NF-kB p65 anticorps (AA 51-100)

N° du produit ABIN668961

Cité dans 30 publications. Cet anticorps anti-NF-kB p65 Polyclonal Lapin (ABIN668961) détecte spécifiquement NF-kB p65 dans WB, FACS, IHC (p), IF (p), IF (cc) et IHC (fro). L’anticorps est réactif avec des échantillons de Humain.

Aperçu rapide pour NF-kB p65 anticorps (AA 51-100) (ABIN668961)

Antigène: NF-kB p65 (NFkBP65) (Nuclear Factor-kB p65 (NFkBP65))

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp NF-kB p65 est non-conjugé

Application: Western Blotting (WB), Flow Cytometry (FACS), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), Immunofluorescence (Cultured Cells) (IF (cc)), Immunohistochemistry (Frozen Sections) (IHC (fro))

Détail du produit anti-NF-kB p65 anticorps

Épitope: AA 51-100

Fonction: NFKB p65 Polyclonal Antibody

Réactivité croisée: Humain, Souris

Homologie: Rat,Dog,Cow,Pig,Horse,Chicken,Rabbit,Zebrafish

Purification: Purified by Protein A.

Immunogène: KLH conjugated synthetic peptide derived from human NFKBp65

Isotype: IgG

Information d'application

Indications d'application: WB(1:300-5000),

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 1 μg/μL

Buffer: 0.01M TBS( pH 7.4) with 1 % BSA, 0.02 % Proclin300 and 50 % Glycerol.

Agent conservateur: ProClin

Précaution d'utilisation: This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: 4 °C,-20 °C

Stockage commentaire: Shipped at 4C. Store at -20C for one year. Avoid repeated freeze/thaw cycles.

Date de péremption: 12 months

Références pour anticorps anti-NF-kB p65 (ABIN668961)

Fontana, Plaza-Díaz, Robles-Bolívar, Valente-Godínez, Sáez-Lara, Abadía-Molina, Gómez-Llorented, Gil, Álvarez-Mercado et al.: "Bifidobacterium breve CNCM I-4035, Lactobacillus paracasei CNCM I-4034 and Lactobacillus rhamnosus CNCM I-4036 Modulate Macrophage Gene Expression and Ameliorate Damage Markers in the Liver of ..." dans: Nutrients, Vol. 13, Issue 1, (2021) (PubMed).

Oyagbemi, Omobowale, Ola-Davies, Asenuga, Ajibade, Adejumobi, Afolabi, Ogunpolu, Falayi, Ayodeji, Hassan, Saba, Adedapo, Yakubu: "Ameliorative effect of Rutin on sodium fluoride-induced hypertension through modulation of Kim-1/NF-κB/Nrf2 signaling pathway in rats." dans: Environmental toxicology, Vol. 33, Issue 12, pp. 1284-1297, (2019) (PubMed).

Xu, Liu, Yu, Wu, Lu: "Effect of recombinant Trichinella spiralis cysteine proteinase inhibitor on TNBS-induced experimental inflammatory bowel disease in mice." dans: International immunopharmacology, Vol. 66, pp. 28-40, (2019) (PubMed).

Fattori, Borghi, Guazelli, Giroldo, Crespigio, Bussmann, Coelho-Silva, Ludwig, Mazzuco, Casagrande, Verri: "Vinpocetine reduces diclofenac-induced acute kidney injury through inhibition of oxidative stress, apoptosis, cytokine production, and NF-κB activation in mice." dans: Pharmacological research, Vol. 120, pp. 10-22, (2018) (PubMed).

Sun, Nemoto, Hong, Sasaki: "Modulation of stromal cell-derived factor 1 alpha (SDF-1α) and its receptor CXCR4 in Porphyromonas gingivalis-induced periodontal inflammation." dans: BMC oral health, Vol. 17, Issue 1, pp. 26, (2018) (PubMed).

Xi, Wang, Chen, Yang, Hu, Zhang, Weng, Xu: "Expressions of IL-6, TNF-α and NF-κB in the skin of Chinese brown frog (Rana dybowskii)." dans: European journal of histochemistry : EJH, Vol. 61, Issue 4, pp. 2834, (2018) (PubMed).

Lin, Geng, Zhao, Lin, Zhu, Tian: "MiR-21 Regulates TNF-α-Induced CD40 Expression via the SIRT1-NF-κB Pathway in Renal Inner Medullary Collecting Duct Cells." dans: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, Vol. 41, Issue 1, pp. 124-136, (2017) (PubMed).

Ganguly, Wen, Myer, Czech, Sahu, Steinmetz, Raman: "Anti-atherogenic effect of trivalent chromium-loaded CPMV nanoparticles in human aortic smooth muscle cells under hyperglycemic conditions in vitro." dans: Nanoscale, Vol. 8, Issue 12, pp. 6542-54, (2016) (PubMed).

Yang, Zhong, Li, Xiong, Wang, Peng, Ye: "Hypothermic machine perfusion increases A20 expression which protects renal cells against ischemia/reperfusion injury by suppressing inflammation, apoptosis and necroptosis." dans: International journal of molecular medicine, Vol. 38, Issue 1, pp. 161-71, (2016) (PubMed).

Oyagbemi, Omobowale, Asenuga, Adejumobi, Ajibade, Ige, Ogunpolu, Adedapo, Yakubu: "Sodium fluoride induces hypertension and cardiac complications through generation of reactive oxygen species and activation of nuclear factor kappa beta." dans: Environmental toxicology, (2016) (PubMed).

Xi, Hu, Guo, Wang, Sheng, Han, Yuan, Weng, Xu: "Immunoreactivities of NF-κB, IL-1β and IL-1R in the skin of Chinese brown frog (Rana dybowskii)." dans: Acta histochemica, Vol. 119, Issue 1, pp. 64-70, (2016) (PubMed).

Zheng, Liu, Li, Tang, Zhang, Tang: "Lithium posttreatment confers neuroprotection through glycogen synthase kinase-3β inhibition in intracerebral hemorrhage rats." dans: Journal of neurosurgery, pp. 1-9, (2016) (PubMed).

Zhang, Wu, Deng, Zheng, Zhang, Deng, Chen, Ma, Wang, Yu, Kang, Wang: "High altitude increases the expression of hypoxia-inducible factor 1α and inducible nitric oxide synthase with intest-inal mucosal barrier failure in rats." dans: International journal of clinical and experimental pathology, Vol. 8, Issue 5, pp. 5189-95, (2016) (PubMed).

Guo, Deng, Cui, Peng, Fang, Zuo, Deng, Wang, Wu, Chen: "Nickel chloride (NiCl2)-caused inflammatory responses via activation of NF-κB pathway and reduction of anti-inflammatory mediator expression in the kidney." dans: Oncotarget, Vol. 6, Issue 30, pp. 28607-20, (2016) (PubMed).

Li, Cheng, Zhao, Guo, Liu, Zhang, Wang, Zhang, Pan, Nie: "ADAMTS-7 exhibits elevated expression in cartilage of osteonecrosis of femoral head and has a positive correlation with TNF- α and NF- κ B P65." dans: Mediators of inflammation, Vol. 2015, pp. 196702, (2016) (PubMed).

Qian, Cai, Zhang, Wang, Qian, Hasegawa: "Effect of Daisaikoto on Expressions of SIRT1 and NF-kappaB of Diabetic Fatty Liver Rats Induced by High-Fat Diet and Streptozotocin." dans: Yonago acta medica, Vol. 59, Issue 2, pp. 149-58, (2016) (PubMed).

Huang, Yang, Wang, Ma, Cui, Huang, Sheng, Weng, Xu: "Immunostimulatory activity of protein hydrolysate from oviductus ranae on macrophage in vitro." dans: Evidence-based complementary and alternative medicine : eCAM, Vol. 2014, pp. 180234, (2015) (PubMed).

Luo, Yang, Tang, Yao, Kong, He, Zhou: "Kaempferol alleviates insulin resistance via hepatic IKK/NF-?B signal in type 2 diabetic rats." dans: International immunopharmacology, Vol. 28, Issue 1, pp. 744-50, (2015) (PubMed).

Détails sur NF-kB p65

Antigène: NF-kB p65 (NFkBP65) (Nuclear Factor-kB p65 (NFkBP65))

Autre désignation: NFKB p65

Sujet:

Synonyms: p65, NFKB3, Transcription factor p65, Nuclear factor NF-kappa-B p65 subunit, Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3, RELA

Background: NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p15, NFKB1/p5, REL and NFKB2/p52 and the heterodimeric p65-p5 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p5 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1.

ID gène: 5970

UniProt: Q04206

Pathways: Signalisation NF-kappaB, Signalisation RTK, TCR Signaling, Signalisation TLR, Fc-epsilon Receptor Signaling Pathway, Neurotrophin Signaling Pathway, Activation of Innate immune Response, Cellular Response to Molecule of Bacterial Origin, Hepatitis C, Toll-Like Receptors Cascades, S100 Proteins