Blocking talin autoinhibition through the E1770A point mutation in Tln1 impairs platelet function. Homozygous and heterozygous Tln1^E1770A mice exhibit prolonged bleeding time, reduced platelet aggregation, and defective clot retraction. Despite intact integrin inside-out activation, these defects suggest talin autoinhibition regulates broader aspects of platelet function and hemostasis.
Increased bleeding time, impaired clot retraction, defective platelet aggregation, no increase in integrin activation
Tln1^E1770A/E1770A point mutant mouse (autoinhibition-deficient talin), C57BL/6 background
Hemostasis, platelet function, integrin signaling, coagulation defect models
CRISPR-generated point mutation (E1770A) in Tln1, homozygous and heterozygous comparison, platelet aggregation and clot retraction assays, tail bleeding test, integrin signaling analysis
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