Phospho-c-Jun (Ser63) Antibody - #AF3089

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Product: Phospho-c-Jun (Ser63) Antibody
Catalog: AF3089
Description: Rabbit polyclonal antibody to Phospho-c-Jun (Ser63)
Application: WB IHC
Cited expt.: WB
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 37kDa; 36kD(Calculated).
Uniprot: P05412
RRID: AB_2834526

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*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(91%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(82%), Xenopus(82%)
Clonality:
Polyclonal
Specificity:
Phospho-c-Jun (Ser63) Antibody detects endogenous levels of c-Jun only when phosphorylated at Serine 63.
RRID:
AB_2834526
Cite Format: Affinity Biosciences Cat# AF3089, RRID:AB_2834526.
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;

Immunogens

Immunogen:

A synthesized peptide derived from human c-Jun around the phosphorylation site of Ser63.

Uniprot:

P05412(JUN_HUMAN) >>Visit HPA database.

Gene(ID):
JUN(3725)
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
Sheep
100
Dog
100
Rabbit
100
Zebrafish
91
Xenopus
82
Chicken
82
Horse
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

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.

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). CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription. Cancer cell international, 2024 (PubMed: 38971758) [IF=5.8]

Application: WB    Species: Human    Sample: breast cancer cells

Fig. 4 CEMIP was identified as a downstream gene of CCDC88C. BT549 cells with stable expression of CCDC88C were used to perform mRNA-seq. A The volcano plot showed the DEGs in cells stably transfected with CCDC88C overexpression vectors when compared with cells stably transfected with ev. B GO enrichments analysis of the DEGs in cells stably transfected with CCDC88C overexpression vectors. C BT-549 cells with stable expression of CCDC88C were transfected with pAP1-Ta-luc and pRL-TK plasmids. After 48 h, the relative luciferase was measured. D Immunoblotting was used to detect the level of c-JUN phosphorylation at Ser 63 and Ser 73 and total c-JUN. E The Venn diagram showed the overlapping DEGs in breast cancer cells stably transfected with CCDC88C overexpression vectors and breast cancer cells transfected with siRNA targeting JUN (siJUN). The heatmap showed 12 overlapping DEG expressions in breast cancer cells stably transfected with CCDC88C overexpression vectors or ev and breast cancer cells transfected with si-JUN or sinc. F BT-549 cells with stable expression of CCDC88C were transiently transfected with siJUN. After 48 h, CEMIP mRNA was detected using qRT-PCR. (G, H) BT-549 cells with stable expression of CCDC88C were transiently transfected with siCEMIP. After 48 h, Cell migration and invasion were measured by wound healing assays (× 100 magnification) and transwell assays (× 100 magnification), respectively. Scale bar: 200 μm. Data are expressed as the mean ± SD. DEGs, differentially expressed genes. FC, fold change. Adj p, adjust p value. CCDC88C coiled-coil domain containing 88C. ev empty vectors. oe overexpression. GO gene ontology. BP biological process. CC cellular component. MF molecular function. JUN Jun proto-oncogene, AP-1 transcription factor subunit. siRNA small interfering RNA. sinc negative control siRNA. CEMIP cell migration-inducing and hyaluronan-binding protein.
2). MFAP5 promotes tumor progression and bone metastasis by regulating ERK/MMP signaling pathways in breast cancer. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2018 (PubMed: 29526753) [IF=2.5]

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.

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