Anti-Mouse CD127 FITC 500 ug
- Known as:
- Antibody toMouse CD127 fluorecein 500 ug
- Catalog number:
- 11-1271-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD127 FITC 500
Related genes to: Anti-Mouse CD127 FITC 500 ug
- Gene:
- IL7R NIH gene
- Name:
- interleukin 7 receptor
- Previous symbol:
- -
- Synonyms:
- CD127, IL7RA
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD127 FITC 500 ug
Related articles to: Anti-Mouse CD127 FITC 500 ug
- Intrauterine growth restriction (IUGR) is a leading cause of maternal and neonatal morbidity and mortality, particularly in low- and middle-income countries. Placental transcriptomics data were analysed to mapped dysregulated pathways via STRING-based PPI networks, identifying hubs and validating pesticide targets by molecular simulations. Rank-based prioritization identified IL7R, LCK and ZAP70 as top hub proteins driving placental dysfunction with cypermethrin exhibiting the lowest binding affinities across them (docking scores: -7.7, -8.7, -9.3 kcal/mol, respectively). Molecular dynamics simulations confirmed the stability of these docked complexes, while toxicity profiling indicated genotoxic potential for permethrin and high aquatic toxicity for deltamethrin. Thus, we show the critical molecular mediators linking pyrethroid exposure to IUGR, suggesting further experimental validation to support maternal health risk assessment. - Source: PubMed
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Shukla Adarsh KumarTyagi Anuj KumarKumar Sandeep - Current single-cell and spatial transcriptomic studies on bladder cancer tissue samples are limited, highlighting the need for advanced molecular and single-cell approaches to enhance our understanding of these complexities and identify reliable prognostic indicators. - Source: PubMed
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Liu SanheWang YiqiPeng ShubinWang JianliCui DianshengDeng KangliHuang LeiAn NengDuan LiqunWei Shaozhong - Antigen 85B (Ag85B), an immunodominant protein secreted by (Mtb), induces robust T-cell-mediated immunity in host cells. Previous studies have demonstrated that recombinant BCG strains overexpressing Ag85B (BCG85B) confer significant protection against tuberculosis in mouse models. This study hypothesized that enhanced protection by recombinant BCG85B results from modulation of host immune gene expression by the Ag85B antigen. To test this, RNA-seq analysis was performed on splenocytes from mice immunized with the wild-type BCG (BCG-WT) and BCG85B strains. Differentially expressed genes (DEGs) in the splenocytes of BCG85B-immunized mice indicated upregulation of immune-related KEGG pathways, including Th1/Th2 and Th17 differentiation, NF-kappa B signaling, and cytokine-cytokine receptor interactions, as well as Gene Ontology (GO) processes such as immune response activation, α-β T cell activation, T-cell production and differentiation, IL-15 mediated signaling, and cytokine-mediated signaling pathways and down regulation of metabolic and digestive processes. Additionally, transcription factor (TF) and protein-protein interaction (PPI) analyses confirmed upregulation of genes involved in T cell receptor signaling and immune activation (, , , , , , and ) in splenocytes from BCG85B-immunized mice. Collectively, these findings indicate that Ag85B overexpression enhances adaptive immune activation and reprograms cellular metabolic pathways, thereby increasing vaccine efficacy. - Source: PubMed
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Chauhan VivekKumar RakeshVeerapandian RajaRamos Enrique IJagannath ChinnaswamyGadad Shrikanth SDhandayuthapani Subramanian - Living cell therapies lack robust, reversible mechanisms for externally controlling therapeutic activity after administration, limiting their safety and clinical adaptability. Here we engineer a drug-gated cellular immunotherapy platform in which T cells function as programmable factories that secrete two inactive antibody modules whose extracellular assembly into a functional bispecific T cell engager (TCE) is controlled by a small-molecule input. Using a rapalog-inducible FKBP-FRB* heterodimerization switch, we design a split CD19 × CD3 engager architecture that remains inactive in the absence of drug and assembles on demand upon rapalog exposure. A 2A-peptide bicistronic construct enables coordinated expression and secretion of both modules, allowing precise drug-dependent control of TCE formation in situ. Drug administration quantitatively regulates T cell activation and cytotoxicity against CD19 targets in vitro, with stringent OFF-state behavior in the absence of rapalog. In xenograft models, systemic rapalog administration induces on-demand anti-tumor activity without evidence of treatment-related toxicity, demonstrating reversible pharmacological control of a locally secreted therapeutic interface. We further extend this strategy to an EGFR-targeting TCE, demonstrating the modularity and broad adaptability of the platform across distinct antigen specificities. This work introduces a generalizable engineering framework for externally programmable cell therapies, enabling tunable, safety-by-design control of T cell-based immunotherapies. - Source: PubMed
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