RIG1 _ RARRES3 (aa 124 to 136)
- Known as:
- RIG1 _ RARRES3 (aa 124 136)
- Catalog number:
- Y213904
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- RIG1 _ RARRES3 ( 124 136)
Related genes to: RIG1 _ RARRES3 (aa 124 to 136)
- Gene:
- ABRAXAS1 NIH gene
- Name:
- abraxas 1, BRCA1 A complex subunit
- Previous symbol:
- CCDC98, FAM175A
- Synonyms:
- FLJ13614, ABRA1, ABRAXAS
- Chromosome:
- 4q21.23
- Locus Type:
- gene with protein product
- Date approved:
- 2006-04-03
- Date modifiied:
- 2017-04-27
- Gene:
- BCORL1 NIH gene
- Name:
- BCL6 corepressor like 1
- Previous symbol:
- CXorf10
- Synonyms:
- FLJ11362
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-27
- Date modifiied:
- 2019-04-23
- Gene:
- BIRC8 NIH gene
- Name:
- baculoviral IAP repeat containing 8
- Previous symbol:
- -
- Synonyms:
- ILP-2, hILP2, RNF136
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-23
- Date modifiied:
- 2019-04-04
- Gene:
- CAAP1 NIH gene
- Name:
- caspase activity and apoptosis inhibitor 1
- Previous symbol:
- C9orf82
- Synonyms:
- FLJ13657, CAAP
- Chromosome:
- 9p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-29
- Date modifiied:
- 2014-11-19
- Gene:
- CCDC121 NIH gene
- Name:
- coiled-coil domain containing 121
- Previous symbol:
- -
- Synonyms:
- FLJ43364, FLJ13646
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-26
- Date modifiied:
- 2016-10-05
Related products to: RIG1 _ RARRES3 (aa 124 to 136)
(1R,3S)-Camphoric Acid CAS: 124-83-4 Formula: C10H16O4(E,E)-Piperic Acid C12H10O4 CAS: 136-72-1(E,E)-Piperic Acid CAS: 136-72-1 Formula: C12H10O4(Leu116)-Prepro-Neuromedin U (104-136) (human)
Prepro-NMU (104-136) (human), (Leu116)-Prepro-NMU (104-136) (human) 98% C177H276N46O45 CAS:([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human)([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human)([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human), CE-marked, Liquid([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human), CE-marked, Liquid([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human), CE-marked, Liquid([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human), CE-marked, Lyophilized([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human), CE-marked, Lyophilized([125I]-Tyr)-Prepro-Neuromedin U (104-136) (human)CE-markedLiquid([125I]-Tyr)-Prepro-NeuromedinU (104-136) (human), CE-marked, Lyophilized([125I]-Tyr)-Prepro-NeuromedinU (104-136) (human)CE-markedLyophilized0.5-10ul P-2/P-10 Pipet Tip Racked Related articles to: RIG1 _ RARRES3 (aa 124 to 136)
- Some patients with colon cancer eventually develop metastasis during treatment, and the 5‑year survival rate of patients with metastatic colon cancer remains relatively low, which is most likely due to the ineffectiveness of the current standard treatment. Systemic treatment for patients with colon cancer has expanded from chemotherapy to targeted therapy and immunotherapy. Immunotherapy holds promise in the treatment of colon cancer. The present study revealed the role of innate immune receptor helicase DExD/H‑box helicase 58 (DDX58), which encodes retinoic acid‑inducible gene‑I (RIG‑I), in colon cancer. It was demonstrated that colon cancer patients with a low protein expression of DDX58/RIG‑I had a worse 5‑year survival rate of patients compared with patients with a high expression of DDX58/RIG‑I. The activation of DDX58/RIG‑I inhibited the proliferation, migration and invasion of colon cancer cells, as well as tumor growth in a nude mouse xenograft model of colon cancer. To investigate the mechanisms of action of DDX58/RIG‑I in colon cancer, the role of signal transducer and activator of transcription 3 (STAT3)/cystathionine‑γ‑lyase (CSE) signaling in the up‑ or downregulation of DDX58 was examined. The data demonstrated that DDX58 regulated the STAT3/CSE signaling pathway by interacting with STAT3 and consequently affecting the proliferation of tumor cells in colon cancer. In addition, the RIG‑I agonist, SB9200, induced proliferation, migration and invasion of human colon cancer. On the whole, the present study demonstrates that DDX58/RIG‑I affects the proliferation of tumor cells by regulating STAT3/CSE signaling in colon cancer. The findings presented herein suggest that DDX58/RIG‑I activation may be an effective treatment strategy, and DDX58/RIG‑I agonists may be potential therapeutic candidates for colon cancer. - Source: PubMed
Publication date: 2022/08/25
Deng YuyingFu HanHan XueLi YuxiZhao WeiZhao XueningYu ChunxueGuo WenqingLei KaijianWang Tianxiao - Vitamin C is well documented to have antiviral functions; however, there is limited information about its effect on airway epithelial cells-the first cells to encounter infections. Here, we examined the effect of vitamin C on human bronchial epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells, and observed that sodium-dependent vitamin C transporter 2 (SVCT2) was the primary vitamin C transporter. Transcriptomic analysis revealed that treating BEAS-2B cells with vitamin C led to a significant upregulation of several metabolic pathways and interferon-stimulated genes (ISGs) along with a downregulation of pathways involved in lung injury and inflammation. Remarkably, vitamin C also enhanced the expression of the viral-sensing receptors retinoic acid-inducible gene 1 (RIG-1) and melanoma differentiation-associated protein 5 (MDA-5), which was confirmed at the protein and functional levels. In addition, the lungs of l-gulono-γ-lactone oxidase knockout (-KO) mice also displayed a marked decrease in these genes compared to wild-type controls. Collectively, our findings indicate that vitamin C acts at multiple levels to exert its antiviral and protective functions in the lungs. - Source: PubMed
Publication date: 2021/08/03
Teafatiller TrevorAgrawal SudhanshuDe Robles GabrielaRahmatpanah FarahSubramanian Veedamali SAgrawal Anshu - Cytoplasmic double-stranded RNA is sensed by RIG-I-like receptors (RLRs), leading to induction of type I interferons (IFN-Is), proinflammatory cytokines, and apoptosis. Here, we elucidate signaling mechanisms that lead to cytokine secretion and cell death induction upon stimulation with the bona fide RIG-I ligand 5'-triphosphate RNA (3p-RNA) in tumor cells. We show that both outcomes are mediated by dsRNA-receptor families with RLR being essential for cytokine production and IFN-I-mediated priming of effector pathways but not for apoptosis. Affinity purification followed by mass spectrometry and subsequent functional analysis revealed that 3p-RNA bound and activated oligoadenylate synthetase 1 and RNase L. RNase L-deficient cells were profoundly impaired in their ability to undergo apoptosis. Mechanistically, the concerted action of translational arrest triggered by RNase L and up-regulation of NOXA was needed to deplete the antiapoptotic MCL-1 to cause intrinsic apoptosis. Thus, 3p-RNA-induced apoptosis is a two-step process consisting of RIG-I-dependent priming and an RNase L-dependent effector phase. - Source: PubMed
Boehmer Daniel F RFormisano Simonede Oliveira Mann Carina CMueller Stephan AKluge MichaelMetzger PhilippRohlfs MeinoHörth ChristineKocheise LorenzLichtenthaler Stefan FHopfner Karl-PeterEndres StefanRothenfusser SimonFriedel Caroline CDuewell PeterSchnurr MaxKoenig Lars M - Due to their immunomodulatory and regenerative properties, Mesenchymal stromal cells (MSC) have generated major interests in several clinical settings including transplantation and inflammatory diseases. MSC functions can be influenced by their tissue origin. Their microenvironment strongly affects their biology notably through TLR sensing. In this study, we show that MSC isolated from four different sources express another type of cytosolic pathogen recognition receptors known as retinoic acid inducible gene-I (RIG-I)-like receptors (RLR). RLR activation in MSC induces the production of Type I IFN (IFN-β) and Type III IFN (IFN-λ1). The highest producers are adipose tissue(AT)-MSC. We further show that Interferon production is induced through TBK1/IKK-ε signaling and IRF7 phosphorylation. Depending on MSC source, the knockdown of TLR3 and/or RIG-I decreases the MSC response to RLR ligand poly(I:C)/Lyovec. Among the different MSC types, AT-MSCs display the highest sensitivity to viral stimuli as shown by the alteration of their viability after prolonged stimulation. Our work indicates that this could be linked to an increase of pro-apoptotic Noxa expression. Finally, the expression of IDO1 and LIF upon RLR activation indicate the increase of MSC immunomodulatory potential, especially in AT-MSCs. Altogether, these data should be considered when designing MSC-based therapy in clinical settings where inflammation or infection are present. - Source: PubMed
Publication date: 2017/06/06
Raicevic GordanaNajar MehdiBusser HélèneCrompot EmerenceBron DominiqueToungouz MichelLagneaux Laurence - Multi-drug resistance (MDR), immune suppression and decreased apoptosis are important causes of therapy-failure in leukaemia. Short interfering RNAs (siRNAs) down-regulate gene transcription, have sequence-independent immune-stimulatory effects and synergize with other anti-cancer therapies in some experimental models. We designed a siRNA targeting MDR1 with 5'-triphosphate ends (3p-siRNA-MDR1). Treatment of leukaemia cells with 3p-siRNA-MDR1 down-regulated MDR1 expression, reduced-drug resistance and induced immune and pro-apoptotic effects in drug-resistant HL-60/Adr and K562/Adr human leukaemia cell lines. We show mechanisms-of-action of these effects involve alterations in the anti-viral cytosolic retinoic acid-inducible protein-I (RIG-I; encoded by RIG-I or DDX58) mediated type-I interferon signal induction, interferon-gamma-inducible protein 10 (IP-10; encoded by IP10 or CXCL10) secretion, major histocompatibility complex-I expression (MHC-I) and caspase-mediated cell apoptosis. 3p-siRNA-MDR1 transfection also enhanced the anti-leukaemia efficacy of doxorubicin. These data suggest a possible synergistic role for 3p-siRNA-MDR1 in anti-leukaemia therapy. - Source: PubMed
Publication date: 2017/03/21
Li DengzheGale Robert PeterLiu YanfengLei BaoxiaWang YuanDiao DongmeiZhang Mei