Rabbit Recombinant Monoclonal JNK2 antibody - conjugated to Alkaline Phosphatase.
pH: 7.4
Preservative: 0.1% Proclin 300 Solution
Constituents: 50% Glycerol (glycerin, glycerine), 1% BSA, 0.016% Magnesium chloride, 0.001% Zinc chloride
| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application Target Binding Affinity | Reactivity Expected | Dilution info - | Notes - |
Application Antibody Labelling | Reactivity Expected | Dilution info - | Notes - |
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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.
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
Rabbit Recombinant Monoclonal JNK2 antibody - conjugated to Alkaline Phosphatase.
pH: 7.4
Preservative: 0.1% Proclin 300 Solution
Constituents: 50% Glycerol (glycerin, glycerine), 1% BSA, 0.016% Magnesium chloride, 0.001% Zinc chloride
This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling.
For suitable applications and species reactivity, please refer to the unconjugated version of this clone. This conjugated antibody is eligible for the Abcam trial program.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
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.
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.
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.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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