Talin controls the exit of the integrin alpha 5 beta 1 from an early compartment of the secretory pathway.

摘要: Talin is a major cytosolic protein that links the intracellular domains of beta1 and beta3 integrins to cytoskeleton. It required for focal adhesion assembly. However, its downregulation not only slows down cell spreading organization adhesions but also impairs maturation some integrins, including fibronectin receptor alpha5beta1. To investigate this, we characterized integrin synthesized in cells expressing talin anti-sense RNA (AT22 cells). We identified large pool abnormally accumulated an earlier compartment secretory pathway. In this report, show talin-deficient AT22 cells, aberrant glycosylation receptors accompanied by delay export normal was found associated with enriched membrane fraction containing Golgi endoplasmic reticulum. Finally, microinjection anti-talin antibodies resulted accumulation within cells. These data strongly suggest plays specific role newly integrins. propose binding may disclose diphenylalanine signal, which present membrane-proximal GFFKR motif conserved all alpha chains.