TNFC antibody Polyclonal Antibodies Primary antibodies
- Known as:
- TNFC (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100093
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TNFC antibody Polyclonal Antibodies Primary antibodies
Related genes to: TNFC antibody Polyclonal Antibodies Primary antibodies
- Gene:
- LTB NIH gene
- Name:
- lymphotoxin beta
- Previous symbol:
- TNFC
- Synonyms:
- p33, TNFSF3
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-22
- Date modifiied:
- 2016-10-05
- Gene:
- LTBR NIH gene
- Name:
- lymphotoxin beta receptor
- Previous symbol:
- D12S370
- Synonyms:
- TNFCR, TNFR-RP, TNFR2-RP, TNF-R-III, TNFRSF3
- Chromosome:
- 12p13
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2015-11-17
Related products to: TNFC antibody Polyclonal Antibodies Primary antibodies
Related articles to: TNFC antibody Polyclonal Antibodies Primary antibodies
- Cholangiocarcinoma (CCA) is an aggressive malignancy arising from the intrahepatic (iCCA) or extrahepatic (eCCA) bile ducts with poor prognosis and limited treatment options. Prior evidence highlighted a significant contribution of the non-canonical NF-κB signalling pathway in initiation and aggressiveness of different tumour types. Lymphotoxin-β (LTβ) stimulates the NF-κB-inducing kinase (NIK), resulting in the activation of the transcription factor RelB. However, the functional contribution of the non-canonical NF-κB signalling pathway via the LTβ/NIK/RelB axis in CCA carcinogenesis and progression has not been established. - Source: PubMed
Publication date: 2024/08/20
Xu KaiyuKessler AnnikaNichetti FedericoHoffmeister-Wittmann PaulaScherr Anna-LenaNader LuisaKelmendi EblinaSchmitt NathalieSchwab MaximilianGarcía-Beccaria MaríaSobol BenjaminNieto Osama AzzamIsele HannaGärtner UlrikeVaquero-Siguero NuriaVolk JuliaKorell FelixMock AndreasHeide DanijelaRamadori PierluigiLenoir BénédicteAlbrecht ThomasHüllein JenniferJäger DirkFröhling StefanSpringfeld ChristophJackstadt ReneHeikenwälder MathiasDill Michael TRoessler StephanieGoeppert BenjaminKöhler Bruno C - Acute cellular rejection (ACR) affects >80% of pediatric liver transplant recipients within 5 years, and late ACR is associated with graft failure. Traditional anti-rejection therapy for late ACR is ineffective and has remained unchanged for six decades. Although CD8+ T cells promote late ACR, little has been done to define their specificity and gene expression. Here, we used single-cell sequencing and immune repertoire profiling (10X Genomics) on 30 cryopreserved 16G liver biopsies from 14 patients (5 pre-transplant or with no ACR, 9 with ACR). We identified expanded intragraft CD8+ T cell clonotypes (CD8) and their gene expression profiles in response to anti-rejection treatment. Notably, we found that expanded CD8 clonotypes (CD8) bore markers of effector and CD56CD161 'NK-like' T cells, retaining their clonotype identity and phenotype in subsequent biopsies from the same patients despite histologic ACR resolution. CD8 clonotypes localized to portal infiltrates during active ACR, and persisted in the lobule after histologic ACR resolution. CellPhoneDB analysis revealed differential crosstalk between KC and CD8 during late ACR, with activation of the LTB-LTBR pathway and downregulation of TGFß signaling. Therefore, persistently-detected intragraft CD8 clones remain active despite ACR treatment and may contribute to long-term allograft fibrosis and failure of operational tolerance. - Source: PubMed
Publication date: 2024/02/29
Peters Anna LDePasquale Erica A KBegum GousiaRoskin Krishna MWoodle E SteveHildeman David A - Unregulated activity of interleukin (IL) 22 promotes intestinal tumorigenesis in mice. IL22 binds the antagonist IL22 subunit alpha 2 (IL22RA2, also called IL22BP). We studied whether alterations in IL22BP contribute to colorectal carcinogenesis in humans and mice. - Source: PubMed
Publication date: 2020/06/22
Kempski JanGiannou Anastasios DRiecken KristofferZhao LilanSteglich BabettLücke JöranGarcia-Perez LauraKarstens Karl-FrederickWöstemeier AnnaNawrocki MikolajPelczar PenelopeWitkowski MarioNilsson SvenKonczalla LeonieShiri Ahmad MustafaKempska JoannaWahib RamezBrockmann LeonieHuber PhilippGnirck Ann-ChristinTurner Jan-EricZazara Dimitra EArck Petra CStein AlexanderSimon RonaldDaubmann AnneMeiners JanPerez DanielStrowig TillKoni PandelakisKruglov Andrey ASauter GuidoIzbicki Jakob RGuse Andreas HRösch ThomasLohse Ansgar WFlavell Richard AGagliani NicolaHuber Samuel - Head and neck squamous cell carcinomas (HNSCC) promote inflammation in the tumor microenvironment through aberrant NF-κB activation, but the genomic alterations and pathway networks that modulate NF-κB signaling have not been fully dissected. Here, we analyzed genome and transcriptome alterations of 279 HNSCC specimens from The Cancer Genome Atlas (TCGA) cohort and identified 61 genes involved in NF-κB and inflammatory pathways. The top 30 altered genes were distributed across 96% of HNSCC samples, and their expression was often correlated with genomic copy-number alterations (CNA). Ten of the amplified genes were associated with human papilloma virus (HPV) status. We sequenced 15 HPV and 11 HPV human HNSCC cell lines, and three oral mucosa keratinocyte lines, and supervised clustering revealed that 28 of 61 genes exhibit altered expression patterns concordant with HNSCC tissues and distinct signatures related to their HPV status. RNAi screening using an NF-κB reporter line identified 16 genes that are induced by TNFα or Lymphotoxin-β (LTβ) and implicated in the classic and/or alternative NF-κB pathways. Knockdown of , or selected downstream signaling components established cross-talk between the classic and alternative NF-κB pathways. TNFα and LTβ induced differential gene expression involving the NF-κB, IFNγ, and STAT pathways, inflammatory cytokines, and metastasis-related genes. Improved survival was observed in HNSCC patients with elevated gene expression in T-cell activation, immune checkpoints, and IFNγ and STAT pathways. These gene signatures of NF-κB activation, which modulate inflammation and responses to the immune therapy, could serve as potential biomarkers in future clinical trials. - Source: PubMed
Publication date: 2019/10/17
Yang XinpingCheng HuiChen JianhongWang RuSaleh AnthonySi HanLee StevenGuven-Maiorov EmineKeskin OzlemGursoy AttilaNussinov RuthFang JugaoVan Waes CarterChen Zhong - Head and neck squamous cell carcinomas (HNSCC) preferentially spread to regional cervical tissues and lymph nodes. Here, we hypothesized that lymphotoxin-β (LTβ), receptor LTβR, and NF-κB-inducing kinase (NIK), promote the aberrant activation of alternative NF-κB2/RELB pathway and genes, that enhance migration and invasion of HNSCC. Genomic and expression alterations of the alternative NF-kB pathway were examined in 279 HNSCC tumors from The Cancer Genome Atlas (TCGA) and a panel of HNSCC lines. LTβR is amplified or overexpressed in HNSCC of the larynx or oral cavity, while LTβ, NIK, and RELB are overexpressed in cancers arising within lymphoid oropharyngeal and tonsillar sites. Similarly, subsets of HNSCC lines displayed overexpression of LTβR, NIK, and RELB proteins. Recombinant LTβ, and siRNA depletion of endogenous LTβR and NIK, modulated expression of LTβR, NIK, and nuclear translocation of NF-κB2(p52)/RELB as well as functional NF-κB promoter reporter activity. Treatment with a NIK inhibitor (1,3[2H,4H]-Iso-Quinoline Dione) reduced the protein expression of NIK and NF-κB2(p52)/RELB, and blocked LTβ induced nuclear translocation of RELB. NIK and RELB siRNA knockdown or NIK inhibitor slowed HNSCC migration or invation in vitro. LTβ-induces expression of migration and metastasis related genes, including hepatocyte growth/scatter factor receptor MET. Knockdown of NIK or MET similarly inhibited the migration of HNSCC cell lines. This may help explain why HNSCC preferentially migrate to local lymph nodes, where LTβ is expressed. Our findings show that LTβ/LTβR promotes activation of the alternative NIK-NF-κB2/RELB pathway to enhance MET-mediated cell migration in HNSCC, which could be potential therapeutic targets in HNSCC. - Source: PubMed
Publication date: 2018/11/28
Das RitaCoupar JamieClavijo Paul ESaleh AnthonyCheng Tsu-FanYang XinpingChen JianhongVan Waes CarterChen Zhong