MLP and CARP are linked to chronic PKCα signalling in dilated cardiomyopathy.

MLP (muscle LIM protein)-deficient mice count among the first mouse models for dilated cardiomyopathy (DCM), yet the exact role of MLP in cardiac signalling processes is still enigmatic. Elevated signalling activity is known to be an important contributor to heart failure. Here we show that MLP directly inhibits the activity of In end-stage DCM, duanyu1531α is concentrated at the intercalated disc of cardiomyocytes, where it is sequestered by the adaptor protein in a multiprotein complex together with PLCβ1. In mice deficient for both MLP and Cduanyu37 the chronic duanyu1531α signalling chain at the intercalated disc is broken and they remain healthy. Our results suggest that the main role of MLP in heart lies in the direct inhibition of duanyu1531α and that chronic uninhibited duanyu1531α activity at the intercalated disc in the absence of functional MLP leads to heart failure.

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