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Rat (Rattus) NFKB1 ELISA Kit for Competition ELISA - ABIN1503629
Zhang, Zhang, Xing: Protective effects of phosphocreatine administered post-treatment combined with ischemic post-conditioning on rat hearts with myocardial ischemia/reperfusion injury. in Journal of clinical medicine research 2015
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Rat (Rattus) NFKB1 ELISA Kit for Sandwich ELISA - ABIN578888
Wang, Zhang, Wang, Li, Min, Wang, Chen, Cheng, Wu: Inhibitory effect of ginsenoside-Rd on carrageenan-induced inflammation in rats. in Canadian journal of physiology and pharmacology 2012
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Mouse (Murine) NFKB1 ELISA Kit - ABIN1503630
Zhang, Liu, McHale, Li, Zhang, Wu, Ye, Yang, Ding: Bone Marrow Injury Induced via Oxidative Stress in Mice by Inhalation Exposure to Formaldehyde. in PLoS ONE 2013
TRIM5alpha (显示 TRIM5 ELISA试剂盒) represses HIV-1 LTR promoter activity by negatively regulating TAK1 (显示 NR2C2 ELISA试剂盒)/TAB1 (显示 TAB1 ELISA试剂盒)/TAB2 (显示 TAB2 ELISA试剂盒)/TAB3 (显示 TAB3 ELISA试剂盒)-complex-mediated NF-kappaB activation.
Prostaglandin E receptor subtype 2 (EP2 (显示 SPAG11A ELISA试剂盒); Ptger2 (显示 PTGER2 ELISA试剂盒)) deficiency suppressed nuclear factor kappaB (NF-kappaB) activation in intracranial arteries 4 and 8 weeks after intracranial aneurysm induction.
Loss of HDAC (显示 HDAC3 ELISA试剂盒)-mediated repression and gain of NF-kappaB activation underlie cytokine induction in ARID1A (显示 ARID1A ELISA试剂盒)- and PIK3CA (显示 PIK3CA ELISA试剂盒)-mutation-driven ovarian cancer.
Absence of Musashi2 (显示 MSI2 ELISA试剂盒) in osteoclast precursors promotes apoptosis and inhibits RANKL (显示 TNFSF11 ELISA试剂盒)-induced NF-kappaB activation, which is essential for osteoclast survival.
NF-kappaB-mediated miR (显示 MLXIP ELISA试剂盒)-130a modulation is critical in lung vascular remodeling.
Inflammasome-derived exosomes activate NF-kappaB signaling in macrophages.
Genetic reduction of the P65 (显示 NFkBP65 ELISA试剂盒) subunit of NF-kappaB diminished chronic inflammation in dystrophic muscle.
selective knockdown of TNFR5 ameliorates glucolipotoxic induction of STAT1 (显示 STAT1 ELISA试剂盒) expression and NF-kappaB activity.
c-REL (显示 NFkBP65 ELISA试剂盒), but not IkappaBNS, controlled the generation of classical CD25 (显示 IL2RA ELISA试剂盒)(+)Foxp3 (显示 FOXP3 ELISA试剂盒)(-) precursors via direct binding to the Cd25 (显示 IL2RA ELISA试剂盒) locus; propose that CD4 (显示 CD4 ELISA试剂盒)(+)GITR (显示 TNFRSF18 ELISA试剂盒)(+)CD122 (显示 IL2RB ELISA试剂盒)(+)CD25 (显示 IL2RA ELISA试剂盒)(-)Foxp3 (显示 FOXP3 ELISA试剂盒)(-) cells represent a Treg pre-precursor population, whose transition into Treg precursors is mediated via c-REL (显示 NFkBP65 ELISA试剂盒)
The results presented in this study represent the first demonstration that NF-kappaB activation acts cell autonomously to protect oligodendrocytes against inflammation in animal models of MS.
proposed that TLR9 (显示 TLR9 ELISA试剂盒) regulates the NF-kappaB-NLRP3 (显示 NLRP3 ELISA试剂盒)-IL-1beta (显示 IL1B ELISA试剂盒) pathway negatively in Salmonella-induced NKG2D (显示 KLRK1 ELISA试剂盒)-mediated intestinal inflammation and plays a critical role in defense against S. typhimurium infection and in the protection of intestinal integrity
Using iterative experimental and computational analyses, the authors show physical and functional interactions between NF-kappaB and the E2 Factor 1 (E2F-1 (显示 E2F1 ELISA试剂盒)) and E2 Factor 4 (E2F-4 (显示 E2F4 ELISA试剂盒)) cell cycle regulators.
Smad7 (显示 SMAD7 ELISA试剂盒) expression in necrotizing enterocolitis macrophages interrupts TGF-beta (显示 TGFB1 ELISA试剂盒) signaling and promotes NF-kappaB-mediated inflammatory signaling in these cells through increased expression of IKK-beta (显示 IKBKB ELISA试剂盒)
The activation of GPER (显示 GPER ELISA试剂盒) can inhibit the epithelial mesenchymal transition and metastasis of triple negative breast cancer cells via NF-kappaB.
Sam68 (显示 KHDRBS1 ELISA试剂盒) deletion diminishes gamma-irradiation-triggered PAR (显示 JTB ELISA试剂盒) synthesis and NF-kappaB activation in colon epithelial cells (CECs), thus hampering the expression of anti-apoptotic molecules in situ and facilitating CECs to undergo apoptosis in mice post whole-body gamma-irradiation (WBIR).
The results suggest that TWEAK (显示 TNFSF12 ELISA试剂盒)/Fn14 (显示 TNFRSF12A ELISA试剂盒) interaction directly favors inorganic phosphate-induced vascular smooth muscle cells calcification by activation of both canonical and non-canonical NF-kappaB pathways.
Low doses of IL1B (显示 IL1B ELISA试剂盒) activate the BMP/Smad (显示 SMAD1 ELISA试剂盒) signaling pathway to promote the osteogenesis of periodontal ligament stem cells, but higher doses of IL1B (显示 IL1B ELISA试剂盒) inhibit BMP/Smad (显示 SMAD1 ELISA试剂盒) signaling through the activation of NF-kappaB and MAPK (显示 MAPK1 ELISA试剂盒) signaling, inhibiting osteogenesis.
Our data propose an additional novel mechanism to explain the known NF-kappaB inhibitory effects of A20: by affecting p105 ubiquitination and subsequently its degradation and limited processing.
IL-18 (显示 IL18 ELISA试剂盒) cooperates with IL-15 (显示 IL15 ELISA试剂盒) to promote group 3 innate lymphoid cell (ILC3) proliferation and IL-22 (显示 IL22 ELISA试剂盒) production; describe an IL-18 (显示 IL18 ELISA试剂盒)-induced, NF-kappaB-mediated mechanism that regulates IL-22 (显示 IL22 ELISA试剂盒) in ILC3s; at steady-state, IL-18 (显示 IL18 ELISA试剂盒) produced by dendritic cells mediates IL-22 (显示 IL22 ELISA试剂盒) production by ILC3s to help maintain normal tissue integrity
These data indicate that RAGE (显示 AGER ELISA试剂盒) plays a central role in maintaining inflammatory signaling in PDAC that benefits tumor growth.
HBx activates NF-kappaB to promote the expression of miR1269b, which augments CDC40 (显示 CDC40 ELISA试剂盒) expression, contributing to malignancy in hepatocellular cancer.
Study indicate an essential role of NF-kappaB in gonadal differentiation.
This study showed that porcine epidemic diarrhea virus inhibited NF-kappaB activity and nsp1 was a potent NF-kappaB antagonist for suppression of both interferon (显示 IFNA ELISA试剂盒) and early production of pro-inflammatory cytokines.
inhibition of NF-kappaB increases autophagy via JNK (显示 MAPK8 ELISA试剂盒) signaling, and promotes steroidogenesis in porcine granulosa cells
SIRT1 (显示 SIRT1 ELISA试剂盒), p53 (显示 TP53 ELISA试剂盒) and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.
porcine CD74 (显示 CD74 ELISA试剂盒) significantly enhanced the inflammatory response by regulating the NF-kappaB signalling pathway during PCV2 infection, which suggests that porcine CD74 (显示 CD74 ELISA试剂盒) may be implicated in the pathogenesis of PCV2 infection.
These results suggest that trans-10, cis (显示 CISH ELISA试剂盒)-12-conjugated linoleic acid can modulate TNF-alpha (显示 TNF ELISA试剂盒) production and NF-kappa B expression by a PPARgamma (显示 PPARG ELISA试剂盒)-dependent pathway in porcine peripheral blood mononuclear cells.
These results indicated that docosahexaenoic acid may attenuate lipopolysaccharide-stimulated inflammatory response in bovine mammary epithelial cells by suppressing NF-kappaB activation through a mechanism partly dependent on PPARgamma (显示 PPARG ELISA试剂盒) activation.
Taken together, Staphylococcus aureus induces TGF-beta1 (显示 TGFB1 ELISA试剂盒) and bFGF (显示 FGF2 ELISA试剂盒) expression through the activation of AP-1 (显示 JUN ELISA试剂盒) and NF-kappaB in bovine mammary gland fibroblasts.
Data indicate the involvement of PKC-alpha (显示 PKCa ELISA试剂盒) in proMMP-2 activation and inhibition of TIMP-2 (显示 TIMP2 ELISA试剂盒) expression by NF-kappaB-MT1-MMP (显示 MMP14 ELISA试剂盒)-dependent and -independent pathway.
MMP-1 (显示 MMP1 ELISA试剂盒) promotes VEGFR2 (显示 KDR ELISA试剂盒) expression and proliferation of endothelial cells through stimulation of PAR-1 (显示 F2R ELISA试剂盒) and activation of NF-kappaB
dynamic compression stimulates cell proliferation and proteoglycan (显示 Vcan ELISA试剂盒) synthesis in the presence of IL-1beta (显示 IL1B ELISA试剂盒) and/or inhibitors of the MAPKs and NFkappaB and AP-1 (显示 JUN ELISA试剂盒) signalling pathways
This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene.
DNA binding factor KBF1
, DNA-binding factor KBF1
, nuclear factor NF-kappa-B p105 subunit
, nuclear factor NF-kappa-B p50 subunit
, nuclear factor kappa-B DNA binding subunit
, nuclear factor of kappa light chain gene enhancer in B-cells 1, p105
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1, p105
, NF-kB p50 subunit
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)
, nuclear factor kappa-B, subunit 1
, nuclear factor of kappa light polypeptide enhancer in B-cells 1
, nuclear factor kappa-B 1
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1
, nuclear factor NF-kappa-B p105 subunit-like
, NF kappaB1
, NF-kappa-B1 p84/NF-kappa-B1 p98
, NF-kappaB p50
, nuclear factor kappaB p50
, nuclear factor-kappaB p50
, p50 subunit of NF kappaB
, p50 subunit of NF-kappaB
, BICD-related protein 1
, NF-kB1 precursor protein
, bicaudal D-related protein 1
, coiled-coil domain-containing protein 64A