CD49b antibody (Azide Free)
- Known as:
- CD49b (anti-) (Azide Free)
- Catalog number:
- 10r-cd49cmsp
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CD49b antibody (Azide Free)
Ask about this productRelated genes to: CD49b antibody (Azide Free)
- Gene:
- ITGA2 NIH gene
- Name:
- integrin subunit alpha 2
- Previous symbol:
- CD49B
- Synonyms:
- CD49b
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2019-04-23
Related products to: CD49b antibody (Azide Free)
Related articles to: CD49b antibody (Azide Free)
- Compared with transplanted tumors, autochthonous tumors are difficult to cure using experimental radiation therapy in mice. Here we analyzed differences in immune-related gene expression profiles between mouse fibrosarcomas subcutaneously induced by 3-methylcholanthrene (3MC) and their corresponding transplanted tumors. The immune genes examined were Pd1, Pdl1, Pdl2, Cd3d, Cd8a, Cd8b, Ifnγ, Itga2, Gzmb, and Foxp3. Among 12 tumors, one was non-transplantable and showed a benign phenotype with an abundance of DX5+ natural killer cells and CD8+ T cells together with increased IFNγ expression and mRNA levels of all immune genes except for Itga2. The other 11 transplantable tumors showed increased expression of Pd1, Pdl1, Pdl2, Cd3d, Cd8b, and Ifnγ following transplantation into syngeneic mice. These effects of transplantation highlight the relevance of immune gene expression status to the curability of tumors. - Source: PubMed
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Lourenço CatarinaConstâncio VeraTavares Nuno TiagoMonteiro-Reis SaraSilva-Santos RuiLobo JoãoCarvalho ÂngelaJerónimo Carmen - Pancreatic adenocarcinoma (PAAD) remains a highly lethal malignancy with limited therapeutic options, motivating the search for robust prognostic markers and tractable therapeutic targets. In this study, we applied an integrative bioinformatic pipeline combining cross-cohort differential expression analysis, high-confidence protein-protein interaction network reconstruction, and topological hub-gene prioritization. Hub candidates were then intersected with curated target repertoires of multi-target chemicals (notably quercetin and sulforaphane [SFN]) to nominate pharmacologically accessible "elite" targets. Downstream in silico validation included comparative mRNA and protein expression profiling, correlations with immune infiltration metrics, survival prognostic assessments, and molecular docking to evaluate ligand-target complementarity. This multilayered approach consistently highlighted extracellular matrix remodeling, integrin-mediated adhesion, and pericellular proteolysis as central processes in PAAD biology and identified COL1A1, ITGA2, and PLAU as top-priority targets that combine high network centrality with overlap to phytochemical target spaces. These genes demonstrated tumor-enriched expression, adverse survival associations, and distinct immune-microenvironment correlations, suggesting a potential involvement in pro-tumorigenic remodeling processes. Molecular docking analyses suggested computationally feasible ligand-target binding hypotheses, with quercetin exhibiting comparatively stronger predicted affinities than SFN across all targets. - Source: PubMed
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