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Myosin Type II
Myosin Light Chains
Myosin Heavy Chains
Distinct temporal-spatial roles for rho kinase and myosin light chain kinase in epithelial purse-string wound closure.
Myosin light chain phosphorylation regulates barrier function by remodeling tight junction structure.
Epithelial myosin light chain kinase activation induces mucosal interleukin-13 expression to alter tight junction ion selectivity.
No static at all.
Mechanisms and functional implications of intestinal barrier defects.
Tight junctions on the move: molecular mechanisms for epithelial barrier regulation.
The epithelial barrier is maintained by in vivo tight junction expansion during pathologic intestinal epithelial shedding.
LIGHT signals directly to intestinal epithelia to cause barrier dysfunction via cytoskeletal and endocytic mechanisms.
Targeted epithelial tight junction dysfunction causes immune activation and contributes to development of experimental colitis.
MLCK-dependent exchange and actin binding region-dependent anchoring of ZO-1 regulate tight junction barrier function.
TNFR2 activates MLCK-dependent tight junction dysregulation to cause apoptosis-mediated barrier loss and experimental colitis.
The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation.
ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.
Antibodies in cerebral cavernous malformations react with cytoskeleton autoantigens in the lesional milieu.
The scaffolding protein ZO-1 coordinates actomyosin and epithelial apical specializations in vitro and in vivo.
Nonmuscle Myosin Type IIB