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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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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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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
Butyrate repress gene expression of NFkappaB1 through modulation of histone H3 (show HIST3H3 ELISA Kits) trimethylation at lysine 27.
The constitutive elevations of Prdx6 (show PRDX6 ELISA Kits) and NF-kappaB during Clonorchis sinensis infection may be associated with more severe persistent hepatobiliary abnormalities mediated by clonorchiasis.
Upregulated KCNJ11 (show KCNJ11 ELISA Kits) predicts a poor prognosis and is regulated by NFkappaB signaling in hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)). LDHA (show LDHA ELISA Kits) partially mediated the oncogenic roles of KCNJ11 (show KCNJ11 ELISA Kits) in HCC (show FAM126A ELISA Kits).
Our finding reveals a crucial roles for SREBP1 (show SREBF1 ELISA Kits) in lipid desaturation of ccRCC through regulation of NF-kappaB signaling, which provides not only new insights in regulatory mode of NF-kappaB signaling but also a novel target for potential metabolic therapies.
Analysis of the early events after receptor engagement revealed that both TNF (show TNF ELISA Kits) and CD40L (show CD40LG ELISA Kits) activate the classical NF-kappaB pathway, and confirm activation of the alternative by the latter. Furthermore, using genetic and pharmacological inhibition of the classical pathway we show that activation of the alternative occurs independently of the former. This reveals insights into NF-kappaB signaling by CD40L (show CD40LG ELISA Kits) and TNF (show TNF ELISA Kits) in endoth...
Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-kappaB in inflammatory breast cancer cells, in particular, to tenascin-C and MPP9.
MyD88 (show MYD88 ELISA Kits) cysteine residues functionally modulate MyD88 (show MYD88 ELISA Kits)-dependent NF-kappaB activation, suggesting a link between MyD88 (show MYD88 ELISA Kits) thiol oxidation state and immune signaling.
These findings demonstrate that NF-kappaB-mediated transcriptional mechanisms are critically involved in the IL-1beta (show IL1B ELISA Kits)-mediated IL-17C (show IL17C ELISA Kits) induction, and that IL-13 (show IL13 ELISA Kits) negatively regulates this induction by suppressing NF-kappaB-based transcriptional activation.
Data show that exendin-4 (Ex-4) could attenuate breast cancer cell proliferation via activation of glucagonlike peptide-1 (GLP-1) receptor (GLP-1R (show GLP1R ELISA Kits)) and subsequent inhibition of nuclear factor kappaB (NF-kappaB ) activation.
The role of NF-kappaB deregulation in the pathogenesis of diffuse large B-cell lymphoma [review]
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 (show PPARG ELISA Kits) activation.
Taken together, Staphylococcus aureus induces TGF-beta1 (show TGFB1 ELISA Kits) and bFGF (show FGF2 ELISA Kits) expression through the activation of AP-1 (show JUN ELISA Kits) and NF-kappaB in bovine mammary gland fibroblasts.
Data indicate the involvement of PKC-alpha (show PKCa ELISA Kits) in proMMP-2 activation and inhibition of TIMP-2 (show TIMP2 ELISA Kits) expression by NF-kappaB-MT1-MMP (show MMP14 ELISA Kits)-dependent and -independent pathway.
MMP-1 (show MMP1 ELISA Kits) promotes VEGFR2 (show KDR ELISA Kits) expression and proliferation of endothelial cells through stimulation of PAR-1 (show F2R ELISA Kits) and activation of NF-kappaB
dynamic compression stimulates cell proliferation and proteoglycan (show Vcan ELISA Kits) synthesis in the presence of IL-1beta (show IL1B ELISA Kits) and/or inhibitors of the MAPKs and NFkappaB and AP-1 (show JUN ELISA Kits) signalling pathways
TRIM5alpha (show TRIM5 ELISA Kits) represses HIV-1 LTR promoter activity by negatively regulating TAK1 (show NR2C2 ELISA Kits)/TAB1 (show TAB1 ELISA Kits)/TAB2 (show TAB2 ELISA Kits)/TAB3 (show TAB3 ELISA Kits)-complex-mediated NF-kappaB activation.
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 (show IFNA ELISA Kits) and early production of pro-inflammatory cytokines.
inhibition of NF-kappaB increases autophagy via JNK (show MAPK8 ELISA Kits) signaling, and promotes steroidogenesis in porcine granulosa cells
SIRT1 (show SIRT1 ELISA Kits), p53 (show TP53 ELISA Kits) and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.
porcine CD74 (show CD74 ELISA Kits) significantly enhanced the inflammatory response by regulating the NF-kappaB signalling pathway during PCV2 infection, which suggests that porcine CD74 (show CD74 ELISA Kits) may be implicated in the pathogenesis of PCV2 infection.
These results suggest that trans-10, cis (show CISH ELISA Kits)-12-conjugated linoleic acid can modulate TNF-alpha (show TNF ELISA Kits) production and NF-kappa B expression by a PPARgamma (show PPARG ELISA Kits)-dependent pathway in porcine peripheral blood mononuclear cells.
SPAK (show STK39 ELISA Kits) plays a pathogenic role in IgA nephropathy through the activation of NF-kappaB/MAPK (show MAPK1 ELISA Kits) signaling pathway.
Identification of a PPAR-gamma (show PPARG ELISA Kits) --> NF-kappaB --> p22phox (show CYBA ELISA Kits) neuroprotective signaling cascade opens a new avenue for protecting the brain against ischemic insult.
interactions of NF-kappaB and N-myc (show MYCN ELISA Kits) with GLT-1/EAAT2 (show SLC1A2 ELISA Kits) promoter sequences was significantly elevated in the ipsi-lateral cortex of both adult and old Traumatic brain injury mice.
Data show that inhibition of the protease activity of MALT1 (show MALT1 ELISA Kits) might be a strategy to treat inflammatory bowel disease and the NLRP3 (show NLRP3 ELISA Kits) inflammasome and NF-kappaB activation are critical components in MALT1 (show MALT1 ELISA Kits) signaling cascades in this disease model.
IFN-gamma (show IFNG ELISA Kits)/TNFalpha (show TNF ELISA Kits) trigger the formation of an NF-kappaB/STAT3 (show STAT3 ELISA Kits) complex.
Importantly, inhibition of NF-kappaB by QDs displayed promising effects against the viral replication and in vivo bacterial endotoxin-induced inflammatory responses. These data suggest the QDs as potent inhibitors of the NF-kappaB signaling pathway, both in vitro and in vivo.
NF-kB mediated upregulation of CADM1 (show CADM1 ELISA Kits) was identified as a mechanism of TNFalpha (show TNF ELISA Kits) induced migration.
NF-kappaB activation and the downstream expression of inflammatory factors were therefore down-regulated in along an efficient path and ameliorating the damage as a consequence of LPS (show TLR4 ELISA Kits)-induced acute lung injury.
FSTL1 (show FSTL1 ELISA Kits) is a secreted osteoclastogenic factor that plays a critical role in osteoclast formation via the NF-kappaB and MAPKs signaling pathways.
Study indicate an essential role of NF-kappaB in gonadal differentiation.
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