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{ <http://www.tkuhn.ch/bel2nanopub/RAv_cMjNHvvwGLIBCe1Z1r9_Sa1jfQIvQPxj4NHLzN-MM#_3> ?p ?o ?g. }
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Pharmacologic inhibition of FAK or expression of kinase-deficient FAK, mutated by substituting Tyr-397 with Phe, inhibit TGF-beta1-induced alpha-smooth muscle actin expression, stress fiber formation, and cellular hypertrophy.
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