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MYLK, a muscle member of the immunoglobulin gene superfamily, encodes myosin light chain kinase which is a calcium/calmodulin dependent enzyme. De plus, nous expédions Myosin Light Chain Kinase Anticorps (124) et Myosin Light Chain Kinase Kits (36) et beaucoup plus de produits pour cette protéine.
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miR155 directly suppressed the expression of MYLK without affecting the RhoA (Montrer RHOA Protéines) pathway.
the MAPKspecific inhibitor SB203580 attenuated the inhibitory effects of 4HPR on the migration of HepG2 cells. Moreover, we also observed that 4HPR inhibited the activation and expression of myosin light chain kinase (MLCK) in HepG2 cells.
Recombinant human MLCK was concentration- and time-dependently degraded by recombinant human MMP9 (Montrer MMP9 Protéines) in vitro, and this process was prevented by the MMP9 (Montrer MMP9 Protéines) inhibitor.
High expression of MLCK is correlated with metastatic triple negative breast cancer.
Interaction between kinase domain and regulatory light chain (RLC) substrate is identified in the absence of calmodulin, indicating restored substrate-binding capability due to mechanically induced removal of the auto-inhibitory regulatory region.
loss of MLCK contributes to the migratory properties of epithelial cells resulting from changes in cell-cell and cell-matrix adhesions, and increased epidermal growth factor receptor (Montrer EGFR Protéines) signaling.
Sixty-seven experienced runners competed in a marathon race. The MLCK genotype (C37885A) of these marathoners was determined. CA heterozygotes for MLCK C37885A might present higher exercise-induced muscle damage after a marathon competition than CC counterparts.
these Acute respiratory distress syndrome (ARDS)-associated MYLK cytosine-guanine dinucleotides with effect modification by ethnicity and local modified cytosine quantitative trait loci suggest that MYLK epigenetic variation and local genetic background may contribute to health disparities observed in ARDS.
mechanical stress and MYLK single nucleotide polymorphism regulate MYLK alternative splicing.
Rebeccamycin attenuates TNF-alpha (Montrer TNF Protéines)-induced disruption of intestinal epithelial barrier integrity by inducing claudin-5 (Montrer CLDN5 Protéines) expression and suppressing MLCK production via Chk1 (Montrer CHEK1 Protéines) activation.
Histamine induces myosin light chain (MLC)phosphorylation via MYLK, suggesting regulatory role for MLC in controlling corneal epithelial permeability.
evaluated the spatial arrangement of the catalytic/regulatory domain, three immunoglobulin-related motifs, one fibronectin-related motif, a repetitive, proline-rich segment, and, at the N-terminus, a unique F-actin-binding domain.
telokin may play a role in attenuating constitutive myosin light chain phosphorylation
MLCK is linked to timely blastocyst formation, though it is dispensable for oocyte meiotic maturation
NF-kappaB (Montrer NFKB1 Protéines) novel partner within endothelial cells
MLCK regulates cell migration in a myosin regulatory light chain phosphorylation-independent mechanism.
nmMlck modulates IL-1beta (Montrer IL1B Protéines)-mediated downregulation of Cldn5 (Montrer CLDN5 Protéines) in brain microvascular endothelial cells.
a prominent effect of the multifunctional microRNA-155 in endothelial cells is modulation of phenotype through alterations in RhoA, myosin light chain kinase expression, and actin cytoskeleton organization
CArG element in intron 15 of the mylk1 gene is necessary for maximal expression of the 130-kDa smMLCK and that the 130-kDa smMLCK isoform is specifically required to regulate smooth muscle contractility
In immune-mediated inflammatory bowel disease, tight junction dysregulation and barrier loss is induced by MLCK, but at advanced stages, barrier loss is MLCK-independent.
Claudin-2 (Montrer CLDN2 Protéines) assumes an important role in colorectal inflammation, and furthermore implicates the involvement of MLCK in colon inflammation.
involved in IL-1beta (Montrer IL1B Protéines)-induced increase in intestinal permeability
Conclude that Mlck1a is the subtype of MLCK that contributes to platelet shape change and thrombus formation.
This gene, a muscle member of the immunoglobulin gene superfamily, encodes myosin light chain kinase which is a calcium/calmodulin dependent enzyme. This kinase phosphorylates myosin regulatory light chains to facilitate myosin interaction with actin filaments to produce contractile activity. This gene encodes both smooth muscle and nonmuscle isoforms. In addition, using a separate promoter in an intron in the 3' region, it encodes telokin, a small protein identical in sequence to the C-terminus of myosin light chain kinase, that is independently expressed in smooth muscle and functions to stabilize unphosphorylated myosin filaments. A pseudogene is located on the p arm of chromosome 3. Four transcript variants that produce four isoforms of the calcium/calmodulin dependent enzyme have been identified as well as two transcripts that produce two isoforms of telokin. Additional variants have been identified but lack full length transcripts.
, myosin light chain kinase, smooth muscle
, myosin, light polypeptide kinase
, smooth muscle myosin light chain kinase
, kinase related protein, telokin
, myosin, light chain kinase
, myosin light chain kinase
, myosin light chain kinase, smooth muscle-like
, smooth muscle myosin light chain kinase (61-kDa active fragment)
, myosin light chain kinase 1
, smooth muscle MLCK