XXXX have overlapping functions in epithelial cells implications for phenotype modification.

@entity15958 @entity1 @entity43166 @entity2639 @entity272 @entity53713 @entity942
Kindlins are a novel family of intracellular adaptor proteins in integrin-containing focal adhesions. @entity15958 are expressed in the skin, but whether and how they cooperate in adult epithelial cells have remained elusive. We uncovered the overlapping roles of @entity15958 in maintaining epithelial integrity and show that the phenotype of @entity53713 -deficient cells can be modulated by regulating @entity43166 gene expression and vice versa. The experimental evidence is provided by use of @entity1 keratinocyte cell lines that express both kindlins, just @entity53713 or @entity43166 , or none of them. Double deficiency of @entity15958 had significant negative effects on focal adhesion formation and actin cytoskeleton organization, cell adhesion, survival, directional migration, and activation of b(1) integrin, whereas @entity942 kindlin only showed variable perturbation of these functions. Cell motility and formation of cell-cell contacts were particularly affected by lack of @entity43166 . These results predict that @entity15958 can functionally compensate for each other, at least in part. The high physiologic and pathologic significance of the compensation was emphasized by the discovery of environmental regulation of @entity43166 expression. UV-B irradiation induced loss of @entity43166 in keratinocytes. This first example of environmental regulation of kindlin expression has implications for phenotype modulation in @entity2639 , a @entity272 caused by @entity53713 deficiency.
