货号 | AHP288 |
同种亚型 | Polyclonal IgG |
反应种属 | Human |
来源宿主 | Rabbit |
应用 | E, GS, IF, IP, WB |
供应商 | Bio-Rad Antibodies |
运输条件 | |
存放说明 | Store at +4oC or at -20oC if preferred. This product should be stored undiluted. Storage in frost free freezers is not recommended. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. |
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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. | |
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 (wt) and DR3 knockout (ko) mice were treated with TL1A or TNF and immunolabeled as described in materials and methods. (A-C) Untreated (UT) 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. | |
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. (6a) Heart tissue from DR3 wild type (wt) and DR3 knock-out (ko) 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. (6b) 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. |