Product: c-Jun Antibody
Catalog: AF6090
Description: Rabbit polyclonal antibody to c-Jun
Application: WB IHC IF/ICC IP
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 37kDa; 36kD(Calculated).
Uniprot: P05412
RRID: AB_2834984

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IP, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Zebrafish(100%), Bovine(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
c-Jun Antibody detects endogenous levels of total c-Jun.
RRID:
AB_2834984
Cite Format: Affinity Biosciences Cat# AF6090, RRID:AB_2834984.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

Activator protein 1; AP 1; AP1; cJun; Enhancer Binding Protein AP1; Jun Activation Domain Binding Protein; JUN; Jun oncogene; JUN protein; Jun proto oncogene; JUN_HUMAN; JUNC; Oncogene JUN; p39; Proto oncogene c jun; Proto oncogene cJun; Proto-oncogene c-jun; Transcription Factor AP 1; Transcription factor AP-1; Transcription Factor AP1; V jun avian sarcoma virus 17 oncogene homolog; V jun sarcoma virus 17 oncogene homolog (avian); V jun sarcoma virus 17 oncogene homolog; V-jun avian sarcoma virus 17 oncogene homolog; vJun Avian Sarcoma Virus 17 Oncogene Homolog;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P05412 JUN_HUMAN:

Expressed in the developing and adult prostate and prostate cancer cells.

Description:
This gene is the putative transforming gene of avian sarcoma virus 17. It encodes a protein which is highly similar to the viral protein, and which interacts directly with specific target DNA sequences to regulate gene expression.
Sequence:
MTAKMETTFYDDALNASFLPSESGPYGYSNPKILKQSMTLNLADPVGSLKPHLRAKNSDLLTSPDVGLLKLASPELERLIIQSSNGHITTTPTPTQFLCPKNVTDEQEGFAEGFVRALAELHSQNTLPSVTSAAQPVNGAGMVAPAVASVAGGSGSGGFSASLHSEPPVYANLSNFNPGALSSGGGAPSYGAAGLAFPAQPQQQQQPPHHLPQQMPVQHPRLQALKEEPQTVPEMPGETPPLSPIDMESQERIKAERKRMRNRIAASKCRKRKLERIARLEEKVKTLKAQNSELASTANMLREQVAQLKQKVMNHVNSGCQLMLTQQLQTF

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Bovine
100
Dog
100
Xenopus
100
Zebrafish
100
Chicken
100
Rabbit
100
Horse
0
Sheep
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P05412 As Substrate

Site PTM Type Enzyme
T2 Phosphorylation Q13177 (PAK2)
T8 Phosphorylation Q13177 (PAK2)
Y26 Phosphorylation P41240 (CSK)
S37 Phosphorylation
S48 Phosphorylation
K50 Acetylation
K50 Ubiquitination
K56 Sumoylation
S58 Phosphorylation
T62 Phosphorylation
S63 Phosphorylation P45983 (MAPK8) , P45984 (MAPK9) , P06493 (CDK1) , Q15139 (PRKD1) , Q96KB5 (PBK) , Q8TD08 (MAPK15) , Q9H4B4 (PLK3) , P53779 (MAPK10) , Q00526 (CDK3) , P27361 (MAPK3) , Q99986 (VRK1)
K70 Ubiquitination
S73 Phosphorylation Q8TD08 (MAPK15) , P53779 (MAPK10) , Q99986 (VRK1) , P27361 (MAPK3) , P45983 (MAPK8) , Q96KB5 (PBK) , P06493 (CDK1) , Q9H4B4 (PLK3) , P45984 (MAPK9) , Q00526 (CDK3)
T89 Phosphorylation Q13177 (PAK2)
T91 Phosphorylation P45983 (MAPK8)
T93 Phosphorylation P45983 (MAPK8) , Q13177 (PAK2)
T95 Phosphorylation
T131 Phosphorylation
Y170 Phosphorylation P00519 (ABL1) , P41240 (CSK)
K226 Sumoylation
T231 Phosphorylation P68400 (CSNK2A1)
T239 Phosphorylation P49840 (GSK3A) , P49841 (GSK3B)
S243 Phosphorylation P06493 (CDK1) , P49841 (GSK3B) , P68400 (CSNK2A1) , Q92630 (DYRK2) , P49840 (GSK3A)
S249 Phosphorylation P68400 (CSNK2A1) , P78527 (PRKDC) , P49840 (GSK3A)
K254 Sumoylation
K268 Acetylation
C269 S-Nitrosylation
K271 Acetylation
K273 Acetylation
T286 Phosphorylation Q13177 (PAK2)
K309 Ubiquitination
C320 S-Nitrosylation

Research Backgrounds

Function:

Transcription factor that recognizes and binds to the enhancer heptamer motif 5'-TGA[CG]TCA-3'. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation. Involved in activated KRAS-mediated transcriptional activation of USP28 in colorectal cancer (CRC) cells. Binds to the USP28 promoter in colorectal cancer (CRC) cells.

PTMs:

Ubiquitinated by the SCF(FBXW7), leading to its degradation. Ubiquitination takes place following phosphorylation, that promotes interaction with FBXW7.

Phosphorylated by CaMK4 and PRKDC; phosphorylation enhances the transcriptional activity. Phosphorylated by HIPK3. Phosphorylated by DYRK2 at Ser-243; this primes the protein for subsequent phosphorylation by GSK3B at Thr-239. Phosphorylated at Thr-239, Ser-243 and Ser-249 by GSK3B; phosphorylation reduces its ability to bind DNA. Phosphorylated by PAK2 at Thr-2, Thr-8, Thr-89, Thr-93 and Thr-286 thereby promoting JUN-mediated cell proliferation and transformation. Phosphorylated by PLK3 following hypoxia or UV irradiation, leading to increase DNA-binding activity.

Acetylated at Lys-271 by EP300.

Subcellular Location:

Nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in the developing and adult prostate and prostate cancer cells.

Subunit Structure:

Heterodimer with either FOS or BATF3 or ATF7. The ATF7/JUN heterodimer is essential for ATF7 transactivation activity. Interacts with DSIPI; the interaction inhibits the binding of active AP1 to its target DNA (By similarity). Interacts with HIVEP3 and MYBBP1A (By similarity). Interacts with SP1, SPIB and TCF20. Interacts with COPS5; the interaction leads indirectly to its phosphorylation. Component of the SMAD3/SMAD4/JUN/FOS/complex which forms at the AP1 promoter site. The SMAD3/SMAD4 heterodimer acts synergistically with the JUN/FOS heterodimer to activate transcription in response to TGF-beta. Interacts (via its basic DNA binding and leucine zipper domains) with SMAD3 (via an N-terminal domain); the interaction is required for TGF-beta-mediated transactivation of the SMAD3/SMAD4/JUN/FOS/complex. Interacts with methylated RNF187. Binds to HIPK3. Interacts (when phosphorylated) with FBXW7. Found in a complex with PRR7 and FBXW7. Interacts with PRR7 and FBXW7; the interaction inhibits ubiquitination-mediated JUN degradation promoting its phosphorylation and transcriptional activity. Interacts with RBM39 (By similarity). Interacts with PAGE4.

Family&Domains:

Belongs to the bZIP family. Jun subfamily.

Research Fields

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Tight junction.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Wnt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Substance dependence > Cocaine addiction.

· Human Diseases > Substance dependence > Amphetamine addiction.

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Renal cell carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (View pathway)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Oxytocin signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). M6A demethylase FTO-mediated downregulation of DACT1 mRNA stability promotes Wnt signaling to facilitate osteosarcoma progression. ONCOGENE (PubMed: 35121825) [IF=8.0]

2). Higenamine alleviates allergic rhinitis by activating AKT1 and suppressing the EGFR/JAK2/c-JUN signaling. PHYTOMEDICINE (PubMed: 33945919) [IF=7.9]

Application: WB    Species: Human    Sample: human nasal epithelial cell

Fig. 8. The effects of higenamine (HG) on potential targets in histamine-induced HNEpCs. (A-J) Levels of protein expression of AKT1, p-AKT1, EGFR, p-EGFR, c-Jun, p-c-Jun, iNOS, JAK2, and p-JAK2 were determined by Western blotting, β-actin was used as an internal control. Data are expressed as means ± SD of three experiments. ## p < 0.01, and # p < 0.05 compared with the control group. ** p < 0.01, and * p < 0.05 compared with the histamine group.

3). The effects of Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract on X-irradiation-induced myocardial fibrosis in rats. BIOMEDICINE & PHARMACOTHERAPY (PubMed: 30780109) [IF=7.5]

Application: WB    Species: rat    Sample: cardiac

Fig. 5.| Representative images of the protein levels of col1α, OPN, P-c-fos and P-c-jun in the three groups. A, The protein expression levels of col1α, OPN, P-c-fos and P-c-jun were significantly increased in the X-ray group. After treatment with RAS-RH, the expression of col1α, OPN and P-c-jun was slightly decreased.B, Relative protein expression levels were analyzed by Image-Pro Plus 6.0 (n = 3, *P < 0.05, **P < 0.01 vs. the control group; #P < 0.05, ##P < 0.01 vs. the RAS-RH + X-ray group).

4). The protection of luteolin against diabetic cardiomyopathy in rats is related to reversing JNK-suppressed autophagy. Food & Function (PubMed: 36852907) [IF=6.1]

5). Emodin Attenuates Lipopolysaccharide-Induced Acute Liver Injury via Inhibiting the TLR4 Signaling Pathway in vitro and in vivo. Frontiers in Pharmacology (PubMed: 30186181) [IF=5.6]

Application: WB    Species: mouse    Sample: RAW264.7cell

FIGURE 4 | Effect of emodin on TLR4 and downstream molecules after LPS stimulation. (A–C) The mRNA levels of TLR4, MyD88, TIRAP, IRF-5, TRAF-6, TRIF,IRF-3, AP-1, and NF–κB were detected by RT-PCR. (D) The protein levels of the above molecules were detected by western blotting. Data are shown as the mean ± SD. #P < 0.05 compared to the normal group. ∗P < 0.05, ∗∗P < 0.01 vs model group; MP < 0.05, MMP < 0.01 vs DEX group.

6). CTGF Triggers Rat Astrocyte Activation and Astrocyte-Mediated Inflammatory Response in Culture Conditions. INFLAMMATION (PubMed: 31183597) [IF=5.1]

Application: WB    Species: rat    Sample: RA cells

Fig. 4.| CTGF activated the NF-κB and AP-1 through ASK1-p38/JNK pathways. b RA cells were treated with either 10 μM ASK1 inhibitor GS-4997, or solvent control as indicated, for 30 min prior to stimulation with 20 ng/ml CTGF for 24 h. The expression of ASK, p65, and c-Jun and their phosphorylation states were examined by Western blotting.

7). Platelets-Derived miR-200a-3p Modulate the Expression of ET-1 and VEGFA in Endothelial Cells by Targeting MAPK14. Frontiers in Physiology (PubMed: 35755441) [IF=4.0]

Application: WB    Species: Human    Sample: HUVEC

FIGURE 5 miR-200a-3p directly targets the 3′UTR of MAPK14 and regulates the expression levels of p38, c-jun, ET-1 and VEGFA. (A) The MAPK14 3′-UTR containing the wildtype or mutant miR-200a-3p binding sequence was inserted into downstream of the luciferase reporter vector. The mutated sequences are italicized. (B) The dual luciferase reporter assay revealed that the luciferase activity controlled by MAPK14 3′-UTR was inhibited by ectopic miR-200a-3p expression in 293T cells. (C) miR-200a-3p was highly expressed or knocked down in HUVEC by lipofectamine 2000 transfection. QRT-PCR analysis was performed to measure the expression levels of miR-200a-3p in HUVEC after treatment with miR-200a-3p mimic, mimic control or miR-200a-3p inhibitor, inhibitor control. (D) The mRNA levels of MAPK14, c-jun, ET-1 and VEGFA were determined by qRT-PCR in HUVEC transfected with miR-200a-3p mimic, mimic control or miR-200a-3p inhibitor, inhibitor control. (E) Western blot analysis of p38, phosphorylated p38, c-jun, phosphorylated c-Jun, ET-1 and VEGFA protein levels in HUVEC transfected with miR-200a-3p mimic, mimic control or miR-200a-3p inhibitor, inhibitor control. (F) Quantification of protein results in panel E. Data were expressed as mean ± SEM. Between group differences were assessed by the student’s t test, respectively. *p < 0.05, **p < 0.01, ns, not significant.

8). Circ-Sirt1 inhibits proliferation, induces apoptosis, and ameliorates inflammation in human rheumatoid arthritis fibroblast-like synoviocytes. AUTOIMMUNITY (PubMed: 34431434) [IF=3.5]

9). MFAP5 promotes tumor progression and bone metastasis by regulating ERK/MMP signaling pathways in breast cancer. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (PubMed: 29526753) [IF=3.1]

Application: WB    Species: human    Sample: MCF7 and MDA-MB-231 cells

Fig. 4. |MFAP5 activated ERK signaling pathway in breast cancer cells. MCF7 and MDA-MB-231 cells were transfected with OE-MFAP5 plasmid or siRNAs or their controls. Then, the expressions of p-FAK (Try861), FAK, p-Eek1/2, Eek1/2, p-cJun (Ser63), p-cJun (Ser73) and cJun were detected by Western blot assay.

10). Gentiopicroside inhibits cell growth and migration on cervical cancer via the reciprocal MAPK/Akt signaling pathways. NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL (PubMed: 32762372) [IF=2.9]

Application: WB    Species: human    Sample: HeLa cells

Figure 6. | MAPK and Akt signaling pathways were regulated by GPS in HeLa cells. HeLa cells under various treatments of GPS for 24 h were harvested for examining the MAPK and Akt signaling pathways associated proteins by western blot. Densitometric analyses of total of Erk1/2, Akt, p38, JNK, c-Jun, and phosphorylation of Erk1/2, Akt, p38, JNK, c-Junproteins were normalized to the level of b-tubulin. Experiments were repeated three times. P < 0.05, P < 0.01vs. the control.

Application: WB    Species: human    Sample: HeLa cells

Figure 6. | MAPK and Akt signaling pathways were regulated by GPS in HeLa cells. HeLa cells under various treatments of GPS for 24 h were harvested for examining the MAPK and Akt signaling pathways associated proteins by western blot. Densitometric analyses of total of Erk1/2, Akt, p38, JNK, c-Jun, and phosphorylation of Erk1/2, Akt, p38, JNK, c-Junproteins were normalized to the level of b-tubulin. Experiments were repeated three times. P < 0.05, P < 0.01vs. the control.

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