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baf a1 treatment group  (MedChemExpress)


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    MedChemExpress baf a1 treatment group
    Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions <t>after</t> <t>Baf-A1</t> treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test
    Baf A1 Treatment Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1214 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/baf+a1+treatment+group/Bafilomycin+A1/pmc12920663-254-2-9
    Average 99 stars, based on 1214 article reviews
    baf a1 treatment group - by Bioz Stars, 2026-09
    99/100 stars

    Images

    1) Product Images from "Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction"

    Article Title: Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction

    Journal: International Journal of Oral Science

    doi: 10.1038/s41368-025-00423-2

    Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test
    Figure Legend Snippet: Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test

    Techniques Used: Inhibition, Micro-CT, Immunofluorescence, Staining

    Related Articles

    Control:

    Article Title: Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction.
    Article Snippet: .. In the Baf-A1 treatment group, 1 nmol/L Baf-A1 (HY-100558, MCE) was incorporated into the osteogenic induction medium, while an equivalent volume of DMSO (D103274, Aladin) was administered to the control cells. .. The EGF treatment group received supplementation with 0.01 nmol/L EGF recombinant protein (HY-P7067, MCE) solubilized in non-enzymatic water within the osteogenic induction medium, and an equal volume of PBS buffer was added to the control cells.

    Article Title: Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction
    Article Snippet: .. In the Baf-A1 treatment group, 1 nmol/L Baf-A1 (HY-100558, MCE) was incorporated into the osteogenic induction medium, while an equivalent volume of DMSO (D103274, Aladin) was administered to the control cells. .. The EGF treatment group received supplementation with 0.01 nmol/L EGF recombinant protein (HY-P7067, MCE) solubilized in non-enzymatic water within the osteogenic induction medium, and an equal volume of PBS buffer was added to the control cells.



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    baf a1 treatment group  (MedChemExpress)
    99
    MedChemExpress baf a1 treatment group
    Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions <t>after</t> <t>Baf-A1</t> treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test
    Baf A1 Treatment Group, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/baf+a1+treatment+group/Bafilomycin+A1/pmc12920663-254-2-9
    Average 99 stars, based on 1 article reviews
    baf a1 treatment group - by Bioz Stars, 2026-09
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test

    Journal: International Journal of Oral Science

    Article Title: Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction

    doi: 10.1038/s41368-025-00423-2

    Figure Lengend Snippet: Inhibition of lysosomal degradation abolishes the enhanced osteogenic phenotype induced by Snx5 deficiency. a Micro-CT reconstructed images of bone architecture in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). Yellow areas indicate ROIs, defined as annular zones extending approximately 75 μm to 175 μm outward from the implant surface; white solid lines delineate defect boundaries in the Sham group. Scale bar: 1 mm. b Quantitative analysis of BV/TV, BS/BV, and Tb.Th in Snx5 -KO mice under Sham and Imp conditions after Baf-A1 treatment ( n = 5). c Immunofluorescence staining and magnified views of peri-defect or peri-implant regions in Snx5 -KO mice after Baf-A1 treatment, showing Runx2 (green), LepR⁺ tdTomato⁺ (red), and DAPI (blue). Yellow dashed boxes indicate zoomed-in areas; white dashed lines outline defect or implant site boundaries ( n = 3). Scale bars: 100 μm. d Quantification of Runx2⁺ LepR⁺ tdTomato⁺ cells as a percentage of total LepR⁺ tdTomato⁺ cells ( n = 3). e Schematic illustration of the proposed mechanism: in Snx5 -KO cells, EGFR is primarily trafficked into Rab7⁺ late endosomes and degraded in LAMP1⁺ lysosomes. Treatment with the lysosomal inhibitor Baf-A1 blocks this pathway and attenuates the enhanced osteogenic phenotype. Baf-A1 Bafilomycin A1, Imp implant, ROI regions of interest. Data are presented as mean ± SD. ns not significant * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1. Statistical analysis for panels b and d was performed using two-way ANOVA followed by Tukey’s multiple comparisons test

    Article Snippet: In the Baf-A1 treatment group, 1 nmol/L Baf-A1 (HY-100558, MCE) was incorporated into the osteogenic induction medium, while an equivalent volume of DMSO (D103274, Aladin) was administered to the control cells.

    Techniques: Inhibition, Micro-CT, Immunofluorescence, Staining