MAB1552
Anti-Myosin Antibody, ventricular heavy chain α/β, clone F26.2D11
culture supernatant, clone F26.2D11, Chemicon®
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UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
antibody form
culture supernatant
antibody product type
primary antibodies
clone
F26.2D11, monoclonal
species reactivity
human
manufacturer/tradename
Chemicon®
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2a
NCBI accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... MYH6(4624)
Specificity
Recognizes the LMM (light meromyosin) fragment of human ventricular myosin heavy chain (type alpha/beta)
Immunogen
Epitope: ventricular heavy chain alpha/beta
Human ventricular myosin
Application
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.
Western blotting: 1:10
Optimal dilutions must be determined by the end user.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
recommended
WGK
nwg
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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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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