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Sci Signal. 2010 Oct 26;3(145):ra77. doi: 10.1126/scisignal.2001200.

Antagonistic regulation of actin dynamics and cell motility by TRPC5 and TRPC6 channels.

Author information

1
Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.

Erratum in

  • Sci Signal. 2010;3(147):er11. Pavenstaedt, Hermann [corrected to Pavenstädt, Hermann].

Abstract

The Rho family of small guanosine triphosphatases (Rho GTPases: RhoA, Cdc42, and Rac1) regulates many aspects of cell behavior, including actin dynamics and cell migration. The generation of calcium ion (Ca(2+)) microdomains is critical in promoting cell migration because they control the localized activity of Rho GTPases. We identified receptor-activated TRPC5 and TRPC6 (transient receptor potential canonical type 5 and 6) channels as antagonistic regulators of actin remodeling and cell motility in fibroblasts and kidney podocytes. We show that TRPC5 is in a molecular complex with Rac1, whereas TRPC6 is in a molecular complex with RhoA. TRPC5-mediated Ca(2+) influx induces Rac1 activation, thereby promoting cell migration, whereas TRPC6-mediated Ca(2+) influx increases RhoA activity, thereby inhibiting cell migration. Our data unveil antagonistic Ca(2+) influx pathways as a conserved signaling mechanism for the integrated regulation of cell migration.

PMID:
20978238
PMCID:
PMC3071756
DOI:
10.1126/scisignal.2001200
[Indexed for MEDLINE]
Free PMC Article

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