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An intrinsic constitutively activated feedforward signaling circuit composed of IkappaBalpha/NF-kappaB (show NFKB1 ELISA Kits)(p65 (show NFkBP65 ELISA Kits)), miR (show MLXIP ELISA Kits)-196b-3p, Meis2 (show MEIS2 ELISA Kits), and PPP3CC (show PPP3CC ELISA Kits) is formed during the emergence of castration-resistant prostate cancer.
Mechanistic analysis suggest that USP12 may be required for the activation of NFkappaB pathway as knockdown of USP12 reduced the inhibitory phosphorylation of IkappaBalpha, a well characterized inhibitor of NFkappaB nuclear translocation.
SM22alpha (show TAGLN ELISA Kits) is a phosphorylation-regulated (show PHAX ELISA Kits) suppressor of IKK (show CHUK ELISA Kits)-IkappaBalpha-NF-kappaB (show NFKB1 ELISA Kits) signaling cascades.
We found potential links between the alterations in expression of Tsc22d3 (show TSC22D3 ELISA Kits), Nfkbia and Pdyn (show PDYN ELISA Kits), and different aspects of susceptibility to stress.
Specific and constitutive deletion of the inhibitor of NF-kappaB (show NFKB1 ELISA Kits) (IkappaBalpha) in eosinophils in vivo reduced apoptosis during helminth infection
GRK6 (show GRK6 ELISA Kits) directly phosphorylates Nfkbia at Ser32/Ser36. Knockdown of GRK6 (show GRK6 ELISA Kits) suppresses TNF-alpha (show TNF ELISA Kits)-induced NF-kappaappaB signaling.
Results demonstrate novel roles of TNFRII (show TNFRSF1B ELISA Kits) in the regulation of Abeta (show APP ELISA Kits) production, suggesting a potential therapeutic strategy for Alzheimer's disease by up-regulating TNFRII (show TNFRSF1B ELISA Kits) levels and elevating phosphorylated IkappaBalpha by SUMOylation.
Defective lymphoid organogenesis underlies the immune deficiency caused by a heterozygous S32I mutation in IkappaBalpha.
Dengue virus protease interacts with both NF-kappaB inhibitor alpha (IkappaBalpha) and NF-kappaB (show NFKB1 ELISA Kits) inhibitor beta (IkappaBbeta (show NFKBIB ELISA Kits)), cleaving them in a mouse hemorrhage model.
The results indicate that following heat shock treatment, HuR (show ELAVL1 ELISA Kits) translocates from the nucleus to the cytoplasm, forming stress granules and regulating the translation of IkBalpha mRNA without affecting the half-life.
The results showed that NFKB1 (show NFKB1 ELISA Kits) and NFKBIA single-nucleotide polymorphisms and gastric cancer are related and that the combined effects of polymorphisms in two genes and the NFKBIA gene monomer increased the risk of gastric cancer, and it was found that in different types of gastric cancer (the cardia and non-cardia cancer), susceptible polymorphism sites and combined effects are different.
Double phosphorylation-induced structural changes in the signal-receiving domain of IkappaBalpha in complex with NF-kappaB (show NFKB1 ELISA Kits) have been described.
Here, the authors report amide hydrogen/deuterium exchange data that reveal long-range allosteric changes in the NFkappaB (show NFKB1 ELISA Kits) (RelA (show NFkBP65 ELISA Kits)-p50 (show CD40 ELISA Kits)) heterodimer induced by DNA or IkappaBalpha binding.
Sam68 (show KHDRBS1 ELISA Kits) is essential for DNA damage-induced NF-kappaB (show NFKB1 ELISA Kits) activation and colon tumorigenesis.
Specifically, BCA2 serves as an E3 SUMO ligase in the SUMOylation of IkappaBalpha, which in turn enhances the sequestration of NF-kappaB (show NFKB1 ELISA Kits) components in the cytoplasm. Since HIV-1 utilizes NF-kappaB (show NFKB1 ELISA Kits) to promote proviral transcription, the BCA2-mediated inhibition of NF-kappaB (show NFKB1 ELISA Kits) significantly decreases the transcriptional activity of HIV-1.
This study found that NFKBIA mRNAs was significantly expressed in normal tissues compared with glioma specimens.
Findings indicate the prognostic value of NFKB inhibitor alpha (NFKBIA) in lower-grade gliomas (LGGs).
W346 effectively inhibited tumor necrosis factor (TNF-a (show TNF ELISA Kits))-induced NF-kappaB (show NFKB1 ELISA Kits) activation by suppressing IKK (show CHUK ELISA Kits) phosphorylation, inhibiting IkB (show NFKBIB ELISA Kits)-a degradation, and restraining the accumulation of NF-kappaB (show NFKB1 ELISA Kits) subunit p65 (show GORASP1 ELISA Kits) nuclear translocation. W346 also affected NF-kappaB (show NFKB1 ELISA Kits)-regulated downstream products involved in cycle arrest and apoptosis.
treating cells with SZC014 resulted in a decrease in phosphorylation of IkBa and NF-kappaB (show NFKB1 ELISA Kits)/p65 (show GORASP1 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits)/p65 (show GORASP1 ELISA Kits) nuclear translocation. The cytotoxic activities of seven OA derivatives were generally stronger than that of OA, among which, SZC014 possessed the most potent anticancer activity in SGC7901 cells and would be a promising chemotherapic agent for the treatment of gastric cancer
Network analysis identified NFKBIA as pathogenic gene in childhood asthma.
IkappaB-alpha protein was stabilized by COMMD1 (show COMMD1 ELISA Kits), which attenuated NF-kappaB (show NFKB1 ELISA Kits) signaling during Toll (show TLR4 ELISA Kits)-like receptor ligand and tumor necrosis factor alpha (show TNF ELISA Kits) treatment and enhanced HIV-1 latency in latently HIV-1-infected cells.
NFKBIA has a role as a marker of NF-kappaB (show NFKB1 ELISA Kits)/p65 (show SYT1 ELISA Kits) activation in the early embryo.
NF-kappaB (show NFKB1 ELISA Kits) has a role in increasing PDGF-B (show PDGFB ELISA Kits) transcription
AIP1 (show PDCD6IP ELISA Kits) is a novel transducer in TNF (show TNF ELISA Kits)-induced TRAF2 (show TRAF2 ELISA Kits)-dependent activation of ASK1 (show MAP3K5 ELISA Kits) that mediates a balance between JNK (show MAPK8 ELISA Kits) versus NF-kappaB (show NFKB1 ELISA Kits) signaling
GRK5 overexpression causes nuclear accumulation of IkappaB alpha, leading to the inhibition of NFkappaB transcriptional activity.
This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease.
NF-kappa-B inhibitor alpha
, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha
, nuclear factor of kappa light chain gene enhancer in B-cells inhibitor, alpha
, nuclear factor of kappa light polyp gene enhancer in B-cell 1
, major histocompatibility complex enhancer-binding protein MAD3
, nuclear factor of kappa light chain gene enhancer in B-cells
, I kappa B-alpha
, NF-kappaB inhibitor alpha
, REL-associated protein pp40
, Rel-associated pp40
, IkappaB alpha
, Inhibitor of nuclear factor of kappa light chain gene enhancer in B-cells alpha
, Inhibitor of nuclear factor of kappa light chain gene enhancer in B-cells, alpha