JNK2 Antibody (YA5409)
(Synonyms: Mitogen-activated protein kinase 9; MAP kinase 9; MAPK 9; JNK-55; Stress-activated protein kinase 1a; SAPK1a; Stress-activated protein kinase JNK2; c-Jun N-terminal kinase 2; )JNK2 Antibody (YA5409) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to JNK2.
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Host:
Mouse
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Application:
IHC-P
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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|---|---|
| Dilution Ratio | 1:50-200 |
Product Details
JNK2 Antibody (YA5409) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to JNK2.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 46,54 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
Synthesized peptide derived from human JNK2
affinity chromatography.
Non-conjugated
Unmodified
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
JNK2 (MAPK9) is a member of the c-Jun N-terminal kinase (JNK) family, a stress-activated branch of the mitogen-activated protein kinase (MAPK) network that transduces extracellular stress, cytokine, and growth-factor signals into cellular responses regulating proliferation, survival, apoptosis, differentiation, and inflammation[1][2]. Mechanistically, JNK signaling is activated through a kinase cascade involving MAP3Ks, MKK4, and MKK7, leading to phosphorylation of transcriptional regulators such as c-Jun and other stress-responsive substrates that control gene expression programs[3][4]. In disease-associated contexts, dysregulated JNK signaling has been linked to cancer, obesity, type 2 diabetes, inflammatory disorders, neurodegenerative diseases, and pathological cell death, making the pathway a widely studied experimental target[1][2][3]. Compared with related isoforms, JNK1 and JNK2 are broadly expressed across tissues, whereas JNK3 shows a more restricted distribution, primarily in the brain, heart, and testis[1][3]. Importantly, JNK1 and JNK2 can exhibit both redundant and opposing biological functions, and experimental studies have demonstrated that JNK1, but not JNK2, is required for specific TNF-α-induced responses including c-Jun kinase activation and apoptosis, highlighting isoform-specific signaling properties[1][4]. For experimental applications, the growing recognition of isoform-dependent JNK biology has stimulated the development of JNK inhibitors, with current research emphasizing improved selectivity and on-target specificity for mechanistic studies and therapeutic evaluation[1][2].
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Subcellular Localization
Cytoplasm; Nucleus
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Isoforms & Post-Translational Modification
P45984 has 5 isomers: P45984-1: 48139 Da (predicted); P45984-2: 44051 Da (predicted); P45984-3: 44223 Da (predicted); P45984-4: 48311 Da (predicted); P45984-5: 27334 Da (predicted).
Dually phosphorylated on Thr-183 and Tyr-185 by MAP2K7 and MAP2K4, which activates the enzyme. Autophosphorylated in vitro -
Subunit
Interacts with NFATC4 (PubMed:17875713). Interacts with ATF7; the interaction does not phosphorylate ATF7 but acts as a docking site for ATF7-associated partners such as JUN (PubMed:10376527). Interacts with BCL10 (PubMed:17189706).
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SwissProt ID
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Synonyms
Mitogen-activated protein kinase 9; MAP kinase 9; MAPK 9; JNK-55; Stress-activated protein kinase 1a; SAPK1a; Stress-activated protein kinase JNK2; c-Jun N-terminal kinase 2;
Documentation
[1]. Harrison R, et al. Enacting open disclosure in the UK National Health Service: A qualitative exploration. J Eval Clin Pract. 2017 Aug;23(4):713-718. [Content Brief]
[2]. Karnam S, et al. Biochemical and biomechanical characteristics of dystrophin-deficient mdx3cv mouse lens. Biochim Biophys Acta Mol Basis Dis. 2021 Jan 1;1867(1):165998. [Content Brief]
[4]. Das D, et al. Secondary Structure Preferences of the Anthrax Toxin Protective Antigen Translocase. J Mol Biol. 2017 Mar 10;429(5):753-762. [Content Brief]