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About This Item
UNSPSC Code:
12352203
biological source
rabbit
conjugate
unconjugated
antibody form
Ig fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
immunohistochemistry: 1:50-1:100, indirect ELISA: 1:1000, western blot: 1:100-1:500
NCBI accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
Gene Information
human ... MEKK3(4215)
General description
MEKK3 directly regulates the stress-activated protein kinase (SAPK) and extracellular signal-regulated protein kinase (ERK) pathways by activating SEK and MEK1/2 respectively; it does not regulate the p38 pathway. In cotransfection assays, it enhances transcription from a nuclear factor kappa-B (NFKB)-dependent reporter gene, consistent with a role in the SAPK pathway.
Immunogen
MEKK3 (NP_976226, 241-275)
This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the center region of human MEKK3.
This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the center region of human MEKK3.
Physical form
Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.
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Storage Class
12 - Non Combustible Liquids
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Xue-Quan Cao et al.
Asian Pacific journal of cancer prevention : APJCP, 15(13), 5271-5276 (2014-07-22)
Mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 3 (MEKK3) is an important protein kinase and a member of the MAPK family, which regulates cellular responses to environmental stress and serves as key integration points along the signal transduction cascade that
Nayara I Viana et al.
The International journal of biological markers, 29(3), e246-e252 (2014-01-30)
The aim of this study was to analyze the roles of miR-143 and miR-145, as well as the gene and protein expression of their targets (KRAS, ERK5, MAP3K3, and MAP4K4) in the pathogenesis of benign prostatic hyperplasia (BPH). We analyzed