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J4750

Sigma-Aldrich

Anti-JNK, Activated (Diphosphorylated JNK) antibody, Mouse monoclonal

clone JNK-PT48, purified from hybridoma cell culture

Synonym(s):

Monoclonal Anti-JNK, Activated (Diphosphorylated JNK) antibody produced in mouse

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.44

biological source

mouse

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

JNK-PT48, monoclonal

form

buffered aqueous solution

mol wt

antigen 46 kDa
antigen 54 kDa

species reactivity

mouse, human, rat

concentration

~2 mg/mL

technique(s)

immunocytochemistry: suitable
indirect ELISA: suitable
microarray: suitable
western blot: 4-20 μg/mL using extract of human Jurkat cells activated with anisomycin

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MAPK8(5599)
mouse ... Mapk8(26419)
rat ... Mapk8(116554)

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General description

Monoclonal Anti-JNK, Activated (Diphosphorylated JNK) (mouse IgG1 isotype) is derived from the JNK-PT48 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to the phosphorylated form of JNK activation loop, conjugated to KLH. JNK (c-Jun N terminal protein kinase) belongs to the mitogen-activated protein kinase (MAPK) superfamily of enzymes. The kinases in the MAPK level are activated by phosphorylation of both tyrosine (Y) and threonine (T) residues organized in a TXY motif. The residue in between the two phosphorylated residue determines the specificity of activation of the MAPKs and is proline for JNK. JNK1-3 of molecular weights 46, 54, and 52 kDa respectively.

Specificity

The antibody reacts specifically with the activated diphosphorylated form of JNK. The epitope recognized by the antibody contains the regulatory site of JNK (Thr183 and Tyr185). Weak cross-reaction is observed with the monophosphorylated threonine peptide, but not with the non-phosphorylated or monophosphorylated tyrosine peptides of JNK. It does not recognize any form of p38-MAPK or ERK-MAPK.

Immunogen

synthetic peptide sequence containing amino acids pTPpYVVTRYYR, corresponding to the phosphorylated form of JNK-activation loop.

Application

Monoclonal Anti-JNK, Activated (Diphosphorylated JNK) antibody has been used in immunoblotting, enzyme linked immunosorbent assay (ELISA), immunocytochemistry, western blotting, immunohistochemistry.

Biochem/physiol Actions

c-Jun N terminal protein kinase (JNK) is mostly stress-responsive kinase and have been implicated in cell death in several cellular systems. The JNK cascade is triggered by small GTPases that are Rac and Cell division control protein 42 (CDC42). After activation, JNKs translocate to the nucleus where they physically associate with and activate their target transcription factors (cJun, AMP-dependent transcription factor (ATF) etc.).

Physical form

Solution in phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

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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Storage Class Code

12 - Non Combustible Liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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JNK signaling: regulation and functions based on complex protein-protein partnerships
Zeke A, et al.
Microbiology and Molecular Biology Reviews, 80(3), 793-835 (2016)
Pigment Epithelium-Derived Factor Alleviates Tamoxifen-Induced Endometrial Hyperplasia
Goldberg K, et al.
Molecular Cancer Therapeutics, 14(12), 2840-2849 (2015)
JNK-signaling: a multiplexing hub in programmed cell death
Dhanasekaran, Danny N and Reddy, E Premkumar
Genes & cancer, 8(9-10), 682-682 (2017)
Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis
Stambe C, et al.
Kidney International, 64(6), 2121-2132 (2003)
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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