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Merck
所有图片(1)

文件

04-893

Sigma-Aldrich

Anti-JNK3/SAPK1b Antibody, clone C05T, rabbit monoclonal

culture supernatant, clone C05T, from rabbit

别名:

JNK3 alpha protein kinase, MAP kinase, MAP kinase p49 3F12, Stress-activated protein kinase JNK3, c-Jun N-terminal kinase 3, c-Jun kinase 3, mitogen-activated protein kinase 10, stress activated protein kinase JNK3, stress activated protein kinase beta

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About This Item

分類程式碼代碼:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物源

rabbit

品質等級

抗體表格

culture supernatant

抗體產品種類

primary antibodies

無性繁殖

C05T, monoclonal

物種活性

rat, human

技術

western blot: suitable

同型

IgG

NCBI登錄號

UniProt登錄號

運輸包裝

dry ice

目標翻譯後修改

unmodified

基因資訊

human ... MAPK10(5602)
rat ... Mapk10(25272)

一般說明

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.

特異性

Recognizes JNK3/SAPK1b. Does not cross react with JNK1 or JNK2.

免疫原

GST fusion protein corresponding to full-length rat JNK3/ SAPK1b

應用

Detect JNK3/SAPK1b using this Anti-JNK3/SAPK1b Antibody, clone C05T validated for use in WB.
Research Category
Signaling
Research Sub Category
Kinases & Phosphatases
Western Blot Analysis: A 1:500-1:2,000 dilution of this lot detected JNK3 in RIPA lysates from A431 cells.

品質

Routinely evaluated by western blot on RIPA lysates from A431 cells.

標靶描述

46-54kDa

聯結

Replaces: 05-893

外觀

Cultured supernantant in 0.05% sodium azide.

儲存和穩定性

Stable for 1 year at -20°C from date of receipt.

分析報告

Control
RIPA cell lysates from A431 cells.

免責聲明

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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儲存類別代碼

12 - Non Combustible Liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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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
Yuan Li et al.
Cell death & disease, 8(7), e2959-e2959 (2017-07-28)
Brain-derived neurotrophic factor (BDNF) and its high affinity receptor, TrkB, play an essential role in memory extinction. Our previous work has shown that JIP3 (JNK interacted protein 3) mediates anterograde axonal transport of TrkB through the direct binding of its
Stella-Amrei Kunde et al.
The Journal of biological chemistry, 300(5), 107263-107263 (2024-04-07)
Synapse formation depends on the coordinated expression and regulation of scaffold proteins. The JNK family kinases play a role in scaffold protein regulation, but the nature of this functional interaction in dendritic spines requires further investigation. Here, using a combination

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