The Boston group saw TRPC5 Ca2+ channels transferring into the plasma membrane, as measured by total internal reflection microscopy, electrophysiology, and surface biotinylation, in response to several growth factors. “Instead of controlling just gating, you are controlling availability,” says Clapham.
Recruitment and activation of TRPC5 Ca2+ currents were dependent on activated Rac and production of PIP2. In combination with previous work, this suggests the following scenario: activated growth factor receptors turn on PI3K-mediated production of PIP3; PIP3 recruits an exchange...
The Rockefeller University Press
2004
The Rockefeller University Press
2004
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