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Key Documents

AV37504

Sigma-Aldrich

Anti-MKL1 antibody produced in rabbit

IgG fraction of antiserum

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

106 kDa

species reactivity

rat, mouse, human

concentration

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

mouse ... MKL1(223701)

General description

Megakaryoblastic Leukemia-1 (MKL1, MAL, MRTF-A, BSAC) is a MRTF family transcription factor with evolutionary conserved domains required for actin-binding, homo- and heterodimerization, high-order chromatin organization and transcriptional activation. MKL1 regulates a wide range of cell processes including epithelial-mesenchymal transition (EMT); megakaryocytic differentiation and migration; neuronal network remodeling; cellular motile functions and muscle cell differentiation including cardiovascular development. It is a component of the Rho/megakaryoblastic leukemia 1 (MKL1) signaling pathway.

Specificity

Anti-MKL1 polyclonal antibody reacts with bovine, chicken, mouse, human, and rat megakaryoblastic leukemia-1 proteins.

Immunogen

Synthetic peptide directed towards the C terminal of human MKL1

Application

Anti-MKL1 polyclonal antibody is used to tag megakaryoblastic leukemia-1 for detection and quantitation by Western blotting and in plasma by immunohistochemical (IHC) techniques. It is used as a probe to determine the roles of megakaryoblastic leukemia-1 in the Rho/megakaryoblastic leukemia 1 (MKL1) signaling pathway and a variety of cell processes such as cell mobilization and the epithelial-mesenchymal transition (EMT).

Biochem/physiol Actions

MKL1 transduces cytoskeletal signals and induces smooth muscle cell differentiation from undifferentiated embryonic stem cells

Sequence

Synthetic peptide located within the following region: QPLSQPGFPAPGPPAQMDLEHPPQPPFATPTSLLKKEPPGYEETVTQQPK

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

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

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Rabea Hinkel et al.
Nature communications, 5, 3970-3970 (2014-06-10)
Gradual occlusion of coronary arteries may result in reversible loss of cardiomyocyte function (hibernating myocardium), which is amenable to therapeutic neovascularization. The role of myocardin-related transcription factors (MRTFs) co-activating serum response factor (SRF) in this process is largely unknown. Here
Maria Carmela Filomena et al.
eLife, 10 (2021-09-25)
Myopalladin (MYPN) is a striated muscle-specific immunoglobulin domain-containing protein located in the sarcomeric Z-line and I-band. MYPN gene mutations are causative for dilated (DCM), hypertrophic, and restrictive cardiomyopathy. In a yeast two-hybrid screening, MYPN was found to bind to titin
Charly Jehanno et al.
Biochimica et biophysica acta. Gene regulatory mechanisms, 1863(5), 194507-194507 (2020-03-03)
Estrogen receptor (ERα) is central in driving the development of hormone-dependent breast cancers. A major challenge in treating these cancers is to understand and overcome endocrine resistance. The Megakaryoblastic Leukemia 1 (MKL1, MRTFA) protein is a master regulator of actin
Anne T Bertrand et al.
Journal of cell science, 127(Pt 13), 2873-2884 (2014-05-09)
The mechanisms underlying the cell response to mechanical forces are crucial for muscle development and functionality. We aim to determine whether mutations of the LMNA gene (which encodes lamin A/C) causing congenital muscular dystrophy impair the ability of muscle precursors

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