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janus kinase 3 jak3 inhibitors  (MedChemExpress)


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    Structured Review

    MedChemExpress janus kinase 3 jak3 inhibitors
    Janus Kinase 3 Jak3 Inhibitors, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/janus kinase 3 jak3 inhibitors/product/MedChemExpress
    Average 91 stars, based on 7 article reviews
    janus kinase 3 jak3 inhibitors - by Bioz Stars, 2026-02
    91/100 stars

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    PIK3CD was positively regulated by <t>JAK3/STAT5</t> signaling. (A) Heat maps of top 50 genes positively correlated with PIK3CD expression in STAD cohort of TCGA by LinkedOmics online tools. STAD, stomach adenocarcinoma. (B) The expression of PIK3CD was positively associated with JAK3, STAT5A and STAT5B in TCGA by Pearson correlation analysis. (C) The potential binding site of STAT5 in the promoter of PIK3CD. The four red nucleotides were mutated from wild‐type binding sites for construction of dual luciferase reporter plasmid (MUT). (D) The relative activities of PIK3CD promoter were examined by dual luciferase reporter kit in GC cells with STAT5A overexpression. * p < 0.05, ** p < 0.01. (E) The protein expression was tested by western blotting upon STAT5A overexpression in MGC803 and AGS cells. (F) Cells were treated with human IL‐2, JANEX‐1 and STAT5 inhibitor (SH‐4‐54) as indicated concentrations. PIK3CD expression was examined by western blot analysis. JANEX‐1, JAK3 inhibitor.
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    PIK3CD was positively regulated by <t>JAK3/STAT5</t> signaling. (A) Heat maps of top 50 genes positively correlated with PIK3CD expression in STAD cohort of TCGA by LinkedOmics online tools. STAD, stomach adenocarcinoma. (B) The expression of PIK3CD was positively associated with JAK3, STAT5A and STAT5B in TCGA by Pearson correlation analysis. (C) The potential binding site of STAT5 in the promoter of PIK3CD. The four red nucleotides were mutated from wild‐type binding sites for construction of dual luciferase reporter plasmid (MUT). (D) The relative activities of PIK3CD promoter were examined by dual luciferase reporter kit in GC cells with STAT5A overexpression. * p < 0.05, ** p < 0.01. (E) The protein expression was tested by western blotting upon STAT5A overexpression in MGC803 and AGS cells. (F) Cells were treated with human IL‐2, JANEX‐1 and STAT5 inhibitor (SH‐4‐54) as indicated concentrations. PIK3CD expression was examined by western blot analysis. JANEX‐1, JAK3 inhibitor.
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    PIK3CD was positively regulated by <t>JAK3/STAT5</t> signaling. (A) Heat maps of top 50 genes positively correlated with PIK3CD expression in STAD cohort of TCGA by LinkedOmics online tools. STAD, stomach adenocarcinoma. (B) The expression of PIK3CD was positively associated with JAK3, STAT5A and STAT5B in TCGA by Pearson correlation analysis. (C) The potential binding site of STAT5 in the promoter of PIK3CD. The four red nucleotides were mutated from wild‐type binding sites for construction of dual luciferase reporter plasmid (MUT). (D) The relative activities of PIK3CD promoter were examined by dual luciferase reporter kit in GC cells with STAT5A overexpression. * p < 0.05, ** p < 0.01. (E) The protein expression was tested by western blotting upon STAT5A overexpression in MGC803 and AGS cells. (F) Cells were treated with human IL‐2, JANEX‐1 and STAT5 inhibitor (SH‐4‐54) as indicated concentrations. PIK3CD expression was examined by western blot analysis. JANEX‐1, JAK3 inhibitor.
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    Cayman Chemical jak3 inhibitor (janex-1
    SVGA astrocytes were pretreated with specific 10 µM JAK2 (AG490) (A,B) or 20 µM <t>JAK3</t> <t>(Janex-1)</t> inhibitors (C, D) or 25 µM JAK1 (E, F) or siRNA to knock down JAK2 and JAK3 (G,H) prior to the transfection with HIV-1 Tat plasmid. The level of CCL5 induction was measured at mRNA (A, C, E, G) and protein levels (B, D, F, H). The values represented for mRNA are expressed relative to the mock-transfected controls. Each experiment was performed in triplicate and each bar in the figure represents the mean ± SE of at least three individual experiments. One-way ANOVA was used to perform the statistical analysis and ** denotes p-value ≤0.01.
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    PIK3CD was positively regulated by JAK3/STAT5 signaling. (A) Heat maps of top 50 genes positively correlated with PIK3CD expression in STAD cohort of TCGA by LinkedOmics online tools. STAD, stomach adenocarcinoma. (B) The expression of PIK3CD was positively associated with JAK3, STAT5A and STAT5B in TCGA by Pearson correlation analysis. (C) The potential binding site of STAT5 in the promoter of PIK3CD. The four red nucleotides were mutated from wild‐type binding sites for construction of dual luciferase reporter plasmid (MUT). (D) The relative activities of PIK3CD promoter were examined by dual luciferase reporter kit in GC cells with STAT5A overexpression. * p < 0.05, ** p < 0.01. (E) The protein expression was tested by western blotting upon STAT5A overexpression in MGC803 and AGS cells. (F) Cells were treated with human IL‐2, JANEX‐1 and STAT5 inhibitor (SH‐4‐54) as indicated concentrations. PIK3CD expression was examined by western blot analysis. JANEX‐1, JAK3 inhibitor.

    Journal: Journal of Cell Communication and Signaling

    Article Title: JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

    doi: 10.1002/ccs3.12017

    Figure Lengend Snippet: PIK3CD was positively regulated by JAK3/STAT5 signaling. (A) Heat maps of top 50 genes positively correlated with PIK3CD expression in STAD cohort of TCGA by LinkedOmics online tools. STAD, stomach adenocarcinoma. (B) The expression of PIK3CD was positively associated with JAK3, STAT5A and STAT5B in TCGA by Pearson correlation analysis. (C) The potential binding site of STAT5 in the promoter of PIK3CD. The four red nucleotides were mutated from wild‐type binding sites for construction of dual luciferase reporter plasmid (MUT). (D) The relative activities of PIK3CD promoter were examined by dual luciferase reporter kit in GC cells with STAT5A overexpression. * p < 0.05, ** p < 0.01. (E) The protein expression was tested by western blotting upon STAT5A overexpression in MGC803 and AGS cells. (F) Cells were treated with human IL‐2, JANEX‐1 and STAT5 inhibitor (SH‐4‐54) as indicated concentrations. PIK3CD expression was examined by western blot analysis. JANEX‐1, JAK3 inhibitor.

    Article Snippet: PI3Kδ inhibitors, including Acalisib (#S5818), compound 7n (#S8693) and Idelalisib (#S2226), STAT3/STAT5 inhibitor SH‐4‐54 (#S7337), STAT3 inhibitor BP‐1‐102 (#S7769), and JAK3 inhibitor JANEX‐1 (#S5903) were purchased from Selleck Chemicals.

    Techniques: Expressing, Binding Assay, Luciferase, Plasmid Preparation, Over Expression, Western Blot

    The correlations between PI3K subunits, JAK3 and immune cell infiltration in GC. (A) PIK3CA and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (B) PIK3CB and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (C) PIK3CD and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (D) JAK3 and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (E) Pro‐inflammatory lymphocyte and LPS had significant impact on PIK3CD expression, but not for PIK3CA and PIK3CB. (F) The effect of overexpression of STAT5 on protein expression of PIK3CA, PIK3CB and PIK3CD. (G) The effect of JANEX‐1 and STAT5 inhibitor (SH‐45‐4) on protein expression of PIK3CA, PIK3CB and PIK3CD. GC, gastric cancer; JANEX‐1, JAK3 inhibitor; LPS, lipopolysaccharide.

    Journal: Journal of Cell Communication and Signaling

    Article Title: JAK3/STAT5 signaling‐triggered upregulation of PIK3CD contributes to gastric carcinoma development

    doi: 10.1002/ccs3.12017

    Figure Lengend Snippet: The correlations between PI3K subunits, JAK3 and immune cell infiltration in GC. (A) PIK3CA and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (B) PIK3CB and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (C) PIK3CD and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (D) JAK3 and immune cell infiltration. The correlation analysis between each gene with immune cell infiltration was performed via TIMER algorithm. (E) Pro‐inflammatory lymphocyte and LPS had significant impact on PIK3CD expression, but not for PIK3CA and PIK3CB. (F) The effect of overexpression of STAT5 on protein expression of PIK3CA, PIK3CB and PIK3CD. (G) The effect of JANEX‐1 and STAT5 inhibitor (SH‐45‐4) on protein expression of PIK3CA, PIK3CB and PIK3CD. GC, gastric cancer; JANEX‐1, JAK3 inhibitor; LPS, lipopolysaccharide.

    Article Snippet: PI3Kδ inhibitors, including Acalisib (#S5818), compound 7n (#S8693) and Idelalisib (#S2226), STAT3/STAT5 inhibitor SH‐4‐54 (#S7337), STAT3 inhibitor BP‐1‐102 (#S7769), and JAK3 inhibitor JANEX‐1 (#S5903) were purchased from Selleck Chemicals.

    Techniques: Expressing, Over Expression

    SVGA astrocytes were pretreated with specific 10 µM JAK2 (AG490) (A,B) or 20 µM JAK3 (Janex-1) inhibitors (C, D) or 25 µM JAK1 (E, F) or siRNA to knock down JAK2 and JAK3 (G,H) prior to the transfection with HIV-1 Tat plasmid. The level of CCL5 induction was measured at mRNA (A, C, E, G) and protein levels (B, D, F, H). The values represented for mRNA are expressed relative to the mock-transfected controls. Each experiment was performed in triplicate and each bar in the figure represents the mean ± SE of at least three individual experiments. One-way ANOVA was used to perform the statistical analysis and ** denotes p-value ≤0.01.

    Journal: PLoS ONE

    Article Title: HIV-1 Tat-Mediated Induction of CCL5 in Astrocytes Involves NF-κB, AP-1, C/EBPα and C/EBPγ Transcription Factors and JAK, PI3K/Akt and p38 MAPK Signaling Pathways

    doi: 10.1371/journal.pone.0078855

    Figure Lengend Snippet: SVGA astrocytes were pretreated with specific 10 µM JAK2 (AG490) (A,B) or 20 µM JAK3 (Janex-1) inhibitors (C, D) or 25 µM JAK1 (E, F) or siRNA to knock down JAK2 and JAK3 (G,H) prior to the transfection with HIV-1 Tat plasmid. The level of CCL5 induction was measured at mRNA (A, C, E, G) and protein levels (B, D, F, H). The values represented for mRNA are expressed relative to the mock-transfected controls. Each experiment was performed in triplicate and each bar in the figure represents the mean ± SE of at least three individual experiments. One-way ANOVA was used to perform the statistical analysis and ** denotes p-value ≤0.01.

    Article Snippet: NF-κB inhibitor (SC514), p38 inhibitor (SB203580), JNK inhibitor (SP600125), PI3K inhibitor (LY294002), JAK1 inhibitor (Picetannol), JAK2 inhibitor (AG490) and JAK3 inhibitor (Janex-1) were obtained from Cayman chemical (Ann Arbor, MI, USA).

    Techniques: Transfection, Plasmid Preparation