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J2128

Anti-phospho-c-Jun (pSer⁶³) antibody produced in rabbit

Name: Anti-phospho-c-Jun (pSer<SUP>63</SUP>) antibody produced in rabbit
Brand: SIGMA

affinity isolated antibody, buffered aqueous glycerol solution

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About This Item

MDL number:

MFCD01092289

UNSPSC Code:

12352203

NACRES:

NA.41

biological source

rabbit

Quality Level

200

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous glycerol solution

mol wt

antigen 48 kDa

species reactivity

rat, mouse, human

technique(s)

flow cytometry: 1:200
microarray: suitable
western blot (chemiluminescent): 1:1,000 using extract of NIH3T3 anisomycin or UV-treated cells

UniProt accession no.

P05412

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pSer63)

Gene Information

human ... JUN(3725)
mouse ... Jun(16476)

Specificity

The antibody does not react with the corresponding phosphorylated form of JunD or JunB.

Immunogen

synthetic phosphoserine⁶³ peptide corresponding to residues around Ser⁶³ of human c-Jun, conjugated to KLH.

Application

Anti-phospho-c-Jun (pSer63) antibody produced in rabbit has been used in microarray analysis to identify the changes in the level of cellular proteins in cells inoculated with Equine influenza virus.

Biochem/physiol Actions

The protooncogene c-Jun encodes a member of the jun family that forms a component of the transcription factor AP-1 (Activator Protein-1). It dimerizes with a member of the Fos family via the leucine-zipper motif to form AP-1, a factor involved in binding to TPA (12-O-tetradecanoylphorbol 13-acetate) response element (TRE) of various genes that include human collagenase, metallothionein IIa, stromelysin, interleukin 2, SV40 and polyoma. The dimers formed are involved in the activation of AP-1 dependent genes. AP-1 regulates the transcription of mammalian DDI (DNA-damage-inducible) genes.

Physical form

Solution in 10 mM HEPES sodium, pH 7.5, containing 150 mM sodium chloride, 100 μg/mL bovine serum albumin, and 50% glycerol.

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Storage Class

10 - Combustible liquids

Certificates of Analysis (COA)

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Rapid and preferential activation of the c-jun gene during the mammalian UV response.

Y Devary et al.

Molecular and cellular biology, 11(5), 2804-2811 (1991-05-01)

Exposure of mammalian cells to DNA-damaging agents leads to activation of a genetic response known as the UV response. Because several previously identified UV-inducible genes contain AP-1 binding sites within their promoters, we investigated the induction of AP-1 activity by

The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1.

P Angel et al.

Cell, 55(5), 875-885 (1988-12-02)

Binding of the human transcription factor Jun/AP-1 to a conserved 8 bp nucleotide sequence (TRE) is responsible for increased transcription of different cellular genes in response to tumor promoters, such as TPA, and serum factors. Enhanced Jun/AP-1 activity in TPA-stimulated

Prolonged activation of jun and collagenase genes by tumour necrosis factor-alpha.

D A Brenner et al.

Nature, 337(6208), 661-663 (1989-02-16)

Tumour necrosis factor-alpha (TNF-alpha) is secreted by macrophages in response to inflammation, infection and cancer. Sublethal doses of recombinant TNF-alpha to rats causes cachexia, anaemia and inflammation. TNF-alpha plays a major part in tissue inflammation and remodelling by stimulating production

jun-D: a third member of the jun gene family.

K Ryder et al.

Proceedings of the National Academy of Sciences of the United States of America, 86(5), 1500-1503 (1989-03-01)

The protooncogene c-jun encodes a component of the transcription factor AP-1. Both murine c-jun and a related gene (jun-B) are rapidly activated in BALB/c3T3 cells by serum growth factors. We report here the cloning and analysis of a cDNA encoding

Long-term administration of fatty acid amide hydrolase inhibitor (URB597) to rats with spontaneous hypertension disturbs liver redox balance and phospholipid metabolism.

Michał Biernacki et al.

Advances in medical sciences, 64(1), 15-23 (2018-09-23)

The effect of chronic administration of [3-(3-carbamoylphenyl)phenyl] N-cyclohexylcarbamate (URB597), inhibitor of fatty acid amide hydrolase (FAAH) that hydrolyzes anandamide, on cross-talk between endocannabinoid system, oxidative status and pro-inflammatory factors in the liver of spontaneously hypertensive rats (SHRs) was investigated. Experiments

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