Product: Phospho-c-Jun (Ser73) Antibody
Catalog: AF3095
Description: Rabbit polyclonal antibody to Phospho-c-Jun (Ser73)
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat, Zebrafish
Prediction: Pig, Zebrafish, Bovine, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 37kDa; 36kD,35kD(Calculated).
Uniprot: P05412 | P17535
RRID: AB_2834532

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, 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,Zebrafish
Prediction:
Pig(100%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Phospho-c-Jun (Ser73) Antibody detects endogenous levels of c-Jun only when phosphorylated at Serine 73.
RRID:
AB_2834532
Cite Format: Affinity Biosciences Cat# AF3095, RRID:AB_2834532.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
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; Activator protein 1; AP 1; AP1; Jun D; jun D proto oncogene; Jund; JunD FL isoform; JUND_HUMAN; Transcription factor jun D; Transcription factor jun-D;

Immunogens

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

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

Description:
JunD Transcription factor binding AP-1 sites. Binds DNA as a dimer. Interacts with MEN1; this interaction represses transcriptional activation.
Sequence:
MTAKMETTFYDDALNASFLPSESGPYGYSNPKILKQSMTLNLADPVGSLKPHLRAKNSDLLTSPDVGLLKLASPELERLIIQSSNGHITTTPTPTQFLCPKNVTDEQEGFAEGFVRALAELHSQNTLPSVTSAAQPVNGAGMVAPAVASVAGGSGSGGFSASLHSEPPVYANLSNFNPGALSSGGGAPSYGAAGLAFPAQPQQQQQPPHHLPQQMPVQHPRLQALKEEPQTVPEMPGETPPLSPIDMESQERIKAERKRMRNRIAASKCRKRKLERIARLEEKVKTLKAQNSELASTANMLREQVAQLKQKVMNHVNSGCQLMLTQQLQTF

METPFYGDEALSGLGGGASGSGGSFASPGRLFPGAPPTAAAGSMMKKDALTLSLSEQVAAALKPAAAPPPTPLRADGAPSAAPPDGLLASPDLGLLKLASPELERLIIQSNGLVTTTPTSSQFLYPKVAASEEQEFAEGFVKALEDLHKQNQLGAGAAAAAAAAAAGGPSGTATGSAPPGELAPAAAAPEAPVYANLSSYAGGAGGAGGAATVAFAAEPVPFPPPPPPGALGPPRLAALKDEPQTVPDVPSFGESPPLSPIDMDTQERIKAERKRLRNRIAASKCRKRKLERISRLEEKVKTLKSQNTELASTASLLREQVAQLKQKVLSHVNSGCQLLPQHQVPAY

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

PTMs - P05412/P17535 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
Site PTM Type Enzyme
S27 Phosphorylation
T38 Phosphorylation
S43 Phosphorylation
T71 Phosphorylation
S90 Phosphorylation P45983 (MAPK8)
K97 Ubiquitination
S100 Phosphorylation P45983 (MAPK8) , P27361 (MAPK3) , P28482 (MAPK1)
T117 Phosphorylation P45983 (MAPK8)
K127 Ubiquitination
S131 Phosphorylation
K142 Ubiquitination
K240 Sumoylation
T245 Phosphorylation
S251 Phosphorylation
S255 Phosphorylation
S259 Phosphorylation
T265 Phosphorylation
S294 Phosphorylation
S305 Phosphorylation
T308 Phosphorylation
S312 Phosphorylation
T313 Phosphorylation
S315 Phosphorylation
K325 Ubiquitination
K327 Ubiquitination

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.

Function:

Transcription factor binding AP-1 sites.

PTMs:

Phosphorylated by MAP kinases MAPK8 and MAPK10; phosphorylation is inhibited in the presence of MEN1.

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
Subunit Structure:

Binds DNA as a dimer (By similarity). Interacts (via MBM motif) with MEN1; this interaction represses transcriptional activation. Interacts with MAPK10; this interaction is inhibited in the presence of MEN1.

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). 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).

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

3). 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.

4). 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.

5). Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway. Oncology Letters (PubMed: 28123584) [IF=2.9]

Application: WB    Species: human    Sample: SV-HUC-1 cells

Figure 4. (A) Fold change in cell viability of SV-HUC-1 cells treated with 0, 0.10 and 0.25% CSE for 7 days in combination with 5 µM U0126, 5 µM SB203580 or 2 µM SP600125. Data are representative of three independent experiments and are expressed as the mean ± standard deviation. * P

6). MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells. Oncology Letters (PubMed: 30197677) [IF=2.9]

Application: WB    Species: human    Sample: SV‑HUC‑1

Figure 4. |Effects of benzidine on the expression and activation of mitogen‑activated protein kinases and activating protein‑1 monomers. (C) Western blotting analysis of Jun family proteins. Significant increases in p‑c‑Jun and JunB levels were observed, whereas the JunD level was not significantly increased.

7). 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.

8). Baicalin enhances the thermotolerance of mouse blastocysts by activating the ERK1/2 signaling pathway and preventing mitochondrial dysfunction. Theriogenology (PubMed: 34808561) [IF=2.8]

9). Resveratrol inhibits cell apoptosis by suppressing long noncoding RNA (lncRNA) XLOC_014869 during lipopolysaccharide-induced acute lung injury in rats. Journal of Thoracic Disease (PubMed: 34992821) [IF=2.5]

Application: WB    Species: Rat    Sample:

Figure 7 Verification of differential mRNA and lncRNA expression levels and analysis of cell apoptosis in rat lung tissue. Quantitative real-time PCR (A-F), and western blotting (G), and TUNEL (H) results of lung tissue in each group. Apoptotic cells were visualized at ×20 magnification. *, P

10). Adipose-derived stem cells promote the proliferation, migration, and invasion of oral squamous cell carcinoma cells by activating the Wnt/planar cell polarity signaling pathway. Translational Cancer Research (PubMed: 35281413) [IF=0.9]

Application: WB    Species: Mice    Sample: OSCC cells

Figure 3 ADSCs promote the growth and development of OSCC cells by activating signal proteins through the Wnt/PCP signaling pathway. (A) Y-axis represents the ratio of gray value of target protein to gray value of actin. Western blot analysis showed that the expression of CTHRC1 and p-c-Jun increased in a dose-dependent manner after ADSC-CM stimulation. The same conclusion can be drawn in the gray value analysis. (B) Stained with 4',6-diamidino-2-phenylindole, the expression and subcellular localization of CTHRC1 and p-c-Jun were observed by fluorescence microscope. After ADSC-CM, translocation of CTHRC1 and p-c-Jun (green) from cytoplasm to nucleus was observed in CAL 27 cells cells. It was also found that the expression of CTHRC1 and p-c-Jun increased after ADSC-CM treatment, as confirmed by Western blot analysis. Scale bar: 50 µm. *P<0.05; **P<0.01. ADSCs, adipose-derived stem cells; OSCC, oral squamous cell carcinoma; PCP, planar cell polarity; CTHRC1, collagen triple helix repeat-containing protein 1; p-c-Jun, phospho-c-Jun; ADSC-CM, ADSC conditioned medium.

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