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BRAND / VENDOR: Abcam

Abcam, ab126424, JNK (Thr183/Tyr185) In-Cell ELISA Kit

CATALOG NUMBER: ab126424
Precio habitual$0.99
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Product Description

Size: 1 x 96Tests
JNK (Thr183/Tyr185) In-Cell ELISA Kit is a Cell-based (qualitative) ELISA for the measurement of JNK (Thr183/Tyr185) In-Cell in Human, Mouse, Rat in Cell Samples samples.
Key facts
Detection method:Colorimetric,
Sample types:Adherent cells,
Reacts with:Mouse, Rat, Human,
Assay type:Cell-based (qualitative),
Assay time:5h 10m,
Assay Platform:Microplate

Product details:
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.

Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Storage information--20°C

Supplementary Information:
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.


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Collaboration

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