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AB126424

JNK (Thr183/Tyr185) In-Cell ELISA试剂盒

JNK (Thr183/Tyr185) In-Cell ELISA Kit

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(5 Publications)

JNK (Thr183/Tyr185) In-Cell ELISA Kit is a Cell-based ELISA for the measurement of JNK (Thr183/Tyr185) In-Cell in Human, Mouse, Rat in Cell Samples samples.

查看别名

JNK1, PRKM8, SAPK1, SAPK1C, MAPK8, Mitogen-activated protein kinase 8, MAP kinase 8, MAPK 8, JNK-46, Stress-activated protein kinase 1c, Stress-activated protein kinase JNK1, c-Jun N-terminal kinase 1, SAPK1c

3 Images
In-Cell ELISA - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)
  • In-Cell ELISA

Unknown

In-Cell ELISA - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)

HeLa cells were stimulated by different concentrations of anisomycin for 1 hour at 37°C.

In-Cell ELISA - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)
  • In-Cell ELISA

Unknown

In-Cell ELISA - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)

HeLa cells were stimulated by different concentrations of anisomycin for 15 minutes at 37°C.

Western blot - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)
  • WB

Supplier Data

Western blot - JNK (Thr183/Tyr185) In-Cell ELISA Kit (AB126424)

Western blot analysis of extracts from 1 µg/ml Anisomycin treated HeLa cells. Anti-Phospho-JNK (Thr183/Tyr185) and Anti-JNK antibodies were used in both detection assays.

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关键信息

检测方法

Colorimetric

样品类型

Adherent cells

反应种属

Mouse, Rat, Human

检测类型

Cell-based

检测时间

5h 10m

检测平台

Microplate

反应性数据

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产品详情

ab126424 is a very rapid, convenient and sensitive assay kit that can monitor the activation or function of important biological pathways in cells. It can be used for measuring the relative amount of JNK (Thr183/Tyr185) phosphorylation and screening the effects of various treatments, inhibitors (such as siRNA or chemicals), or activators in cultured Human, Mouse and Rat cell lines. By determining JNK protein phosphorylation in your experimental model system, you can verify pathway activation in your cell lines without spending excess time and effort in preparing cell lysate and performing an analysis of Western Blot.

In the JNK (Thr183/Tyr185) In-Cell ELISA Kit, cells are seeded into a 96 well tissue culture plate. The cells are fixed after various treatments, inhibitors or activators. After blocking, anti-Phospho-JNK(Thr183/Tyr185) or anti-JNK (primary antibody) is pipetted into the wells and incubated. The wells are washed, and HRP-conjugated anti-Mouse IgG (secondary antibody) is added to the wells. The wells are washed again, a

TMB substrate solution is added to the wells and color develops in proportion to the amount of protein. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm.

规格

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性能和储存信息

运输条件
Blue Ice
推荐的短期储存条件
-20°C
推荐的长期储存条件
-20°C
储存信息
-20°C

补充信息

This supplementary information is collated from multiple sources and compiled automatically.

JNK1 JNK2 and JNK3 collectively known as c-Jun N-terminal kinases are important members of the mitogen-activated protein kinase (MAPK) family. JNK1 JNK2 and JNK3 have molecular weights of approximately 46 to 55 kDa with JNK1 being around 46 kDa JNK2 about 54 kDa and JNK3 also around 54 kDa. They are expressed differently across tissues: JNK1 and JNK2 are widely present in many tissues while JNK3 is mostly in brain heart and testis. These kinases primarily phosphorylate serine and threonine residues acting on various transcription factors including c-Jun to regulate cellular processes.
Biological function summary

These kinases function as significant regulators of cellular responses to stress and cytokines. They do not act alone but often form part of larger signaling complexes that include other MAPKs and various scaffold proteins. Their roles are substantial in cell differentiation proliferation apoptosis and migration. Precise regulation by JNK molecules influences these critical cellular events which play a role in maintaining homeostasis and response to external stresses.

Pathways

JNK proteins are central to the MAPK signaling pathway and are tightly linked to the MAPK/ERK pathway. Activation of the JNK pathways leads to the regulation of various other proteins including those in the apoptosis pathway such as Bcl-2 and Bax. These interactions focus on cellular stress response regulation and contribute to processes like inflammation stress-induced apoptosis and some metabolic processes.

JNKs have important roles in inflammatory diseases and neurodegenerative disorders such as Alzheimer's disease and Parkinson’s disease. Their activity links to the regulation of pro-inflammatory cytokines and neuronal apoptosis. JNK1 and JNK2 are particularly connected to inflammatory responses whereas JNK3 with its expression in the brain has associations with neuronal death in neurodegenerative diseases. Modulating JNK activity may offer therapeutic approaches for these conditions targeting pathways involving proteins like TNF-alpha and Aβ-amyloid.

产品实验方案

靶点信息

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as pro-inflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway (PubMed : 28943315). In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity (PubMed : 18307971). Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins (PubMed : 21856198). Loss of this interaction abrogates the acetylation required for replication initiation (PubMed : 21856198). Promotes stressed cell apoptosis by phosphorylating key regulatory factors including p53/TP53 and Yes-associates protein YAP1 (PubMed : 21364637). In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Contributes to the survival of erythroid cells by phosphorylating the antagonist of cell death BAD upon EPO stimulation (PubMed : 21095239). Mediates starvation-induced BCL2 phosphorylation, BCL2 dissociation from BECN1, and thus activation of autophagy (PubMed : 18570871). Phosphorylates STMN2 and hence regulates microtubule dynamics, controlling neurite elongation in cortical neurons (By similarity). In the developing brain, through its cytoplasmic activity on STMN2, negatively regulates the rate of exit from multipolar stage and of radial migration from the ventricular zone (By similarity). Phosphorylates several other substrates including heat shock factor protein 4 (HSF4), the deacetylase SIRT1, ELK1, or the E3 ligase ITCH (PubMed : 16581800, PubMed : 17296730, PubMed : 20027304). Phosphorylates the CLOCK-BMAL1 heterodimer and plays a role in the regulation of the circadian clock (PubMed : 22441692). Phosphorylates the heat shock transcription factor HSF1, suppressing HSF1-induced transcriptional activity (PubMed : 10747973). Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteasomal degradation (By similarity). Phosphorylates JUND and this phosphorylation is inhibited in the presence of MEN1 (PubMed : 22327296). In neurons, phosphorylates SYT4 which captures neuronal dense core vesicles at synapses (By similarity). Phosphorylates EIF4ENIF1/4-ET in response to oxidative stress, promoting P-body assembly (PubMed : 22966201). Phosphorylates SIRT6 in response to oxidative stress, stimulating its mono-ADP-ribosyltransferase activity (PubMed : 27568560). Phosphorylates NLRP3, promoting assembly of the NLRP3 inflammasome (PubMed : 28943315). Phosphorylates ALKBH5 in response to reactive oxygen species (ROS), promoting ALKBH5 sumoylation and inactivation (PubMed : 34048572).. JNK1 isoforms display different binding patterns : beta-1 preferentially binds to c-Jun, whereas alpha-1, alpha-2, and beta-2 have a similar low level of binding to both c-Jun or ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms.
See full target information MAPK8 phospho Y185 + T183

文献 (5)

Recent publications for all applications. Explore the full list and refine your search

PloS one 18:e0286454 PubMed37352173

2023

Aged black garlic extract inhibits the growth of estrogen receptor-positive breast cancer cells by downregulating MCL-1 expression through the ROS-JNK pathway.

Applications

Unspecified application

Species

Unspecified reactive species

Qiwei Yang,Fang Li,Guohui Jia,Rui Liu

Animals : an open access journal from MDPI 11: PubMed34073895

2021

Artemisinin Protects Porcine Mammary Epithelial Cells against Lipopolysaccharide-Induced Inflammatory Injury by Regulating the NF-κB and MAPK Signaling Pathways.

Applications

Unspecified application

Species

Unspecified reactive species

Wenfei Zhang,Liang Xiong,Jiaming Chen,Zhezhe Tian,Jiaxin Liu,Fang Chen,Man Ren,Wutai Guan,Shihai Zhang

Oxidative medicine and cellular longevity 2021:8049079 PubMed33643519

2021

Yixin-Shu Capsules Ameliorated Ischemia-Induced Heart Failure by Restoring Trx2 and Inhibiting JNK/p38 Activation.

Applications

Unspecified application

Species

Unspecified reactive species

Changpei Xiang,Fangbo Zhang,Jinhuan Gao,Feifei Guo,Mao Zhang,Rui Zhou,Junying Wei,Ping Wang,Yi Zhang,Jingjing Zhang,Hongjun Yang

Molecular medicine reports 21:1011-1020 PubMed31922242

2020

miR‑155 inhibition represents a potential valuable regulator in mitigating myocardial hypoxia/reoxygenation injury through targeting BAG5 and MAPK/JNK signaling.

Applications

Unspecified application

Species

Unspecified reactive species

Jing Xi,Qiang-Qiang Li,Bing-Qiang Li,Ning Li

Bone 114:90-108 PubMed29908298

2018

Hydrogen sulfide epigenetically mitigates bone loss through OPG/RANKL regulation during hyperhomocysteinemia in mice.

Applications

Unspecified application

Species

Unspecified reactive species

Jyotirmaya Behera,Akash K George,Michael J Voor,Suresh C Tyagi,Neetu Tyagi
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