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Key Documents

Safety Information

MAB1552

Sigma-Aldrich

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

culture supernatant, clone F26.2D11, Chemicon®

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About This Item

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

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.

NM_000257.2

UniProt accession no.

P12883
P13533

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.

Legal Information

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

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Storage Class Code

12 - Non Combustible Liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Listings

Regulatory Listings are mainly provided for chemical products. Only limited information can be provided here for non-chemical products. No entry means none of the components are listed. It is the user’s obligation to ensure the safe and legal use of the product.

JAN Code

MAB1552:

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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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)
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
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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