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MAB1552

Sigma-Aldrich

Anti-Myosin Antibody, ventricular heavy chain α/β, clone F26.2D11

culture supernatant, clone F26.2D11, Chemicon®

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

生物来源

mouse

抗体形式

culture supernatant

抗体产品类型

primary antibodies

克隆

F26.2D11, monoclonal

种属反应性

human

制造商/商品名称

Chemicon®

技术

immunohistochemistry: suitable
western blot: suitable

同位素/亚型

IgG2a

NCBI登记号

UniProt登记号

运输

dry ice

靶向翻译后修饰

unmodified

基因信息

human ... MYH6(4624)

特异性

Recognizes the LMM (light meromyosin) fragment of human ventricular myosin heavy chain (type alpha/beta)

免疫原

Epitope: ventricular heavy chain alpha/beta
Human ventricular myosin

应用

Anti-Myosin Antibody, ventricular heavy chain α/β, clone F26.2D11 is an antibody against Myosin for use in WB, IH.
Immunochemistry: undiluted to 1:10

Western blotting: 1:10

Optimal dilutions must be determined by the end user.

法律信息

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

WGK

nwg

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Elizabeth M Grey et al.
American journal of physiology. Heart and circulatory physiology, 285(1), H90-H96 (2003-03-15)
Conflicting reports exist regarding the influence of beta-adrenergic stimulation on the maximum velocity of shortening (Vmax) in ventricular myocytes. This may be due to an unrecognized effect of maturation. In the present study, the effects of beta-adrenergic receptor stimulation on
Regulation of gap junction protein (connexin) genes and function in differentiating ES cells.
M Oyamada et al.
Methods in molecular biology (Clifton, N.J.), 185, 63-69 (2002-01-05)
Carl W Tong et al.
Circulation research, 103(9), 974-982 (2008-09-20)
Normal cardiac function requires dynamic modulation of contraction. beta1-adrenergic-induced protein kinase (PK)A phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate crossbridge kinetics to modulate contraction. We tested this idea with mechanical measurements and echocardiography in a mouse model lacking
Armita M Gorabi et al.
Journal of cellular physiology, 234(2), 1534-1546 (2018-08-06)
The discovery of gene- and cell-based strategies has opened a new area to investigate novel approaches for the treatment of many conditions caused by cardiac cell failure. The TBX18 (T-box 18) transcription factor is considered as a prominent factor in

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