AV37504
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.
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
Anti-MKL1 polyclonal antibody reacts with bovine, chicken, mouse, human, and rat megakaryoblastic leukemia-1 proteins.
MKL1 transduces cytoskeletal signals and induces smooth muscle cell differentiation from undifferentiated embryonic stem cells
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Other Notes
Synthetic peptide located within the following region: QPLSQPGFPAPGPPAQMDLEHPPQPPFATPTSLLKKEPPGYEETVTQQPK
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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