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Distinct Roles of the Adaptor Protein Shc and Focal Adhesion Kinase in Integrin Signaling to ERK*
Although not necessary for signaling to ERK in primary fibroblasts, FAK may enhance and prolong integrin-mediated activation of ERK through p130CAS, Crk, and Rap1 in cells expressing B-Raf.
The integrin cytoplasmic domain-associated protein ICAP-1 binds and regulates Rho family GTPases during cell spreading
Data show for the first time that ICAP-1 regulates Rho family GTPases during integrin-mediated cell matrix adhesion, acting as guanine dissociation inhibitor.
Melusin, a muscle-specific integrin β1–interacting protein, is required to prevent cardiac failure in response to chronic pressure overload
Analysis of intracellular signaling events induced by pressure overload indicated that phosphorylation of glycogen synthase kinase-3 β (GSK-3β) was specifically blunted in melusin-null hearts, which prevents cardiac dilation during chronic pressure overload by specifically sensing mechanical stress.
Protection from angiotensin II–mediated vasculotoxic and hypertensive response in mice lacking PI3Kγ
It is shown that mice lacking the GPCR-activated phosphoinositide 3-kinase (PI3K)γ are protected from hypertension that is induced by administration of angiotensin II in vivo and suggested that blocking PI3Kγ function might be exploited to improve therapeutic intervention on hypertension.
IQGAP1 regulates ERK1/2 and AKT signalling in the heart and sustains functional remodelling upon pressure overload.
These data demonstrate, for the first time, a key role for the scaffold protein IQGAP1 in integrating hypertrophy and survival signals in the heart and regulating long-term left ventricle remodelling upon pressure overload.
ERK1/2 activation in heart is controlled by melusin, focal adhesion kinase and the scaffold protein IQGAP1
Melusin is characterized as a muscle-specific chaperone protein capable of ERK1/2 signalling activation in the heart and both focal adhesion kinase (FAK) and IQ motif-containing GTPase activating protein 1 (IQGAP1) are part of the melusin complex and are required for ERK 1/2 activation in response to pressure overload.
Cardiac Overexpression of Melusin Protects From Dilated Cardiomyopathy Due to Long-Standing Pressure Overload
It is demonstrated that melusin overexpression allows prolonged concentric compensatory hypertrophy and protects against the transition toward cardiac dilation and failure in response to long-standing pressure overload.