We used structure-based mutagenesis to engineer talin and β3 variants that interact with comparable affinity to the wild-type proteins but inhibit integrin activation by competing with endogenous talin. Here we define the structure of a complex between talin and the membrane-proximal integrin β3 cytoplasmic domain and identify specific contacts between talin and the integrin tail required for activation. Binding of the talin phosphotyrosine-binding (PTB) domain to integrin β subunit cytoplasmic domains (tails) causes activation, whereas numerous other PTB-domain-containing proteins bind integrins without activating them. Regulation of integrin affinity (activation) is essential for metazoan development and for many pathological processes.
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