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 | UniProt | Comment | Textmining |
---|---|---|---|
Sus scrofa | - |
- |
- |
Sus scrofa Yorkshire crossbred | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
Caco-2/BBe cell | i.e. C2Bbe1 cell | Sus scrofa | - |
ileum | - |
Sus scrofa | - |
intestine | - |
Sus scrofa | - |
Synonyms | Comment | Organism |
---|---|---|
MLCK | - |
Sus scrofa |
myosin light chain kinase | - |
Sus scrofa |
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 |