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M5795

Sigma-Aldrich

Anti-MAP Kinase Kinase (MEK, MAPKK) antibody produced in rabbit

whole antiserum

Synonym(s):
Anti-MAPKK, Anti-MEK
MDL number:

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

whole antiserum

antibody product type

primary antibodies

clone

polyclonal

mol wt

antigen 45 kDa (MEK1a)
antigen 46 kDa (MEK2)

contains

15 mM sodium azide

species reactivity

mouse, rat, human

technique(s)

microarray: suitable
western blot: 1:20,000 using rat brain extract and mouse NIH 3T3 fibroblast lysate

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

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General description

MAP kinase kinase (MAPKK, MEK) consists of three different isoforms with a high degree of homology between them, MEK-1a (45 kDa), MEK-1b (41 kDa), and MEK-2 (46 kDa). MEK isoforms are generally expressed, in the central nervous system, thymus, spleen, heart, lung, kidney. In addition, it is also expressed at high levels in PC12 cells and in fibroblasts.

Specificity

Reacts with MEK-1a and MEK-2. Staining of MEK-1a and MEK-2 is specifically inhibited with MEK-1 peptide (34-48), but not with MAP kinase peptide (317-399) corresponding to subdomain XI of ERK1.

Immunogen

synthetic peptide corresponding to amino acids 34-48 of human MAP kinase kinase 1 (MEK-1).

Application

Anti-MAP Kinase Kinase (MEK, MAPKK) antibody produced in rabbit has been used in immunoblotting and for analysis of signaling pathways.

Biochem/physiol Actions

MAP Kinase Kinase (MAPKK, MEK1 and MEK2) belong to a family of enzymes that activates their substrate by dual phosphorylation at threonine and tyrosine residues. MEK1 and MEK2 have 86% homology in their catalytic domain. Activation of MEK1/2 is mediated in mitogen-stimulated cells by Raf-1 kinase. MEK1/2 then activates ERK1/2 leading to the activation of several downstream targets that contribute to cell proliferation, apoptosis and motility. In addition to ERK1/2, there may be non-catalytic effectors of MEK1/2. MEK isoforms appear to be widely expressed in the central nervous system, thymus, spleen, heart, lung, and kidney. Active forms of MEK1/2 are sufficient for the transformation of NIH3T3 cells of the differentiation of PC-12 cells.
Antibodies that react specifically with MEK may be used to study the specific activation requirements, differential tissue expression and intracellular localization of MEK in normal and neoplastic tissue.

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.

Certificate of Analysis

Certificate of Origin

Transcriptional and metabolic rewiring of colorectal cancer cells expressing the oncogenic KRAS G13D mutation
Charitou T, et al.
British Journal of Cancer, 20(10), 1-1 (2019)
WNK2 modulates MEK1 activity through the Rho GTPase pathway
Moniz S, et al.
Cellular Signalling, 20(10), 1762-1768 (2008)
Sónia Moniz et al.
Cellular signalling, 20(10), 1762-1768 (2008-07-03)
WNK protein kinases form a kinase subfamily expressed in multi-cellular organisms and the human genome encodes four distinct WNK genes. Human WNK2 has been recently identified as a cell growth regulator that modulates activation of the ERK1/2 protein kinase and
Jian-Hui Zhu et al.
The American journal of pathology, 161(6), 2087-2098 (2002-12-06)
A better understanding of cellular mechanisms that occur in Parkinson's disease and related Lewy body diseases is essential for development of new therapies. We previously found that 6-hydroxydopamine (6-OHDA) elicits sustained extracellular signal-regulated kinase (ERK) activation that contributes to neuronal
Christophe Frémin et al.
Journal of hematology & oncology, 3, 8-8 (2010-02-13)
The Ras-dependent Raf/MEK/ERK1/2 mitogen-activated protein (MAP) kinase signaling pathway is a major regulator of cell proliferation and survival. Not surprisingly, hyperactivation of this pathway is frequently observed in human malignancies as a result of aberrant activation of receptor tyrosine kinases

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