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AB130019

Recombinant Human JNK2 protein

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Recombinant Human JNK2 protein is a Human Full Length protein, in the 1 to 382 aa range, expressed in Escherichia coli, with >95%, suitable for SDS-PAGE, Mass Spec.

View Alternative Names

JNK2, PRKM9, SAPK1A, MAPK9, Mitogen-activated protein kinase 9, MAP kinase 9, MAPK 9, JNK-55, Stress-activated protein kinase 1a, Stress-activated protein kinase JNK2, c-Jun N-terminal kinase 2, SAPK1a

1 Images
SDS-PAGE - Recombinant Human JNK2 protein (AB130019)
  • SDS-PAGE

Supplier Data

SDS-PAGE - Recombinant Human JNK2 protein (AB130019)

SDS-PAGE analysis of ab130019 at 3μg under reducing condition.

Key facts

Purity

>95% SDS-PAGE

Expression system

Escherichia coli

Tags

His tag N-Terminus

Applications

SDS-PAGE, Mass Spec

applications

Biologically active

No

Accession

P45984

Animal free

No

Carrier free

No

Species

Human

Storage buffer

pH: 8 Constituents: 10% Glycerol (glycerin, glycerine), 0.58% Sodium chloride, 0.32% Tris HCl, 0.02% (R*,R*)-1,4-Dimercaptobutan-2,3-diol

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "Mass Spec": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

Sequence info

[{"sequence":"MGSSHHHHHHSSGLVPRGSHMGSHMSDSKCDSQFYSVQVADSTFTVLKRYQQLKPIGSGAQGIVCAAFDTVLGINVAVKKLSRPFQNQTHAKRAYRELVLLKCVNHKNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIHMELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTACTNFMMTPYVVTRYYRAPEVILGMGYKENVDIWSVGCIMGELVKGCVIFQGTDHIDQWNKVIEQLGTPSAEFMKKLQPTVRNYVENRPKYPGIKFEELFPDWIFPSESERDKIKTSQARDLLSKMLVIDPDKRISVDEALRHPYITVWYDPAEAEAPPPQIYDAQLEEREHAIEEWKELIYKEVMDWEERSKNGVVKDQPSAQMQQ","proteinLength":"Full Length","predictedMolecularWeight":"46.6 kDa","actualMolecularWeight":null,"aminoAcidEnd":382,"aminoAcidStart":1,"nature":"Recombinant","expressionSystem":"Escherichia coli","accessionNumber":"P45984","tags":[{"tag":"His","terminus":"N-Terminus"}]}]

Properties and storage information

Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle
False

Supplementary information

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

C-Jun N-terminal kinase 2 also known as JNK2 is a member of the MAPK (mitogen-activated protein kinase) family. JNK2 plays a significant role in transmitting signals within cells. It is a protein with a mass of approximately 48 kDa and exists in various tissues including the brain heart and liver. JNK2 is ubiquitously expressed and has two main isoforms produced by alternative splicing. These isoforms are involved in different biological functions emphasizing the protein's versatility.
Biological function summary

C-Jun N-terminal kinase 2 is key in regulating processes such as cell growth apoptosis and differentiation. JNK2 is part of the MAP kinase signal transduction pathways and forms interactions with several proteins including the scaffolding proteins known as JNK-interacting proteins (JIPs). These complexes help coordinate the response of JNK2 in cellular stress and inflammatory responses. JNK2 is also critical in modulating the expression of genes by activating transcription factors such as c-Jun and ATF2.

Pathways

JNK2 operates within the MAPK signaling pathway by integrating various upstream signals to exert effects on gene expression. JNK2 phosphorylates and activates transcription factors playing an important role in cellular responses to stress. It is closely connected to other proteins within the pathway such as JNK1 and JNK3 together contributing to the complex regulation of stress-induced apoptosis and pro-inflammatory responses. These interactions highlight JNK2's essential function across multiple signaling networks.

Research connects c-Jun N-terminal kinase 2 to both cancer and neurodegenerative diseases. Its role in controlling apoptosis and cell proliferation links JNK2 to tumor progression where abnormal JNK2 activity can lead to oncogenesis. Additionally in neurodegenerative diseases like Alzheimer's dysregulated JNK2 signaling may accelerate neuronal death. JNK2's association with other proteins involved in these disorders such as amyloid precursor protein in Alzheimer's disease highlights its influence in pathological processes.

Specifications

Form

Liquid

Additional notes

ab130019 was purified using conventional chromatography techniques.

General info

Function

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death (PubMed : 10376527, PubMed : 15805466, PubMed : 17525747, PubMed : 19675674, PubMed : 20595622, PubMed : 21364637, PubMed : 22441692, PubMed : 34048572). 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. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK9/JNK2 (PubMed : 10376527, PubMed : 15805466, PubMed : 17525747, PubMed : 19675674, PubMed : 20595622, PubMed : 21364637, PubMed : 22441692, PubMed : 34048572). In turn, MAPK9/JNK2 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity (PubMed : 10376527). In response to oxidative or ribotoxic stresses, inhibits rRNA synthesis by phosphorylating and inactivating the RNA polymerase 1-specific transcription initiation factor RRN3 (PubMed : 15805466). Promotes stressed cell apoptosis by phosphorylating key regulatory factors including TP53 and YAP1 (PubMed : 17525747, PubMed : 21364637). In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells (PubMed : 19290929). Upon T-cell receptor (TCR) stimulation, is activated by CARMA1, BCL10, MAP2K7 and MAP3K7/TAK1 to regulate JUN protein levels (PubMed : 19290929). Plays an important role in the osmotic stress-induced epithelial tight-junctions disruption (PubMed : 20595622). When activated, promotes beta-catenin/CTNNB1 degradation and inhibits the canonical Wnt signaling pathway (PubMed : 19675674). Participates also in neurite growth in spiral ganglion neurons (By similarity). Phosphorylates the CLOCK-BMAL1 heterodimer and plays a role in the regulation of the circadian clock (PubMed : 22441692). Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteasomal degradation (By similarity). Phosphorylates ALKBH5 in response to reactive oxygen species (ROS), promoting ALKBH5 sumoylation and inactivation (PubMed : 34048572).. MAPK9 isoforms display different binding patterns : alpha-1 and alpha-2 preferentially bind to JUN, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 alpha-2, and JUND binds only weakly to it.

Sequence similarities

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.

Post-translational modifications

Dually phosphorylated on Thr-183 and Tyr-185 by MAP2K7 and MAP2K4, which activates the enzyme. Autophosphorylated in vitro.

Subcellular localisation

Nucleus

Product protocols

Target data

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death (PubMed : 10376527, PubMed : 15805466, PubMed : 17525747, PubMed : 19675674, PubMed : 20595622, PubMed : 21364637, PubMed : 22441692, PubMed : 34048572). 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. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK9/JNK2 (PubMed : 10376527, PubMed : 15805466, PubMed : 17525747, PubMed : 19675674, PubMed : 20595622, PubMed : 21364637, PubMed : 22441692, PubMed : 34048572). In turn, MAPK9/JNK2 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity (PubMed : 10376527). In response to oxidative or ribotoxic stresses, inhibits rRNA synthesis by phosphorylating and inactivating the RNA polymerase 1-specific transcription initiation factor RRN3 (PubMed : 15805466). Promotes stressed cell apoptosis by phosphorylating key regulatory factors including TP53 and YAP1 (PubMed : 17525747, PubMed : 21364637). In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells (PubMed : 19290929). Upon T-cell receptor (TCR) stimulation, is activated by CARMA1, BCL10, MAP2K7 and MAP3K7/TAK1 to regulate JUN protein levels (PubMed : 19290929). Plays an important role in the osmotic stress-induced epithelial tight-junctions disruption (PubMed : 20595622). When activated, promotes beta-catenin/CTNNB1 degradation and inhibits the canonical Wnt signaling pathway (PubMed : 19675674). Participates also in neurite growth in spiral ganglion neurons (By similarity). Phosphorylates the CLOCK-BMAL1 heterodimer and plays a role in the regulation of the circadian clock (PubMed : 22441692). Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteasomal degradation (By similarity). Phosphorylates ALKBH5 in response to reactive oxygen species (ROS), promoting ALKBH5 sumoylation and inactivation (PubMed : 34048572).. MAPK9 isoforms display different binding patterns : alpha-1 and alpha-2 preferentially bind to JUN, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 alpha-2, and JUND binds only weakly to it.
See full target information MAPK9

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