IL21 predesign siRNA
- Known as:
- IL21 predesign small interfearing RNA
- Catalog number:
- RI12705
- Product Quantity:
- 5 OD
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- IL21 predesign siRNA
Related genes to: IL21 predesign siRNA
- Gene:
- IL21 NIH gene
- Name:
- interleukin 21
- Previous symbol:
- -
- Synonyms:
- Za11, IL-21
- Chromosome:
- 4q27
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2019-04-23
Related products to: IL21 predesign siRNA
Related articles to: IL21 predesign siRNA
- CD4 effector T helper 1 (T1) cells drive inflammatory bowel disease (IBD). Here, we investigated how integrated signaling, metabolic, and epigenetic programs sustain their pathogenic persistence. We found that enforcing mitochondrial pyruvate metabolism with methyl pyruvate (MePyr) suppressed T1 cell effector function and induced the acquisition of a regulatory-like phenotype. MePyr suppressed the activity of glycogen synthase kinase 3β (GSK3β), promoting a metabolic shift from glycolysis toward oxidative phosphorylation (OXPHOS) and limiting the accumulation of intracellular acetyl-CoA. This metabolic reprogramming decreased histone H3 acetylation at genes encoding inflammatory cytokines, thereby decreasing T1 cell-associated gene expression. Restoration of inflammatory cytokine production by acetate supplementation or histone deacetylase inhibition established acetyl-CoA-dependent histone acetylation as a mechanistic link between metabolic flux and effector function. Conversely, the cytokine interleukin-21 enhanced T1 cell effector activity by promoting a GSK3β-dependent shift from OXPHOS to glycolysis. Single-cell transcriptomic analysis of Crohn's disease tissue revealed enrichment of glycolytic gene programs in nonregulatory CD4 T cells. Consistent with these findings, pharmacologic inhibition of GSK3β attenuated disease severity in a T cell-transfer mouse model of colitis. Together, these findings identify a GSK3β-dependent metabolic-epigenetic axis that sustains T1 cell pathogenicity and highlight GSK3β as a potential therapeutic target for IBD. - Source: PubMed
Publication date: 2026/10/06
Mishra Shravan KAbdelrahman Leena MLee Hyun Se KimValenzuela-Pérez LucíaManna Dina FAbram Tanner JAli Lama MohamedDavidson Heidi MHassan Omar MFaubion William AHirsova PetraBamidele Adebowale O - Cytokines can elicit potent antitumor immunity, but their clinical use is often limited by systemic immune activation and dose-limiting toxicity. Protease-responsive masking offers a way to improve selectivity by linking cytokine activity to disease-associated protease cleavage, but current approaches have faced several challenges. Here we describe a de novo protein design strategy for generating protease-activatable cytokine prodrugs that overcomes these challenges. We use this strategy to design and characterize cytokine prodrugs and well-behaved AND-gated split systems that require both target-dependent colocalization and proteolytic unmasking to generate active cytokines. In challenging syngeneic tumor models, our IL-21 prodrugs reduced treatment-associated toxicity while maintaining antitumor efficacy. - Source: PubMed
Publication date: 2026/09/22
Shin HojeongTello Julissa GKim Chan JohngChun Jung-HoPeprah FrankParent Brendan DAtajanova TavusMahmud Robiah Arefin IbnQiang LiAguirre Andrew JDougan Stephanie KDougan MichaelBaker David - Arsenic (As) is an extremely hazardous trace metalloid frequently found in water bodies, where it poses substantial threats to all living organisms, including fish. Its removal has therefore become a significant global challenge. - Source: PubMed
Publication date: 2026/09/30
Habotta Ola ARawan Ahmad FAbdelmoneim DoaaAdly Mina SAteya AhmedIbrahim ImanAmer ShroukAzab Rasha EHabak SaraMorsi RehabHetta Helal FIbrahim Samah FShukry MustafaEl-Nemr AhmedRaia AmrAbdeen Ahmed - This study aimed to characterize the distributions of Th17 and regulatory T (Treg) cells and the associated interleukin-21 (IL-21) signaling in patients with human immunodeficiency virus (HIV) and Mycobacterium tuberculosis (Mtb) coinfection. - Source: PubMed
Publication date: 2026/09/25
Chen GaoChen Shikai - Hepatocellular carcinoma (HCC) remains a significant global health threat characterized by aggressive progression and high mortality rates. Despite therapeutic advancements, survival for advanced stages is unacceptably low, necessitating innovative approaches like Natural Killer (NK) cell-based immunotherapy. NK cells are crucial innate immune components providing rapid tumor cytotoxicity without prior sensitization. However, the HCC tumor microenvironment (TME) presents a formidable barrier, inducing NK cell dysfunction through immunosuppressive cytokines like TGF-[Formula: see text], chronic hypoxia, and metabolic exhaustion driven by lipid accumulation. This literature review consolidates and integrates findings regarding current NK cell-based strategies in HCC, with particular emphasis on mechanisms of NK cell dysfunction within the TME and therapeutic approaches designed to restore their antitumor activity. Emerging therapeutic strategies involve cytokine-supported approaches, including the adoptive transfer of autologous or allogeneic NK cells expanded ex vivo using stimuli such as IL-15 and IL-21. In parallel, advances in genetic engineering have enabled the development of modified NK cells, including chimeric antigen receptor (CAR)-NK platforms targeting HCC-associated antigens such as glypican-3 (GPC3) and CD147 and bispecific and trispecific killer cell engagers (BiKEs and TriKEs). This review underscores the translational potential of NK cell-based therapies by highlighting unresolved knowledge gaps in the complex interplay between NK cells and the TME. These developments provide a foundation for optimizing NK cell immunotherapy and improving prognostic outcomes for patients with HCC. - Source: PubMed
Publication date: 2026/09/24
Widowati WahyuWargasetia Teresa LilianaSadri BaharehNainggolan Ita MargarethaAzis RizalRifana Safira DindaRismani ElhamVosough Massoud