推荐产品
生物来源
mouse
质量水平
抗体形式
purified immunoglobulin
抗体产品类型
primary antibodies
克隆
19D3.1, monoclonal
种属反应性
human, rat
技术
immunohistochemistry: suitable
western blot: suitable
同位素/亚型
IgG1κ
NCBI登记号
UniProt登记号
运输
wet ice
靶向翻译后修饰
unmodified
基因信息
human ... MYL2(4633)
一般描述
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).
特异性
Other homologies: Mouse 92% sequence homologies.
免疫原
GST-tagged recombinant protein corresponding to human MLC-2.
应用
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
Cell Structure
Research Sub Category
ECM Proteins
ECM Proteins
质量
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.
Western Blotting Analysis: A 1:2,000 dilution from a representative lot detected MLC-2 in 10 µg of human skeletal muscle tissue lysate.
目标描述
~19 kDa observed
外形
Protein G Purified
Format: Purified
Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
储存及稳定性
Stable for 1 year at 2-8°C from date of receipt.
分析说明
Control
Human skeletal muscle tissue lysate.
Human skeletal muscle tissue lysate.
免责声明
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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储存分类代码
12 - Non Combustible Liquids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
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
Transforming Growth Factor-β1 Decreases β2-Agonist-induced Relaxation in Human Airway Smooth Muscle.
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
Christie A Ojiaku et al.
American journal of respiratory cell and molecular biology, 58(5), 575-584 (2017-10-07)
Transforming growth factor β1 (TGF-β1), a cytokine whose levels are elevated in the airways of patients with asthma, perpetuates airway inflammation and modulates airway structural cell remodeling. However, the role of TGF-β1 in excessive airway narrowing in asthma, or airway
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
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