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anti-Human MYL2 Antibodies:
anti-Mouse (Murine) MYL2 Antibodies:
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Human Monoclonal MYL2 Primary Antibody for ELISA, FACS - ABIN450002
Samwer, Dehne, Spira, Kollmar, Gerlich, Urlaub, Görlich: The nuclear F-actin interactome of Xenopus oocytes reveals an actin-bundling kinesin that is essential for meiotic cytokinesis. in The EMBO journal 2013
Show all 3 Pubmed References
Human Monoclonal MYL2 Primary Antibody for ELISA, WB - ABIN969302
Sachdev, Raychowdhury, Sarkar: Human fast skeletal myosin light chain 2 cDNA: isolation, tissue specific expression of the single copy gene, comparative sequence analysis of isoforms and evolutionary relationships. in DNA sequence : the journal of DNA sequencing and mapping 2004
Show all 2 Pubmed References
Human Polyclonal MYL2 Primary Antibody for IHC, IHC (p) - ABIN4337526
He, Tian, Zhang, Hu, Huang, Zhang, Wang, Zhou: BAF200 is required for heart morphogenesis and coronary artery development. in PLoS ONE 2014
Human Polyclonal MYL2 Primary Antibody for IHC, WB - ABIN1742562
Yeo, Ting, Brena, Koh, Chen, Toh, Lim, Oh, Lee: Genome-Wide Transcriptome and Binding Sites Analyses Identify Early FOX Expressions for Enhancing Cardiomyogenesis Efficiency of hESC Cultures. in Scientific reports 2016
Human Polyclonal MYL2 Primary Antibody for IHC - ABIN966635
Janiak, Zemskov, Belkin: Cell surface transglutaminase promotes RhoA activation via integrin clustering and suppression of the Src-p190RhoGAP signaling pathway. in Molecular biology of the cell 2006
Human Monoclonal MYL2 Primary Antibody for ELISA, WB - ABIN966625
Ueda, Murata-Hori, Tatsuka, Hosoya: Rho-kinase contributes to diphosphorylation of myosin II regulatory light chain in nonmuscle cells. in Oncogene 2002
Show all 2 Pubmed References
Human Monoclonal MYL2 Primary Antibody for IF, IP - ABIN561897
Gannon, Doran, Kirwan, Ohlendieck: Drastic increase of myosin light chain MLC-2 in senescent skeletal muscle indicates fast-to-slow fibre transition in sarcopenia of old age. in European journal of cell biology 2009
The hypocontractile activity of D94A MYL-2 mutant resulted in the rightward shift of the force-pCa (show FLVCR1 Antibodies) dependence and decreased actin-activated myosin ATPase (show DNAH8 Antibodies) activity.
These results indicate shear stress induced vascular smooth muscle cell contraction was mediated by cell surface glycocalyx via a ROCK-MLC phosphatase (MLCP) pathway, providing evidence of the glycocalyx mechanotransduction in myogenic response.
The results show that the MYL2 mutation c.64G > A on its own is incapable of triggering clinical HCM in most carriers. However, the presence of an additional risk factor for hypertrophy, particularly hypertension, adds to the development of HCM.
Our study provides the first evidence that miR (show MLXIP Antibodies)-223 can regulate pulmonary artery smooth muscle cells proliferation, migration, and actomyosin reorganization through its novel targets, RhoB and MLC2 (show MYL9 Antibodies), resulting in vascular remodeling and the development of pulmonary arterial hypertension.
NKX2-5 (show NKX2-5 Antibodies) and MLC2v double-positive cells possess ventricular-like properties. The results demonstrate that the NKX2-5 (show NKX2-5 Antibodies)(eGFP/w) and MLC2v(mCherry/w) hPSCs provide a powerful model system to capture region-specific cardiac differentiation from early to late stages. Our study would facilitate subtype-specific cardiac development and functional analysis using the hPSC-derived sources.
This exome-wide association study indicated that C12orf51 rs11066280, MYL2 rs12229654, and ALDH2 (show ALDH2 Antibodies) rs671 polymorphisms are linked to blood Pb levels in the Korean population.
differential regulation of PKA and cell stiffness in unconfined versus confined cells is abrogated by dual, but not individual, inhibition of Piezo1 and myosin II.
Mutation in myosin regulatory light chain gene is associated with defective myosin motor function that ultimately result in pathological hypertrophic remodeling.
Lipolysis-stimulated lipoprotein receptors (LSRs) localized to bicellular junctions in association with myosin regulatory light chain 2 (MRLC2 (show MYL12B Antibodies)) at low cell densities and to tricellular contacts when myosin phosphatase target subunit 1 (MYPT1 (show PPP1R12A Antibodies)) localized to the bicellular regions.
Structural dynamics-based approach reveals that the E56G mutation in human ventricular essential light chain affects the structure of the actin-myosin complex in the presence of ATP. The mutation increases the population in the S structural state (increasing the duty ratio), and changes the structure of the W state, so that it more closely resembles the S state.
transgenic mouse models of hypertrophic cardiomyopathy may be caused by mutations in myosin regulatory light chain
MLC2 phosphorylation regulates actin-based cytokinesis in mouse oocytes, and this regulation may be mediated via a RhoA-MLC2-actin pathway.
Treatment of mice with an AT1R (show AGTRAP Antibodies) biased ligand, acting via beta-arrestin signalling, is able to induce an increase in cardiac contractility associated with an increase in ventricular myosin light chain-2 (show MYL12B Antibodies) phosphorylation
Hypertrophic cardiomyopathy associated Lys104Glu mutation in the myosin regulatory light chain causes diastolic disturbance in mice.
Mammalian target of rapamycin (mTOR (show FRAP1 Antibodies)) inhibition with rapamycin improves cardiac function in type 2 diabetic mice: potential role of attenuated oxidative stress and altered contractile protein (show TNNT2 Antibodies) expression.
Data indicate that NRG-1beta up-regulated the gene expressions of Nkx2.5, GATA4, alpha-actin, MLC-2v, and ANF in a time-dependent regulation of ErbB/ERK1/2 pathways.
Results indicated that sine oculis homeobox (show PRRX1 Antibodies) 1 (Six1 (show SIX1 Antibodies)) overexpression could significantly promote the expression of fast-type muscle genes Atp2a1 (show ATP2A1 Antibodies), Srl (show SRL Antibodies), and Mylpf (show MYLPF Antibodies).
High resolution characterization of myosin IIC protein tailpiece and its effect on filament assembly
Accelerated cMLCK protein turnover by the ubiquitin-proteasome system underlies the transition from compensated hypertrophy to decompensated heart failure as a result of reduced phosphorylation of MLC2v.
Results show that the binding force between selenium and cardiac myosin (CM), which consists of two heavy chains (MHC) and two pairs of light chains: MLC1 and MLC2, was 100 times stronger than that of daunorubicin (DNR) and CM.
We show that the phosphorylation of cTnI and alphaTm vary in the different chambers of the heart, whereas the phosphorylation of MLC2 and cTnT does not.
Thus gene encodes the regulatory light chain associated with cardiac myosin beta (or slow) heavy chain. Ca+ triggers the phosphorylation of regulatory light chain that in turn triggers contraction. Mutations in this gene are associated with mid-left ventricular chamber type hypertrophic cardiomyopathy.
, RLC of myosin
, cardiac ventricular myosin light chain 2
, myosin light chain 2
, myosin regulatory light chain 2, ventricular/cardiac muscle isoform
, myosin, light polypeptide 2, regulatory, cardiac, slow
, regulatory light chain of myosin
, slow cardiac myosin regulatory light chain 2
, fast skeletal myosin light chain 2
, myosin regulatory light chain 2, skeletal muscle isoform
, myosin light chain 2v
, myosin light chain, phosphorylatable, cardiac ventricles
, ventricular myosin regulatory light chain
, cardiac myosin light chain-2
, myosin, light chain 2b, regulatory, cardiac, slow
, myosin, light polypeptide 2b, regulatory, cardiac, slow
, myosin light chain 2 S homeolog
, myosin, light chain 2, regulatory, cardiac, slow
, cardiac muscle isoform
, light polypeptide 2
, myosin regulatory light chain 2A, cardiac muscle isoform
, myosin light chain 2V
, ventricular myosin light chain 2