biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
culture supernatant
antibody product type
primary antibodies
clone
C05T, monoclonal
species reactivity
rat, human
technique(s)
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... MAPK10(5602)
rat ... Mapk10(25272)
General description
46-54kDa
The stress-activated protein kinase 1 family is also referred to as the jun N-terminal kinase family, in light of the substrate preference of these serine/threonine kinases. The SAPK family shares 42-45% identity in the kinase domains with the MAPK family, and the SAPKs are activated by phosphorylation of a threonine and tyrosine by MKK4 and SKK4, just as the MAP kinases are phosphorylated on a threonine and tyrosine by MEK1 and MEK2. By contrast to the mitogen-activated kinases, the stress-activated kinases are only weakly activated by mitogenic stimuli, but potently activated by stress stimuli, such as inflammatory cytokines, ischemia, chemotherapeutic agents and irradiation.
The JNK/SAPK1 kinases, like the other MAPK-like kinases, are thought to phosphorylate multiple substrates and regulate many processes, including proliferation (in some cell types) and apoptosis. The SAPK2/3 family is most widely referred to as the p38 family. These kinases are also activated by stresses, most notably inflammatory cytokines, irradiation, and certain toxins such as anisomycin and arsenite. The activating kinases of SAPK2/3 are SKK2/MEK3 for SAPK2a and 2b, and MKK6 for SAPK3. The targets of the SAPK2/3 family include the MAPKAP kinases 2 and 3/3pK. In addition, SKK4 is related to this family, exhibiting 60% identity, and is activated by MKK6.
The JNK/SAPK1 kinases, like the other MAPK-like kinases, are thought to phosphorylate multiple substrates and regulate many processes, including proliferation (in some cell types) and apoptosis. The SAPK2/3 family is most widely referred to as the p38 family. These kinases are also activated by stresses, most notably inflammatory cytokines, irradiation, and certain toxins such as anisomycin and arsenite. The activating kinases of SAPK2/3 are SKK2/MEK3 for SAPK2a and 2b, and MKK6 for SAPK3. The targets of the SAPK2/3 family include the MAPKAP kinases 2 and 3/3pK. In addition, SKK4 is related to this family, exhibiting 60% identity, and is activated by MKK6.
Immunogen
GST fusion protein corresponding to full-length rat JNK3/ SAPK1b
Application
Western Blot Analysis: A 1:500-1:2,000 dilution of this lot detected JNK3 in RIPA lysates from A431 cells.
Detect JNK3/SAPK1b using this Anti-JNK3/SAPK1b Antibody, clone C05T validated for use in WB.
Research Category
Signaling
Signaling
Research Sub Category
Kinases & Phosphatases
Kinases & Phosphatases
Biochem/physiol Actions
Recognizes JNK3/SAPK1b. Does not cross react with JNK1 or JNK2.
Physical form
Cultured supernantant in 0.05% sodium azide.
Preparation Note
Stable for 1 year at -20°C from date of receipt.
Analysis Note
Control
RIPA cell lysates from A431 cells.
RIPA cell lysates from A431 cells.
Routinely evaluated by western blot on RIPA lysates from A431 cells.
Other Notes
Replaces: 05-893
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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存储类别
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Stella-Amrei Kunde et al.
Human genetics, 132(4), 461-471 (2013-01-19)
The c-Jun N-terminal kinases (JNKs) are stress-activated serine-threonine kinases that have recently been linked to various neurological disorders. We previously described a patient with intellectual disability (ID) and seizures (Patient 1), carrying a de novo chromosome translocation affecting the CNS-expressed
Qiu-Ju Zhu et al.
FEBS letters, 586(9), 1259-1264 (2012-04-10)
Protein SUMOylation has been implicated in the pathogenesis of ischemic stroke. However, the underlying mechanisms remain unclear. Here, we found that global brain ischemia evokes a sustained elevation of GluK2 SUMOylation in the rat hippocampal CA1 region. Over-expression of wild-type
Small peptide inhibitor of JNK3 protects dopaminergic neurons from MPTP induced injury via inhibiting the ASK1-JNK3 signaling pathway.
Pan, J; Li, H; Zhang, B; Xiong, R; Zhang, Y; Kang, WY; Chen, W; Zhao, ZB; Chen, SD
Testing null
全球贸易项目编号
| 货号 | GTIN |
|---|---|
| 04-893 | 04053252515194 |