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MABT180

Sigma-Aldrich

Anti-MLC-2 Antibody, clone 19D3.1

clone 19D3.1, from mouse

Synonym(s):

Myosin regulatory light chain 2, ventricular/cardiac muscle isoform, MLC-2, MLC-2v

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

19D3.1, monoclonal

species reactivity

human, rat

technique(s)

immunohistochemistry: suitable
western blot: suitable

isotype

IgG1κ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... MYL2(4633)

General description

Myosin light chain 2 (MLC2), also known as myosin regulatory light chain (MRLC), RLC, or LC20, has several isoforms and is a component of myosin, which is made up of two heavy chains and four light chains. MLC2 is involved in smooth muscle contraction, stress fiber assembly, and cytokinesis. MLC2 defects can cause of familial hypertrophic cardiomyopathy type 10 (CMH10).

Specificity

Other homologies: Mouse 92% sequence homologies.

Immunogen

GST-tagged recombinant protein corresponding to human MLC-2.

Application

Detect Myosin using this mouse monoclonal antibody, Anti-MLC-2 Antibody, clone 19D3.1 validated for use in western blotting & IHC.
Immunohistochemistry Analysis: A 1:1,000 dilution from a representative lot detected MLC-2 in human cardiac myocyte and in rat skeletal muscle tissues.
Research Category
Cell Structure
Research Sub Category
ECM Proteins

Quality

Evaluated by Western Blotting in human skeletal muscle tissue lysate.

Western Blotting Analysis: A 1:2,000 dilution from a representative lot detected MLC-2 in 10 µg of human skeletal muscle tissue lysate.

Target description

~19 kDa observed

Physical form

Format: Purified
Protein G Purified
Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Analysis Note

Control
Human skeletal muscle tissue lysate.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Elena Chung et al.
Respiratory research, 21(1), 256-256 (2020-10-10)
Glucocorticoids (GCs) and β2-adrenergic receptor (β2AR) agonists improve asthma outcomes in most patients. GCs also modulate gene expression in human airway smooth muscle (HASM), thereby attenuating airway inflammation and airway hyperresponsiveness that define asthma. Our previous studies showed that the
Edwin J Yoo et al.
British journal of pharmacology, 174(23), 4383-4395 (2017-09-19)
PI3K-dependent activation of Rho kinase (ROCK) is necessary for agonist-induced human airway smooth muscle cell (HASMC) contraction, and inhibition of PI3K promotes bronchodilation of human small airways. The mechanisms driving agonist-mediated PI3K/ROCK axis activation, however, remain unclear. Given that G12
Christie A Ojiaku et al.
American journal of respiratory cell and molecular biology, 61(2), 209-218 (2019-02-12)
Helper T effector cytokines implicated in asthma modulate the contractility of human airway smooth muscle (HASM) cells. We have reported recently that a profibrotic cytokine, transforming growth factor (TGF)-β1, induces HASM cell shortening and airway hyperresponsiveness. Here, we assessed whether
Paul R Clark et al.
PloS one, 10(3), e0120075-e0120075 (2015-03-31)
Capillary leak in severe sepsis involves disruption of endothelial cell tight junctions. We modeled this process by TNF treatment of cultured human dermal microvascular endothelial cell (HDMEC) monolayers, which unlike human umbilical vein endothelial cells form claudin-5-dependent tight junctions and
Feng Liu et al.
Stem cell research & therapy, 11(1), 284-284 (2020-07-18)
Biological pacemakers derived from pluripotent stem cell (PSC) have been considered as a potential therapeutic surrogate for sick sinus syndrome. So it is essential to develop highly efficient strategies for enrichment of sinoatrial node-like cells (SANLCs) as seed cells for

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