推荐产品
生物来源
rabbit
偶联物
unconjugated
抗体形式
whole antiserum
抗体产品类型
primary antibodies
克隆
polyclonal
分子量
antigen, JNK1 46 kDa
antigen, JNK2 55 kDa
包含
15 mM sodium azide
种属反应性
rat, human, mouse
技术
microarray: suitable
western blot: 1:16,000 using rat brain extract and mouse NIH-3T3 fibroblast extract, respectively
western blot: 1:2,000 using mouse NIH 3T3 fibroblast cell lysate
UniProt登记号
运输
dry ice
储存温度
−20°C
靶向翻译后修饰
unmodified
基因信息
human ... MAPK8(5599)
mouse ... Mapk8(26419)
rat ... Mapk8(116554)
一般描述
Anti-c-Jun N-Terminal Kinase (JNK1, JNK2) is developed in rabbit using a synthetic peptide, corresponding to amino acids of human c-Jun N-terminal kinase 1 (JNK1), coupled to KLH as the immunogen.
JNK (c-Jun N terminal protein kinase, also known as stress activated protein kinase, SAPK1) is a protein that belongs to serine/threonine-protein kinase family. It has a critical role in inhibiting WOX1 (WW domain-containing oxidoreductase) mediated apoptosis. It also mediates starvation-induced BCL2 phosphorylation and activates autophagy. Anti-c-Jun N-terminal kinase antibody can be used in microarray. Rabbit anti-c-Jun N-terminal kinase antibody reacts specifically with JNK1 (46 kD) and JNK2 (55 kD) of cell culture lysates and rat brain tissue extracts. The product has also shown weak cross reactivity for JNK2β (50 kD) isoform in mouse NIH-3T3 fibroblast cell lysate.
免疫原
Synthetic peptide corresponding to amino acids 339-354 of human JNK1 (c-Jun N-terminal kinase 1), conjugated to KLH. The sequence is highly conserved in JNK1, JNK2 α, β, γ (p54 SAPK α, β, γ) and identical in human, rat, and mouse JNK1.
应用
Anti-c-Jun N-Terminal Kinase antibody produced in rabbit has been used in western blotting.
生化/生理作用
Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases which play a central role in mitogenic signaling. The MAPKs function to transduce extracellular signals to intracellular targets, including transcription factors controlling the expression of genes essential to many cellular processes including proliferation, development and differentiation. JNK1 is essential for tumor necrosis factor alpha (TNF-α)-induced c-Jun kinase activation, c-Jun expression, and apoptosis. JNK1 and JNK2 participates in the survival of neuronal cells.
免责声明
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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储存分类代码
10 - Combustible liquids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
MEK7-dependent activation of p38 MAP kinase in keratinocytes
Dashti SR, et al.
The Journal of Biological Chemistry, 276(11), 8059-8063 (2001)
Induction of COX-2 enzyme and down-regulation of COX-1 expression by lipopolysaccharide (LPS) control prostaglandin E2 production in astrocytes
Font-Nieves M, et al.
The Journal of Biological Chemistry, 287(9), 6454-6468 (2012)
c-Jun N-terminal protein kinase 1 (JNK1), but not JNK2, is essential for tumor necrosis factor alpha-induced c-Jun kinase activation and apoptosis
Liu J, et al.
Molecular and Cellular Biology, 24(24), 10844-10856 (2004)
Mitogen-Activated Protein Kinases and Their Role in Radiation Response.
Anupama M and Rajagopal R
Genes & Cancer, 4(9-10), 401-408 (2013)
Ilan Feine et al.
PloS one, 7(7), e41633-e41633 (2012-08-23)
Major circulation pathologies are initiated by oxidative insult expansion from a few injured endothelial cells to distal sites; this possibly involves mechanisms that are important to understanding circulation physiology and designing therapeutic management of myocardial pathologies. We tested the hypothesis
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