MAP3K14 & CHUK Protein Protein Interaction Antibody Pair
- Known as:
- MAP3K14 & CHUK Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0605
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAP3K14 & CHUK Protein Interaction Antibody Pair
Related genes to: MAP3K14 & CHUK Protein Protein Interaction Antibody Pair
- Gene:
- CHUK NIH gene
- Name:
- component of inhibitor of nuclear factor kappa B kinase complex
- Previous symbol:
- TCF16
- Synonyms:
- IKK1, IKK-alpha, IkBKA, NFKBIKA, IKKA
- Chromosome:
- 10q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-15
- Date modifiied:
- 2019-02-21
- Gene:
- MAP3K14 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 14
- Previous symbol:
- -
- Synonyms:
- NIK, HSNIK, FTDCR1B, HS
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-11
- Date modifiied:
- 2019-04-23
Related products to: MAP3K14 & CHUK Protein Protein Interaction Antibody Pair
Related articles to: MAP3K14 & CHUK Protein Protein Interaction Antibody Pair
- Influenza A virus (IAV) is an important zoonotic pathogen responsible for substantial respiratory morbidity and mortality. Elucidating the mechanisms by which IAV evades host innate immunity is critical for developing novel antiviral strategies. Although the IAV non-structural protein 2 (NS2) is well-characterized for the export of viral ribonucleoproteins (vRNPs) from the host cell nucleus, the function of NS2 in evading host innate immunity, especially the NFKB/NF-κB (nuclear factor kappa B) signaling pathway, remains poorly understood. The present study uncovered that NS2 is a novel viral inhibitor of the NFKB pathway. Mechanistically, NS2 interacted with and mediated the degradation of the NFKB essential modulator (IKBKG/NEMO), thereby suppressing downstream signal transduction. The macroautophagy/autophagy receptor OPTN (optineurin) was exploited by NS2 to mediate the selective autophagic degradation. Furthermore, the K72 residue was critical for the NS2-mediated degradation of IKBKG/NEMO, as the K72R substitution in NS2 disrupted the IKBKG/NEMO-NS2 interaction and abrogated the autophagic degradation. In addition, NS2 mutant virus displayed less viral load and milder pathogenicity in mice. In conclusion, these findings highlighted the novel biological function of IAV NS2 in exploiting selective autophagy to evade host defenses, and offered a potential target for controlling IAV infections.: 3-MA: 3-methyladenine; AIV: avian influenza virus; ATG7: autophagy related 7; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CHX: cycloheximide; co-IP: co-immunoprecipitation; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; DAPI: 4', 6-diamidino-2-phenylindole, dihydrochloride; dsRNA: double-stranded RNA; dpi: days post-infection; EID: 50% egg infective dose; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; hpi: hours post-infection; IAV: influenza A virus; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IFNG: interferon gamma; IKBKG/NEMO: inhibitor of nuclear factor kappa B kinase subunit gamma; IKK: IκB kinase; IP: immunoprecipitation; IRF3: interferon regulatory factor 3; IRF7: interferon regulatory factor 7; LAMP1: lysosome associated membrane protein 1; LIR: LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K14/NIK: mitogen-activated protein kinase kinase kinase 14; MAVS: mitochondrial antiviral signaling protein; MLD: 50% mouse lethal dose; MOI: multiplicity of infection; MRV/Sendai virus: murine respirovirus; NBR1: NBR1 autophagy cargo receptor; NEP: nuclear export protein; NFKB/NF-κB: nuclear factor kappa B; NFKB2/p100: nuclear factor kappa B subunit 2; NFKBIA/IκBα: NFK inhibitor alpha; NP: nucleoprotein; NS1: non-structural protein 1; OPTN: optineurin; PB1: basic polymerase 1; PBS: phosphate-buffered saline; poly(I:C): polyriboinosinic polyribocytidylic acid; PRRs: pattern recognition receptors; RELA/p65: RELA proto-oncogene, NF-kB subunit; RELB: RELB proto-oncogene, NF-kB subunit; RIGI: RNA sensor RIG-I; RIGI-IN: RIGI-CARD; RLR: RIGI-like-receptor; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; SIM: SUMO-interacting motif; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TBK1: TANK binding kinase 1; TNF: tumor necrosis factor; TRAF6: TNF receptor associated factor 6; TOLLIP: toll interacting protein; Vec: empty vector; vRNP: viral ribonucleoprotein. - Source: PubMed
Publication date: 2026/05/27
Zhang BoHan LebinCui ChenyingHuang JiaxinZhu QiyunLei CaoqiXu Shuai - : Chronic lymphocytic leukemia (CLL) is the most common adult leukemia in Western countries and it can progress to Richter's syndrome (RS), a more aggressive condition. The NF-κB pathway is pivotal in CLL pathogenesis, driven mainly by B-cell receptor (BCR) signaling. However, recent evidence indicates that BCR signaling is reduced in RS, raising questions about whether and how NF-κB activity is maintained in RS. This study aims to elucidate the triggers and dynamics of NF-κB activation and the progression from CLL to RS. : Integrated single-cell RNA sequencing data from peripheral blood samples of four CLL-RS patients were analyzed. NF-κB pathway activity and gene expression profiles were assessed to determine changes in NF-κB components and their targets. Tumor microenvironment composition and cell-cell communication patterns were inferred to explore NF-κB regulatory mechanisms. : RS samples showed increased proportions of malignant cells expressing NF-κB components, including , , , , , , and , with significantly higher expression levels than in CLL. Enhanced NF-κB pathway activity in RS cells was associated with targets involved in immune modulation. The tumor microenvironment in RS displayed significant compositional changes, and signaling inference revealed enhanced cell-cell communication via BAFF and APRIL pathways, involving interactions with receptors such as BAFF-R and TACI on RS cells. : The findings from this study reveal an active state of NF-κB in RS and suggest that this state plays a critical role in the evolution of CLL to RS, which is modulated by alternative signaling pathways and the influence of the tumor microenvironment. - Source: PubMed
Publication date: 2024/11/05
Rohan PauloBinato RenataAbdelhay Eliana - Necrotic enteritis (NE) is a devastating disease that has seen a resurgence of cases following the removal of antibiotics from feed resulting in financial loss and significant animal health concerns across the poultry industry. The objective was to evaluate the efficacy of a microencapsulated blend of organic (25% citric and 16.7% sorbic) acids and botanicals (1.7% thymol and 1% vanillin [AviPlusP]) to reduce clinical NE and determine the signaling pathways associated with any changes. Day-of-hatch by-product broiler breeder chicks were randomly assigned to a control (0) or supplemented (500 g/MT) diet (n = 23-26) and evaluated in a NE challenge model (n = 3). Birds were administered 2X cocci vaccine on d 14 and challenged with a cocktail of Clostridium perfringens strains (10) on d 17 to 19. On d 20 to 21 birds were weighed, euthanized, and scored for NE lesions. Jejunal tissue was collected for kinome analysis using an immuno-metabolism peptide array (n = 5; 15/treatment) to compare tissue from supplement-fed birds to controls. Mortality and weight were analyzed using Student's t test and lesion scores analyzed using F-test two-sample for variances (P < 0.05). The kinome data was analyzed using PIIKA2 peptide array analysis software and fold-change between control and treated groups determined. Mortality in the supplemented group was 47.4% and 70.7% in controls (P = 0.004). Lesions scores were lower (P = 0.006) in supplemented birds (2.47) compared to controls (3.3). Supplement-fed birds tended (P = 0.19) to be heavier (848.6 g) than controls (796.2 g). Kinome analysis showed T cell receptor, TNF and NF-kB signaling pathways contributed to the improvements seen in the supplement-fed birds. The following peptides were significant (P < 0.05) in all 3 pathways: CHUK, MAP3K14, MAP3K7, and NFKB1 indicating their importance. Additionally, there were changes to IL6, IL10, and IFN- γ mRNA expression in tissue between control- and supplement-fed chickens. In conclusion, the addition of a microencapsulated blend of organic acids and botanicals to a broiler diet reduced the clinical signs of NE that was mediated by specific immune-related pathways. - Source: PubMed
Publication date: 2022/01/30
Swaggerty Christina LByrd J AllenArsenault Ryan JPerry FamattaJohnson Casey NGenovese Kenneth JHe HaiqiKogut Michael HPiva AndreaGrilli Ester - Melanoma remains incurable skin cancer, and targeting heat shock protein 90 (HSP90) is a promising therapeutic approach. In this study, we investigate the effect of 17-aminogeldanamycin, a potent HSP90 inhibitor, on nuclear factor-kappa B (NF-κB) activity in BRAF and NRAS patient-derived melanoma cell lines. We performed time-lapse microscopy and flow cytometry to monitor changes in cell confluence and viability. The NF-κB activity was determined by immunodetection of phospho-p65 and assessment of expression of NF-κB-dependent genes by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and enzyme-linked immunosorbent assay (ELISA). Constitutive activity of p65/NF-κB was evident in all melanoma cell lines. Differences in its level might be associated with genetic alterations in , , , , , and , while differences in transcript levels of NF-κB-inducible genes revealed by PCR array might result from the contribution of other regulatory mechanisms. 17-Aminogeldanamycin markedly diminished the level of phospho-p65, but the total p65 protein level was unaltered, indicating that 17-aminogeldanamycin inhibited activation of p65/NF-κB. This conclusion was supported by significantly reduced expression of selected NF-κB-dependent genes: cyclin D1 (, C-X-C motif chemokine ligand 8 (), and vascular endothelial growth factor (), as shown at transcript and protein levels, as well as secretion of IL-8 and VEGF. Our study indicates that 17-aminogeldanamycin can be used for efficient inhibition of NF-κB activity and the simultaneous diminution of IL-8 and VEGF levels in the extracellular milieu of melanoma. - Source: PubMed
Publication date: 2020/05/26
Hartman Mariusz LRogut MagdalenaMielczarek-Lewandowska AleksandraWozniak MichalCzyz Malgorzata - NF-κB-inducing kinase (NIK; also known as MAP3K14) is a central regulator of non-canonical NF-κB signaling in response to stimulation of TNF receptor superfamily members, such as the lymphotoxin-β receptor (LTβR), and is implicated in pathological angiogenesis associated with chronic inflammation and cancer. Here, we identify a previously unrecognized role of the LTβR-NIK axis during inflammatory activation of human endothelial cells (ECs). Engagement of LTβR-triggered canonical and non-canonical NF-κB signaling promoted expression of inflammatory mediators and adhesion molecules, and increased immune cell adhesion to ECs. Sustained LTβR-induced inflammatory activation of ECs was NIK dependent, but independent of p100, indicating that the non-canonical arm of NF-κB is not involved. Instead, prolonged activation of canonical NF-κB signaling, through the interaction of NIK with IκB kinase α and β (also known as CHUK and IKBKB, respectively), was required for the inflammatory response. Endothelial inflammatory activation induced by synovial fluid from rheumatoid arthritis patients was significantly reduced by NIK knockdown, suggesting that NIK-mediated alternative activation of canonical NF-κB signaling is a key driver of pathological inflammatory activation of ECs. Targeting NIK could thus provide a novel approach for treating chronic inflammatory diseases. - Source: PubMed
Publication date: 2019/04/03
Kucharzewska PaulinaMaracle Chrissta XJeucken Kim C Mvan Hamburg Jan PietIsraelsson ElisabethFurber MarkTas Sander WOlsson Henric K