M5795
Anti-MAP Kinase Kinase (MEK, MAPKK) antibody produced in rabbit
whole antiserum
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Synonym(s):
Anti-MAPKK, Anti-MEK
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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, human, rat
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
target post-translational modification
unmodified
Gene Information
human ... MAP2K1(5604) , MAP2K2(5605)
mouse ... Map2k1(26395) , Map2k2(26396)
rat ... Map2k1(170851) , Map2k2(58960)
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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
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.
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.
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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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WNK2 modulates MEK1 activity through the Rho GTPase pathway
Moniz S, et al.
Cellular Signalling, 20(10), 1762-1768 (2008)
Kazi M Ahmed et al.
Molecular cancer research : MCR, 4(12), 945-955 (2006-12-26)
The molecular mechanism by which tumor cells increase their resistance to therapeutic radiation remains to be elucidated. We have previously reported that activation of nuclear factor-kappaB (NF-kappaB) is causally associated with the enhanced cell survival of MCF+FIR cells derived from
S J Mansour et al.
Science (New York, N.Y.), 265(5174), 966-970 (1994-08-12)
Mitogen-activated protein (MAP) kinase kinase (MAPKK) activates MAP kinase in a signal transduction pathway that mediates cellular responses to growth and differentiation factors. Oncogenes such as ras, src, raf, and mos have been proposed to transform cells by prolonging the
Jan Pinkas et al.
Cancer research, 62(16), 4781-4790 (2002-08-17)
Activation of the mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)-mitogen-activated protein kinase (MAPK) pathway is a frequent event in tumorigenesis, and analysis of human breast carcinomas demonstrates that 25-50% of these tumors express elevated levels of activated MAPK1/2. However, a direct
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)
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