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rapamycin  (Selleck Chemicals)


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    Structured Review

    Selleck Chemicals rapamycin
    Rapamycin, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1624 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rapamycin/Rapamycin/pmc13678578-1002-0-2
    Average 96 stars, based on 1624 article reviews
    rapamycin - by Bioz Stars, 2026-11
    96/100 stars

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    Related Articles

    Cell-Signaling:

    Article Title: Blockade of radio-adaptive EZH2-mTOR signaling restores glioblastoma radiosensitivity
    Article Snippet: The antibodies used in this study included: anti-EZH2 (Cell Signaling Technology, 5246); anti-H3K27me3 (Cell Signaling Technology, 6944); anti-USP1 (Cell Signaling Technology, 8033); anti-p70S6K pT389 (Cell Signaling Technology, 9234); anti-p70S6K pS371 (Cell Signaling Technology, 9208); anti-p70S6K (Servicebio, GB111181); anti-p4EBP1 (Cell Signaling Technology, 2855); anti-4EBP1 (Immunoway, YT0022); and anti-β-Actin (Sigma, A1978). .. The reagents included GSK343 (Selleck, S7164); EPZ-6438 (APExBIO, A8221); Rapamycin (Selleck, S1039); and CHX (Cell Signaling Technology, 2112). ..

    Staining:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Activity Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Lactate Dehydrogenase Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    other:


    Control:

    Article Title: The role of rapamycin in neural tube defects: insights from bioinformatics analysis and experimental validation.
    Article Snippet: Neural tube defects (NTDs) are the most severe congenital malformations of the central nervous system.. Fetal developmental homeostasis disruptions heighten NTDs risk through aberrant maternal-fetal signaling and periconceptional medication exposure.. Rapamycin, an inhibitor of the mTOR signaling pathway, is a widely used clinical drug whose effects on embryonic neural development remain unclear.

    shRNA:

    Article Title: ACTB promotes ESCC progression by regulating the AKT-mTOR signaling pathway through an m 6 A-dependent mechanism.
    Article Snippet: .. The following validated shRNA sequences were used: shACTB-1: 5′-GGCTTTCGTGTAAATTATA-3′ shACTB-2: 5′-GTAATCTTCGCCTTAATAA-3′ shYTHDC2-1: 5′-GCATATATGGTTTAATAAA-3′ shYTHDC2-2: 5′-GGCATATATGGTTTAATAA-3′ Ivermectin (MCE, Cat#HY-15310), Rapamycin (Selleck, Cat# S1039) was dissolved in DMSO and applied at 100 nM concentration in vitro or 5- 10mg/kg intraperitoneally in vivo. .. Antibodies against ACTB (Cat#20536–1-AP), YTHDC2 (Cat#27779–1-AP), AKT (Cat#10176-2-AP), mTOR (Cat#28273-1-AP), LaminB1 (Cat#12987-1AP), Alpha Tubulin (Cat#11224-1-AP) were purchased from Proteintech (Wuhan, China).

    Concentration Assay:

    Article Title: ACTB promotes ESCC progression by regulating the AKT-mTOR signaling pathway through an m 6 A-dependent mechanism.
    Article Snippet: .. The following validated shRNA sequences were used: shACTB-1: 5′-GGCTTTCGTGTAAATTATA-3′ shACTB-2: 5′-GTAATCTTCGCCTTAATAA-3′ shYTHDC2-1: 5′-GCATATATGGTTTAATAAA-3′ shYTHDC2-2: 5′-GGCATATATGGTTTAATAA-3′ Ivermectin (MCE, Cat#HY-15310), Rapamycin (Selleck, Cat# S1039) was dissolved in DMSO and applied at 100 nM concentration in vitro or 5- 10mg/kg intraperitoneally in vivo. .. Antibodies against ACTB (Cat#20536–1-AP), YTHDC2 (Cat#27779–1-AP), AKT (Cat#10176-2-AP), mTOR (Cat#28273-1-AP), LaminB1 (Cat#12987-1AP), Alpha Tubulin (Cat#11224-1-AP) were purchased from Proteintech (Wuhan, China).

    In Vitro:

    Article Title: ACTB promotes ESCC progression by regulating the AKT-mTOR signaling pathway through an m 6 A-dependent mechanism.
    Article Snippet: .. The following validated shRNA sequences were used: shACTB-1: 5′-GGCTTTCGTGTAAATTATA-3′ shACTB-2: 5′-GTAATCTTCGCCTTAATAA-3′ shYTHDC2-1: 5′-GCATATATGGTTTAATAAA-3′ shYTHDC2-2: 5′-GGCATATATGGTTTAATAA-3′ Ivermectin (MCE, Cat#HY-15310), Rapamycin (Selleck, Cat# S1039) was dissolved in DMSO and applied at 100 nM concentration in vitro or 5- 10mg/kg intraperitoneally in vivo. .. Antibodies against ACTB (Cat#20536–1-AP), YTHDC2 (Cat#27779–1-AP), AKT (Cat#10176-2-AP), mTOR (Cat#28273-1-AP), LaminB1 (Cat#12987-1AP), Alpha Tubulin (Cat#11224-1-AP) were purchased from Proteintech (Wuhan, China).

    In Vivo:

    Article Title: ACTB promotes ESCC progression by regulating the AKT-mTOR signaling pathway through an m 6 A-dependent mechanism.
    Article Snippet: .. The following validated shRNA sequences were used: shACTB-1: 5′-GGCTTTCGTGTAAATTATA-3′ shACTB-2: 5′-GTAATCTTCGCCTTAATAA-3′ shYTHDC2-1: 5′-GCATATATGGTTTAATAAA-3′ shYTHDC2-2: 5′-GGCATATATGGTTTAATAA-3′ Ivermectin (MCE, Cat#HY-15310), Rapamycin (Selleck, Cat# S1039) was dissolved in DMSO and applied at 100 nM concentration in vitro or 5- 10mg/kg intraperitoneally in vivo. .. Antibodies against ACTB (Cat#20536–1-AP), YTHDC2 (Cat#27779–1-AP), AKT (Cat#10176-2-AP), mTOR (Cat#28273-1-AP), LaminB1 (Cat#12987-1AP), Alpha Tubulin (Cat#11224-1-AP) were purchased from Proteintech (Wuhan, China).

    Drug discovery:

    Article Title: Senotherapeutic potential against xeroderma pigmentosum.
    Article Snippet: Senotherapeutic drug screening agents The following agents were applied for senolytic drug screening: ABT-263 (Selleck, S1001), A-1331852 (Selleck, S7801), A-1155463 (Selleck, S7800), S63845 (MedchemExpress, HY-100741), BPTES (Selleck, S7753), RSL3 (Selleck, S8155), digoxin (Sigma, D6003), ouabain (Sigma, O3125), 17-DMAG (Selleck, S1142), ganetespib (Selleck, S1159), panobinostat (Selleck, S1030), and romidepsin (MedchemExpress, HY-15149). .. In addition, the following agents were applied for senomorphic drug screening: A485 (Selleck, S8740), acetylcysteine (Selleck, S1623), curcumin (Selleck, S1848), EF24 (MedchemExpress, HY-119272), metformin (Selleck, S5958), apremilast (Selleck, S8034), difamilast (MedchemExpress, HY-109085), abrocitinib (Selleck, S8765), baricitinib (Selleck, S2851), upadacitinib (Selleck, S8162), IFN alpha-IFNAR-IN-1 (Selleck, E2982), VBIT-4 (Selleck, S3544), rapamycin (Selleck, S1039), dasatinib (Selleck, S1021), and quercetin (Selleck, S2391). ..



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    ( A and B ) mTORC1 inhibitor <t>rapamycin</t> and dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO organoids to MRTX1133. Representative pictures of organoids treated with mono- or combined therapy of MRTX1133 and rapamycin (A) or BGT226 (B). Representative organoid images are shown (top panels) and results were quantified (bottom panels). ( C to E ) Dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO tumors to MRTX1133. Mice were intranasally inoculated with Adeno-Cre for 4 weeks and then treated with vehicle, MRTX1133, BGT226 or a combination of both for 4 weeks. Representative H&E images of lungs collected from KRAS G12D ;C1 WT or KRAS G12D ;C1 KO mice (C). Tumor size (D) and burden (tumor area/total lung area × 100) (E) were quantified. Results presented as mean and SD. Statistical analysis was performed by nested ANOVA, followed by Tukey’s post hoc test for multiple comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.
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    ATRA enhanced the autophagy by facilitating the production of autophagosomes. (A, B) Quantitative analysis of ATRA‐induced autophagy in MDCK cells through the IFA assay. Scale bar: 10 μm. The statistical significance of differences was evaluated with the one‐way ANOVA. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. ns, no significance.
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    ATRA enhanced the autophagy by facilitating the production of autophagosomes. (A, B) Quantitative analysis of ATRA‐induced autophagy in MDCK cells through the IFA assay. Scale bar: 10 μm. The statistical significance of differences was evaluated with the one‐way ANOVA. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. ns, no significance.
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    ATRA enhanced the autophagy by facilitating the production of autophagosomes. (A, B) Quantitative analysis of ATRA‐induced autophagy in MDCK cells through the IFA assay. Scale bar: 10 μm. The statistical significance of differences was evaluated with the one‐way ANOVA. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. ns, no significance.
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    Image Search Results


    ( A and B ) mTORC1 inhibitor rapamycin and dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO organoids to MRTX1133. Representative pictures of organoids treated with mono- or combined therapy of MRTX1133 and rapamycin (A) or BGT226 (B). Representative organoid images are shown (top panels) and results were quantified (bottom panels). ( C to E ) Dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO tumors to MRTX1133. Mice were intranasally inoculated with Adeno-Cre for 4 weeks and then treated with vehicle, MRTX1133, BGT226 or a combination of both for 4 weeks. Representative H&E images of lungs collected from KRAS G12D ;C1 WT or KRAS G12D ;C1 KO mice (C). Tumor size (D) and burden (tumor area/total lung area × 100) (E) were quantified. Results presented as mean and SD. Statistical analysis was performed by nested ANOVA, followed by Tukey’s post hoc test for multiple comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Journal: Science Advances

    Article Title: CASTOR1 functional inactivation drives KRAS -mutant NSCLC and therapy resistance by a noncanonical mechanism of tumor suppression

    doi: 10.1126/sciadv.aeb9836

    Figure Lengend Snippet: ( A and B ) mTORC1 inhibitor rapamycin and dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO organoids to MRTX1133. Representative pictures of organoids treated with mono- or combined therapy of MRTX1133 and rapamycin (A) or BGT226 (B). Representative organoid images are shown (top panels) and results were quantified (bottom panels). ( C to E ) Dual PI3K/mTOR inhibitor BGT226 sensitized KRAS G12D ;C1 WT and KRAS G12D ;C1 KO tumors to MRTX1133. Mice were intranasally inoculated with Adeno-Cre for 4 weeks and then treated with vehicle, MRTX1133, BGT226 or a combination of both for 4 weeks. Representative H&E images of lungs collected from KRAS G12D ;C1 WT or KRAS G12D ;C1 KO mice (C). Tumor size (D) and burden (tumor area/total lung area × 100) (E) were quantified. Results presented as mean and SD. Statistical analysis was performed by nested ANOVA, followed by Tukey’s post hoc test for multiple comparisons. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Article Snippet: For drug treatment assays, organoids were treated with the following drug concentrations: 10 nM MRTX1133 (ChemGood, catalog no. C1420), 20 nM rapamycin (MCE, catalog no. HY10219), and 10 nM BGT226 (MCE, catalog no. 13334).

    Techniques: Organoids, Analysis

    ( A ) Knockdown of CASTOR1 enhanced cell proliferation of human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines following siRNA knockdown of CASTOR1 . ( B ) Overexpression of CASTOR1 inhibited cell proliferation of human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines following the overexpression of CASTOR1 . ( C ) Knockdown of CASTOR1 enhanced resistance to mTORC1 inhibitor Torin1 in human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines treated with Torin1 following siRNA knockdown of CASTOR1 . ( D ) Overexpression of CASTOR1 sensitized human lung cancer cell lines to mTORC1 inhibitors Torin1 and rapamycin. Clonogenic assay and immunoblotting of human lung cancer cell lines with mTOR inhibitors Torin1 and rapamycin following the overexpression of CASTOR1 . Rapamycin was used at 20 nM, while Torin1 was used at 0.2 μM.

    Journal: Science Advances

    Article Title: CASTOR1 functional inactivation drives KRAS -mutant NSCLC and therapy resistance by a noncanonical mechanism of tumor suppression

    doi: 10.1126/sciadv.aeb9836

    Figure Lengend Snippet: ( A ) Knockdown of CASTOR1 enhanced cell proliferation of human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines following siRNA knockdown of CASTOR1 . ( B ) Overexpression of CASTOR1 inhibited cell proliferation of human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines following the overexpression of CASTOR1 . ( C ) Knockdown of CASTOR1 enhanced resistance to mTORC1 inhibitor Torin1 in human lung cancer cell lines. Clonogenic assay and immunoblotting of human lung cancer cell lines treated with Torin1 following siRNA knockdown of CASTOR1 . ( D ) Overexpression of CASTOR1 sensitized human lung cancer cell lines to mTORC1 inhibitors Torin1 and rapamycin. Clonogenic assay and immunoblotting of human lung cancer cell lines with mTOR inhibitors Torin1 and rapamycin following the overexpression of CASTOR1 . Rapamycin was used at 20 nM, while Torin1 was used at 0.2 μM.

    Article Snippet: For drug treatment assays, organoids were treated with the following drug concentrations: 10 nM MRTX1133 (ChemGood, catalog no. C1420), 20 nM rapamycin (MCE, catalog no. HY10219), and 10 nM BGT226 (MCE, catalog no. 13334).

    Techniques: Knockdown, Clonogenic Assay, Western Blot, Over Expression

    ATRA enhanced the autophagy by facilitating the production of autophagosomes. (A, B) Quantitative analysis of ATRA‐induced autophagy in MDCK cells through the IFA assay. Scale bar: 10 μm. The statistical significance of differences was evaluated with the one‐way ANOVA. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. ns, no significance.

    Journal: Transboundary and Emerging Diseases

    Article Title: All‐Trans Retinoic Acid Inhibits Canine Influenza Virus Replication Through Keratin 27–Mediated Autophagy Modulation

    doi: 10.1155/tbed/2088414

    Figure Lengend Snippet: ATRA enhanced the autophagy by facilitating the production of autophagosomes. (A, B) Quantitative analysis of ATRA‐induced autophagy in MDCK cells through the IFA assay. Scale bar: 10 μm. The statistical significance of differences was evaluated with the one‐way ANOVA. ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. ns, no significance.

    Article Snippet: The reagents ATRA, rapamycin, chloroquine, and CCK‐8 kit were purchased from Topscience (China).

    Techniques: Analysis