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Anti-NFkB p65 Antibody (Serum)

Rabbit Anti-Human Polyclonal Antibody

     
  • IF - Anti-NFkB p65 Antibody (Serum) ABD11272
    Published customer image:Rabbit anti NFκBp65 antibody used for the evaluation of NF&kappab expression in muring kidney by immunofluorescence.Image caption:Response of vascular endothelial cells in human kidney in organ culture to TL1A. Confocal images of kidney organ culture incubated with either culture media alone or with TL1A (0.2 µg/ml) or TNF (5 ng/ml) for 3 hours at 37°C. (A-C) cultures incubated in media alone show EC staining for NF-κBp65 (green) in both the glomerular (inset) and in peritubular vassels. Some peritubular vessels EC showed positive staining for DR3 (red). (D-F) Cultures treated with TL1A show co-staining for NF-κBp65 (green) and DR3 (red) in EC of some blood vessel (arrows). Inset; show no signal for NF-κBp65 on glomerular EC. (G-I) In contrast, TNF-treated cultures show a strong signal for NF-κB p65 (green) in EC of glomerular (inset) and peritubular blood vessels. DR3 (red) is present only in EC of peritubular blood vessels negative for NF-κB p65. (Original Mags; x40).From: Wang J, Al-Lamki RS, Zhu X, Liu H, Pober JS, Bradley JR. TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells. BMC Nephrol. 2014 Nov 16;15:178.
  • IF - Anti-NFkB p65 Antibody (Serum) ABD11272
    Published customer image:Rabbit anti NFκBp65 antibody used for the evaluation of NF&kappab expression in muring kidney by immunofluorescence.Image caption:TL1a induced NF-κB activation in renal interstitial vascular endothelial cells in mouse organ cultures. Kidney tissue from DR3 wild type and DR3 knockout mice were treated with TL1A or TNF and immunolabeled as described in materials and methods. (A-C) Untreated DR3wt showed no positive staining for NF-κB activation in CD31 positive EC from glomerulus or interstitial vessels. (D-F) some interstitial EC were positive for NF-κB activation after TL1A treatment. (G-I) more vascular EC were positive for NF-κB activation after TNF treatment. (J-L) untreated DR3ko showed no staining for NF-κB activation in vascular EC. (M-O) TL1A-treated DR3ko showed no staining for NF-κB activation in vascular EC. (P-R) TNF-treated DR3ko showed positive staining for NF-κB activation in vascular EC. Arrow for BvEC: blood vessel endothelial cells. Results were representative of 3 experiments.From: Wang J, Al-Lamki RS, Zhu X, Liu H, Pober JS, Bradley JR. TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells. BMC Nephrol. 2014 Nov 16;15:178.
  • IF - Anti-NFkB p65 Antibody (Serum) ABD11272
    Published customer image:Rabbit anti NFκBp65 antibody used for the evaluation of NF&kappab expression in muring kidney by immunofluorescence.Image caption:TL1A induced NF-κB activation in vascular endothelial cells in mouse heart organ cultures. Heart tissue from DR3 wild type and DR3 knock-out mice were treated with TL1A or TNF and immunolabeled as described in materials and methods. DR3wt showed more nuclear NF-κB activation in CD31 positive EC after TL1A treatment (B) compared to the untreated (A). There was similar odd nuclear NF-κB activation in DR3ko mice EC between TL1A treated (E) and untreated cultures (D). TNF induced a more profound nuclear NF-κB activation in EC of both DR3wt and DR3ko (C and F). Results were representative of 3 experiments. Graph showed a statistical difference in number of EC in TL1A treated tissue with NF-κB activation in DR3wt compared to DR3ko (p?<?0.05) (*).From: Wang J, Al-Lamki RS, Zhu X, Liu H, Pober JS, Bradley JR. TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells. BMC Nephrol. 2014 Nov 16;15:178.
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
WB, IF, E, IP, GS
Primary Accession Q04206
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Polyclonal IgG
Calculated MW 60219 Da
Additional Information
Other Species M,Rat
Purification Antisera to NFkB p65 were raised by repeated immunisation of rabbits with highly purified antigen.
Immunogen NFkB p65 peptide corresponding to the C-terminus region of the human protein conjugated to KLH.
Shelf Life 18 months from date of despatch.
Gene ID 5970
Other Names Transcription factor p65, Nuclear factor NF-kappa-B p65 subunit, Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3, RELA, NFKB3
Target/Specificity Rabbit anti-Human NFkB p65 antibody recognizes the human Transcription factor p65, also known as Nuclear factor NF-kappa-B p65 subunit, NFκB p65, RelA or Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3. NFκB p65 is a 551 amino acid ~65 kDa subunit of the NFκB transcription factor present in most cell types and is involved as the endpoint in an array of signal transduction events related to many processes including apotosis, immunity, inflammation and tumorigenesis. The most abundant form of NFκB appears to be the p65-p50 heterodimer. In the active form NFκB p65 is found in the nucleus co-localizing with the ATP-dependent RNA helicase DDX1. NFκB p65 is also found in an inactive form in the cytoplasm associated with the inhibitor IκB (UniProt: Q04206)In a gel supershift assay Rabbit anti-Human NFκB p65 antibody was found to be active against all p65 containing human, mouse or rat NFκB complexes using 0.5ul to 1.0ul per assay. The binding of Rabbit anti-Human NFκB p65 antibody to the NFκB p65 subunit can be blocked using the NFκB p65 control peptide (PHP073).
Preservative & Stabilisers 0.01% Sodium Azide
Storage Store at +4℃ or at -20 ℃.
PrecautionsAnti-NFkB p65 Antibody (Serum) is for research use only and not for use in diagnostic or therapeutic procedures.
Research Areas
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References

1. Cruz, M.T. et al. (1999) Involvement of JAK2 and MAPK on type II nitric oxide synthase expression in skin-derived dendritic cells.
Am J Physiol. 277: C1050-7. 2. Parmentier. M, et al. (2000) Regulation of lipopolysaccharide-mediated interleukin-1beta release by N-acetylcysteine in THP-1 cells.
Eur. Respir. J. 16: 933-9. 3. Gründker, C. et al. (2000) Luteinizing hormone-releasing hormone induces nuclear factor kappaB-activation and inhibits apoptosis in ovarian cancer cells.
J Clin Endocrinol Metab. 85: 3815-20. 4. Sun, J. et al. (2007) Neuropeptide substance P upregulates chemokine and chemokine receptor expression in primary mouse neutrophils.
Am J Physiol Cell Physiol. 293: C696-704. 5. Wang, J. et al. (2014) TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells.
BMC Nephrol. 15: 178. 6. Abdel-Latif, M. (2015) Diethylcarbamazine citrate ameliorates insulin resistance in high-fat diet-induced obese mice via modulation of adipose tissue inflammation.
Int Immunopharmacol. : . 7. Takada Y et al. (2009) Odoroside A and ouabain inhibit Na+/K+-ATPase and prevent NF-kappaB-inducible protein expression by blocking Na+-dependent amino acid transport.
Biochem Pharmacol. 78 (9): 1157-66. 8. Zhang H et al. (2007) Hydrogen sulfide acts as an inflammatory mediator in cecal ligation and puncture-induced sepsis in mice by upregulating the production of cytokines and chemokines via NF-kappaB.
Am J Physiol Lung Cell Mol Physiol. 292 (4): L960-71.

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