Target intelligence / Profile preview

Talin-1 (TLN1)

Target
TLN1
Molecular classification
Cytoskeletal protein, Scaffold/adapter protein, Other
01

Overview

Talin-1 is a high molecular weight cytoskeletal adaptor protein encoded by the TLN1 gene. It is ubiquitously expressed and localized to regions of cell–matrix and cell–cell contacts, especially at focal adhesions and costameres in muscle tissues. Talin-1 acts as a crucial mediator connecting integrins (especially β1 and β3 integrins) to the actin cytoskeleton, facilitating cell adhesion, migration, and activation of integrins[1][2][6]. Its structural domains enable binding to actin, integrins, vinculin, and other proteins involved in cytoskeletal organization. In various tissues, talin-1 is vital for maintaining cell structure and signaling. In mouse models, loss of talin-1 leads to defects in platelet aggregation, muscle integrity, and is embryonically lethal[1]. In humans, altered TLN1 expression is observed in certain disease states, such as increased expression in heart failure. No direct pharmacological modulators are approved clinically, but its functions connect it to roles in cardiovascular disease, myopathies, and immune-related hemostatic disorders[1][2][5][6].

Other names
Talin 1KIAA1027TLNILWEQtalin-1TLN1
02

Mechanism of action

Not applicable—no direct modulatory drugs are currently known. Modulation would theoretically involve interfering with integrin–cytoskeleton linkage or integrin activation.

03

Biological functions

Linking integrins to the actin cytoskeletonIntegrin activationCell adhesionActin filament assemblyCell migration and spreadingOrganization of focal adhesions
04

Disease associations

Cardiovascular disease (heart failure, cardiac hypertrophy)Capillary leak syndromeCholestasis, benign recurrent intrahepaticImmune disorders (defective platelet activation linked to hemostatic defects)Muscular dystrophy/myopathyOther
05

Safety considerations

Essential for embryonic development—complete knockout is embryonic lethalDisruption may impair platelet function and cause hemostatic defectsPotential for muscle weakness or myopathy if function is lost
06

Biomarkers

Increased expression in cardiomyocytes may have biomarker utility in heart failureNo established, widely used clinical biomarkers found

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