extension of CRACR2A. Full-length cloning demonstrated expression of the long variant in endothelial cells. It was designated CRACR2A-L. Sequence analysis suggested it to be a previously unrecognised member of the Rab GTPase family. It made a positive contribution to endothelial tube formation. The data suggest that endothelial cells contain a long variant of CRACR2A which is an EF-hand-containing Rab protein that lacks impact on CRAC channels.
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