c-Jun Antibody (YA7604)
(Synonyms: Transcription factor Jun, Activator protein 1, Proto-oncogene c-Jun, Transcription factor AP-1 subunit Jun, V-jun avian sarcoma virus 17 oncogene homolog, p39, AP1, JUN)c-Jun Antibody (YA7604) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to c-Jun.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, IP, ELISA
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|---|
| Dilution Ratio | 1:200-1:1000 | 1:2000-1:10000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 |
Product Details
c-Jun Antibody (YA7604) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to c-Jun.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 43 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 36 kDa
The exact sequence is proprietary to MCE.
Endogenous
Protein A affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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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
c-Jun, a basic leucine zipper transcription factor, regulates gene expression in response to multiple extracellular signals[1]. It is a central component of the activator protein-1 (AP-1) complex, mediating cellular proliferation, differentiation, and stress responses[2][3]. Mechanistically, c-Jun is primarily activated by phosphorylation through the c-Jun N-terminal kinase (JNK) pathway, linking stress signals to transcriptional outputs[3][4]. Isoform-specific functions of JNK1, JNK2, and JNK3 modulate c-Jun activity in tissue- and cell-specific contexts, influencing apoptosis, inflammation, and neuroplasticity[1][5][6]. In disease models, c-Jun contributes to pathological angiogenesis, rheumatoid arthritis, and neurodegeneration, where its inhibition reduces endothelial proliferation, metalloproteinase expression, and neuronal apoptosis[7][8][9][10][11][6]. Compared with related Jun-family members, c-Jun exhibits distinct phosphorylation patterns and transcriptional targets, enabling isoform-specific experimental interventions[6][12]. Pharmacological inhibitors targeting JNK or c-Jun itself, such as SP600125 or DNAzymes, demonstrate utility in blocking pro-apoptotic signaling, reducing inflammation, and modulating angiogenic pathways, supporting their research and therapeutic application[7][8][10][6]. In cancer and viral models, c-Jun interacts with oncogenic pathways, including Bcl-2/Bcl-xL upregulation and FGF-2-mediated proliferation, highlighting its role in cell survival and transcriptional regulation[2][13]. Collectively, c-Jun integrates stress, mitogenic, and inflammatory signals, serving as a critical target for isoform-specific modulation in experimental and disease contexts[1][3][6][7].
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Subcellular Localization
Nucleus
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Expression
Tissue_Specificity: Expressed in the developing and adult prostate and prostate cancer cells -
Isoforms & Post-Translational Modification
P05412: 331 amino acids, molecular weight 35676 Da.
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Subunit
Heterodimer with either BATF3 or ATF7 (PubMed:10376527, PubMed:12087103, PubMed:15467742)
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SwissProt ID
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Synonyms
Transcription factor Jun, Activator protein 1, Proto-oncogene c-Jun, Transcription factor AP-1 subunit Jun, V-jun avian sarcoma virus 17 oncogene homolog, p39, AP1, JUN
Documentation
[1]. Bogoyevitch MA. The isoform-specific functions of the c-Jun N-terminal Kinases (JNKs): differences revealed by gene targeting. Bioessays. 2006 Sep;28(9):923-34. doi: 10.1002/bies.20458. PMID: 16937364. et al. The isoform-specific functions of the c-Jun N-terminal Kinases (JNKs): differences revealed by gene targeting. Bioessays. 2006 Sep;28(9):923-34. [Content Brief]
[2]. Hortala M, et al. Identification of c-Jun as a critical mediator for the intracrine 24 kDa FGF-2 isoform-induced cell proliferation. Int J Cancer. 2005 May 10;114(6):863-9. [Content Brief]
[3]. Shashikanth N, et al. Role of C-Jun N-Terminal Kinases on a Stressed Epithelium: Time for Testing Isoform Specificity. Biology (Basel). 2025 Jun 3;14(6):649. [Content Brief]
[4]. Yao R, et al. Specific activation of a c-Jun NH2-terminal kinase isoform and induction of neurite outgrowth in PC-12 cells by staurosporine. J Biol Chem. 1997 Jul 18;272(29):18261-6. [Content Brief]
[5]. Raivich G. c-Jun expression, et al. c-Jun expression, activation and function in neural cell death, inflammation and repair. J Neurochem. 2008 Nov;107(4):898-906. [Content Brief]
[6]. Tan J, et al. Isoform-specific functions of c-Jun N-terminal kinase 1 and 2 in lung ischemia-reperfusion injury through the c-Jun/activator protein-1 pathway. J Thorac Cardiovasc Surg. 2021 Aug;162(2):e143-e156. [Content Brief]
[7]. Folkman J. Angiogenesis and c-Jun. J Natl Cancer Inst. 2004 May 5;96(9):644. doi: 10.1093/jnci/djh148. PMID: 15126593. et al. Angiogenesis and c-Jun. J Natl Cancer Inst. 2004 May 5;96(9):644. [Content Brief]
[8]. Zhang GY, et al. Agents targeting c-Jun N-terminal kinase pathway as potential neuroprotectants. Expert Opin Investig Drugs. 2005 Nov;14(11):1373-83. [Content Brief]
[9]. Ouyang W, et al. Anthrax lethal toxin rapidly reduces c-Jun levels by inhibiting c-Jun gene transcription and promoting c-Jun protein degradation. J Biol Chem. 2017 Oct 27;292(43):17919-17927. [Content Brief]
[10]. Han Z, et al. c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis. J Clin Invest. 2001 Jul;108(1):73-81. [Content Brief]
[11]. Hepp Rehfeldt SC, et al. c-Jun N-Terminal Kinase Inhibitors as Potential Leads for New Therapeutics for Alzheimer's Diseases. Int J Mol Sci. 2020 Dec 18;21(24):9677. [Content Brief]
[12]. Zhang Y, et al. MAPK/c-Jun signaling pathway contributes to the upregulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL induced by Epstein-Barr virus-encoded BARF1 in gastric carcinoma cells. Oncol Lett. 2018 May;15(5):7537-7544. [Content Brief]
[13]. Zoukhri D, et al. c-Jun NH2-terminal kinase mediates interleukin-1beta-induced inhibition of lacrimal gland secretion. J Neurochem. 2006 Jan;96(1):126-35. [Content Brief]
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