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Histamine induces myosin light chain (MLC)phosphorylation via MYLK, suggesting regulatory role for MLC in controlling corneal epithelial permeability.
This study demonstrates that cyclic stretch disrupts tight junctions and adherens junctions by a JNK2 (show MAPK9 Proteins), c-Src (show SRC Proteins), and MLCK (show MYLK Proteins)-dependent mechanism.
Biochemical and physiological regulation of cardiac myocyte contraction by cardiac-specific myosin light chain kinase.
These findings suggest that hepatitis B virus X protein disrupts stress fiber formation and triggers apoptosis via an MLCK and a PTEN-dependent pathway.
Integrated cDNA expression analysis of failing human myocardia uncovered a novel protein kinase (show CDK7 Proteins), cardiac-specific myosin light chain kinase (cardiac-MLCK), which acts on MLC2v (show MYL2 Proteins).
data indicate that the IL-1beta (show IL1B Proteins)-induced increase in MLCK (show MYLK Proteins) protein expression and Caco-2 TJ permeability was mediated by an increase in MLCK (show MYLK Proteins) expression and activity and by an NF-kappaB (show NFKB1 Proteins)-dependent increase in MLCK (show MYLK Proteins) gene transcription
Acanthopanax senticosus polysaccharide pretreatment may be associated with inhibition of the NF-kappaB (show NFKB1 Proteins)/MLCK (show MYLK Proteins) pathway and concomitant amelioration of LPS (show TLR4 Proteins)-induced tight junction dysfunction of intestinal epithelium in endotoxemia
that MLCK (show MYLK Proteins) is competing with centrally active ROCK for a limiting pool of monomer with which to drive lamellar filament assembly
This study demonstrated that catchlike property during dynamic performance in mouse hindlimb muscles with (wild-type) and without MLCK(-/-) ) the primary mechanism for PTP (myosin phosphorylation).
Ablation of cardiac Mylk3 suggests that Mylk3 plays a pivotal role in the transition from compensated to decompensated hypertrophy via cardiac myocyte atrophy and sarcomeric disorganization.
Data suggest that galectin-3 (show LGALS3 Proteins) in hepatocellular carcinoma cells promotes cell migration by inducing RhoA GTPase activity, activating Mlck (show MYLK Proteins), up-regulating phosphorylation of MLC2 (myosin light chain 2 (show MYL12B Proteins)), and inducing actin rearrangement.
epithelial MLCK (show MYLK Proteins)-activated brush border fanning by IFN-gamma (show IFNG Proteins) promotes adherence and internalization of normally noninvasive enteric bacteria
MLCK may regulate the structure and the motility of stereocilia through F-actin polymerization.
Silencing TNFR2 (show TNFRSF1B Proteins), but not TNFR1 (show TNFRSF1A Proteins), resulted in restoration of epithelial tight junction (TJ) associated with decreased MLCK (show MYLK Proteins) expression.
Calcium regulation of MLCK (show MYLK Proteins) facilitates GLUT4 (show SLC2A4 Proteins)-mediated glucose uptake in 3T3-L1 adipocytes.
nmMLCK has a critical role in thrombin (show F2 Proteins)-induced endothelial cell inflammation and lung PMN (show TBCE Proteins) infiltration
Phosphorylation of cardiac myosin heavy chains (see MYH7B, MIM 609928) and light chains (see MYL2, MIM 160781) by a kinase, such as MYLK3, potentiates the force and rate of cross-bridge recruitment in cardiac myocytes (Chan et al., 2008
myosin light chain kinase 3
, Putative myosin light chain kinase 3
, cardiac-MyBP-C-associated Ca/CaM kinase
, myosin light chain kinase, smooth muscle
, myosin, light chain kinase
, myosin, light polypeptide kinase
, smooth muscle myosin light chain kinase (61-kDa active fragment)
, MLC kinase
, cardiac-MyBP-C associated Ca/CaM kinase
, putative myosin light chain kinase 3
, cardiac MLCK
, cardiac-specific myosin light chain kinase