Literature summary for 2.7.11.18 extracted from

Jin, Y.; Blikslager, A.T.
Myosin light chain kinase mediates intestinal barrier dysfunction via occludin endocytosis during anoxia/reoxygenation injury (2016), Am. J. Physiol. Cell Physiol., 311, C996-C1004.

Search for more literature for 2.7.11.18

Inhibitors

Inhibitors	Comment	Organism	Structure
MLCK inhibitor peptide 18	a membrane permeant nonapeptide inhibitor of MLCK. Treatment with the MLCK inhibitor peptide 18 attenuates the increased epithelial monolayer permeability and occludin endocytosis caused by anoxia/reoxygenation injury	Sus scrofa

Organism

Organism	UniProt	Comment	Textmining
Sus scrofa	-	-	-
Sus scrofa Yorkshire crossbred	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
Caco-2/BBe cell	i.e. C2Bbe1 cell	Sus scrofa	-
ileum	-	Sus scrofa	-
intestine	-	Sus scrofa	-

Synonyms

Synonyms	Comment	Organism
MLCK	-	Sus scrofa
myosin light chain kinase	-	Sus scrofa

General Information

General Information	Comment	Organism
malfunction	MLCK enzyme inhibitors reduce paracellular barrier dysfunction in ischemic porcine ileum. Pharmacological inhibitions of MLCK significantly reduce paracellular permeability and occludin internalization in in vitro anoxia/reoxygenation injury and ex vivo porcine ischemic injury experimental models	Sus scrofa
physiological function	myosin light chain kinase (MLCK) has been shown to alter barrier function via regulation of interepithelial tight junctions. Intestinal anoxia/reoxygenation injury disrupts tight junctions barrier function via MLCK activation and myosin light chain phosphorylation, MLC phosphorylation was significantly increased by anoxia/reoxygenation injury. MLCK-induced occludin endocytosis mediates intestinal epithelial barrier dysfunction during anoxia/reoxygenation injury. The perijunctional actomyosin ring contracts in response to myosin light chain (MLC) phosphorylation, primarily by myosin light chain kinase (MLCK) activation. This in turn leads to tight junction opening	Sus scrofa

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Release 2023.1 (January 2023)