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The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, <t>AIFM2,</t> and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.
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The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, <t>AIFM2,</t> and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.
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The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, <t>AIFM2,</t> and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.
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Proteintech mouse monoclonal anti yap1 antibody
The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, <t>AIFM2,</t> and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.
Mouse Monoclonal Anti Yap1 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SMFs amplify the response of orthodontic mechanical signaling pathways. (a) Representative immunofluorescence images of vinculin (green), F‐actin (purple), and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), with mechanical force only, and with mechanical force plus SMFs. Scale bar: 10 µm. (b) Cell area, (c) FA area per cell, and (d) cell shape index in PDLCs. Mean ± SD. n = 24. * p < 0.05, ** p < 0.01, **** p < 0.0001. (e) FAK: Focal Adhesion Kinase. It is a mechanotransducer that becomes activated upon orthodontic force, regulating downstream bone remodeling and inflammatory responses in PDLCs. Representative immunofluorescence images of FAK (red) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (f) Relative FAK integrated density per cell in PDLCs. Mean ± SD. n = 24. **** p < 0.0001. (g) Representative immunofluorescence images <t>of</t> <t>YAP/TAZ</t> (green) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (h) The nuclear‐cytoplasmic ratios of YAP/TAZ in PDLCs analyzed from the immunofluorescence images. Mean ± SD. n = 24. ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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SMFs amplify the response of orthodontic mechanical signaling pathways. (a) Representative immunofluorescence images of vinculin (green), F‐actin (purple), and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), with mechanical force only, and with mechanical force plus SMFs. Scale bar: 10 µm. (b) Cell area, (c) FA area per cell, and (d) cell shape index in PDLCs. Mean ± SD. n = 24. * p < 0.05, ** p < 0.01, **** p < 0.0001. (e) FAK: Focal Adhesion Kinase. It is a mechanotransducer that becomes activated upon orthodontic force, regulating downstream bone remodeling and inflammatory responses in PDLCs. Representative immunofluorescence images of FAK (red) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (f) Relative FAK integrated density per cell in PDLCs. Mean ± SD. n = 24. **** p < 0.0001. (g) Representative immunofluorescence images <t>of</t> <t>YAP/TAZ</t> (green) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (h) The nuclear‐cytoplasmic ratios of YAP/TAZ in PDLCs analyzed from the immunofluorescence images. Mean ± SD. n = 24. ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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SMFs amplify the response of orthodontic mechanical signaling pathways. (a) Representative immunofluorescence images of vinculin (green), F‐actin (purple), and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), with mechanical force only, and with mechanical force plus SMFs. Scale bar: 10 µm. (b) Cell area, (c) FA area per cell, and (d) cell shape index in PDLCs. Mean ± SD. n = 24. * p < 0.05, ** p < 0.01, **** p < 0.0001. (e) FAK: Focal Adhesion Kinase. It is a mechanotransducer that becomes activated upon orthodontic force, regulating downstream bone remodeling and inflammatory responses in PDLCs. Representative immunofluorescence images of FAK (red) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (f) Relative FAK integrated density per cell in PDLCs. Mean ± SD. n = 24. **** p < 0.0001. (g) Representative immunofluorescence images <t>of</t> <t>YAP/TAZ</t> (green) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (h) The nuclear‐cytoplasmic ratios of YAP/TAZ in PDLCs analyzed from the immunofluorescence images. Mean ± SD. n = 24. ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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Mechanistic analysis of YOD1-mediated regulation by Y-Exos in macrophage polarization and osteogenic differentiation. (A) PCA analysis of transcriptomic profiles of LPS-stimulated BMMs treated with or without YOD1. (B) Number of differentially expressed genes identified after YOD1 treatment (P < 0.05, |log₂(FC)| > 1). (C) KEGG pathway enrichment analysis of differentially expressed genes. (D) Western blot analysis of Hippo/YAP signaling-related proteins and macrophage polarization markers in BMMs treated with YOD1 or Y-Exos under LPS stimulation. (E) Effects of <t>YAP1</t> nuclear translocation inhibition by Verteporfin on ARG1 and iNOS expression in BMMs. (F-G) Quantification of protein expression in (D-E). (H) Western blot analysis of AKT/mTOR signaling-related proteins in BMMs after YOD1 or Y-Exos treatment. (I) Quantification of AKT/mTOR-related protein expression. (J) Effects of AKT and mTOR inhibition by MK2206 and Rapamycin on macrophage polarization-related proteins. (K) Western blot analysis of Hippo/YAP signaling-related proteins and osteogenic markers in BMSCs after YOD1 or Y-Exos treatment during osteogenic induction. (L-M) Quantification of protein expression in (J-K). (N) F-actin ring staining showing the effects of Rapamycin on the indirect regulation of osteoclast differentiation by YOD1 and Y-Exos (scale bar = 100 μm). (O-P) Western blot analysis and quantification of NFATC1 expression after Rapamycin treatment. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.
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Mechanistic analysis of YOD1-mediated regulation by Y-Exos in macrophage polarization and osteogenic differentiation. (A) PCA analysis of transcriptomic profiles of LPS-stimulated BMMs treated with or without YOD1. (B) Number of differentially expressed genes identified after YOD1 treatment (P < 0.05, |log₂(FC)| > 1). (C) KEGG pathway enrichment analysis of differentially expressed genes. (D) Western blot analysis of Hippo/YAP signaling-related proteins and macrophage polarization markers in BMMs treated with YOD1 or Y-Exos under LPS stimulation. (E) Effects of <t>YAP1</t> nuclear translocation inhibition by Verteporfin on ARG1 and iNOS expression in BMMs. (F-G) Quantification of protein expression in (D-E). (H) Western blot analysis of AKT/mTOR signaling-related proteins in BMMs after YOD1 or Y-Exos treatment. (I) Quantification of AKT/mTOR-related protein expression. (J) Effects of AKT and mTOR inhibition by MK2206 and Rapamycin on macrophage polarization-related proteins. (K) Western blot analysis of Hippo/YAP signaling-related proteins and osteogenic markers in BMSCs after YOD1 or Y-Exos treatment during osteogenic induction. (L-M) Quantification of protein expression in (J-K). (N) F-actin ring staining showing the effects of Rapamycin on the indirect regulation of osteoclast differentiation by YOD1 and Y-Exos (scale bar = 100 μm). (O-P) Western blot analysis and quantification of NFATC1 expression after Rapamycin treatment. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.
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Image Search Results


The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, AIFM2, and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.

Journal: Molecular & Cellular Oncology

Article Title: GINS1 suppresses ferroptosis by inhibiting the Hippo pathway in neuroblastoma

doi: 10.1080/23723556.2026.2715868

Figure Lengend Snippet: The impact of GINS1 on ferroptosis and the Hippo signaling pathway in neuroblastoma cells. A GO and KEGG pathway enrichment analysis of GINS1. B The ssGSEA scores of the ferroptosis pathway in Low_GINS1 and High_GINS1 groups. C The correlation between GINS1 expression and the expression of ACSL4, AIFM2, and TP53 proteins. D The gene expression in ferroptosis and Hippo pathways between neuroblastoma in Low_GINS1 and High_GINS1 groups; red boxes highlight ferroptosis genes. E The relative RFU of C11-BODIPY 581/591 were measured to assess lipid peroxidation in SH-SY5Y neuroblastoma cells transfected with shNC, shGINS1-1 and shGINS1-2. The concentration of malondialdehyde (MDA) and the iron content were also determined, respectively, as indicators of lipid peroxidation and iron metabolism. F Western blot assessed ACSL4, YAP, p -YAP, and AIFM2 in SH-SY5Y cells with shNC, shGINS1-1, and shGINS1-2. Data are presented as mean ± SD from three independent experiments, and statistical significance was determined using unpaired t-test or one-way ANOVA. The p -values are denoted by asterisks as follows: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns, not significant.

Article Snippet: Membranes were incubated with primary antibodies against ACSL4 (1:2000, Proteintech, 22401-1-AP), p -YAP (1:1000, Proteintech, 80694-2-RR), YAP (1:1000, Proteintech, 13584-1-AP), AIFM2 (1:1000, Proteintech, 20886-1-AP), p -MST1 (1:1000, Cell Signaling Technology, #3681S), MST1 (1:1000, Cell Signaling Technology, #3682S), p -LATS1 (1:1000, Cell Signaling Technology, #8654S), LATS1 (1:1000, Cell Signaling Technology, #3477S), GPX4 (1:1000, Proteintech, 67763-1-Ig), SLC7A11 (1:1000, Proteintech, 26864-1-AP) and GAPDH (1:30000, Proteintech, 60004-1-lg), followed by HRP-conjugated secondary antibodies.

Techniques: Analysis, Expressing, Gene Expression, Transfection, Concentration Assay, Western Blot

SMFs amplify the response of orthodontic mechanical signaling pathways. (a) Representative immunofluorescence images of vinculin (green), F‐actin (purple), and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), with mechanical force only, and with mechanical force plus SMFs. Scale bar: 10 µm. (b) Cell area, (c) FA area per cell, and (d) cell shape index in PDLCs. Mean ± SD. n = 24. * p < 0.05, ** p < 0.01, **** p < 0.0001. (e) FAK: Focal Adhesion Kinase. It is a mechanotransducer that becomes activated upon orthodontic force, regulating downstream bone remodeling and inflammatory responses in PDLCs. Representative immunofluorescence images of FAK (red) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (f) Relative FAK integrated density per cell in PDLCs. Mean ± SD. n = 24. **** p < 0.0001. (g) Representative immunofluorescence images of YAP/TAZ (green) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (h) The nuclear‐cytoplasmic ratios of YAP/TAZ in PDLCs analyzed from the immunofluorescence images. Mean ± SD. n = 24. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: Arrayed Magnetic Accelerator Synergistically Enhances Orthodontic Tooth Movement via Microtubule Assembly‐Mediated Periodontal Remodeling

doi: 10.1002/advs.77447

Figure Lengend Snippet: SMFs amplify the response of orthodontic mechanical signaling pathways. (a) Representative immunofluorescence images of vinculin (green), F‐actin (purple), and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), with mechanical force only, and with mechanical force plus SMFs. Scale bar: 10 µm. (b) Cell area, (c) FA area per cell, and (d) cell shape index in PDLCs. Mean ± SD. n = 24. * p < 0.05, ** p < 0.01, **** p < 0.0001. (e) FAK: Focal Adhesion Kinase. It is a mechanotransducer that becomes activated upon orthodontic force, regulating downstream bone remodeling and inflammatory responses in PDLCs. Representative immunofluorescence images of FAK (red) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (f) Relative FAK integrated density per cell in PDLCs. Mean ± SD. n = 24. **** p < 0.0001. (g) Representative immunofluorescence images of YAP/TAZ (green) and nuclei (blue) in PDLCs under three conditions: control (without mechanical force and without SMFs), mechanical force only, and mechanical force plus SMFs. Scale bar: 10 µm. (h) The nuclear‐cytoplasmic ratios of YAP/TAZ in PDLCs analyzed from the immunofluorescence images. Mean ± SD. n = 24. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: PDLCs were respectively incubated with the primary antibody for Vinculin (Proteintech, 26520‐1‐Ap, 1:300), FAK (Proteintech, 12636‐1‐AP, 1:400), YAP/TAZ (Proteintech, 13584‐1‐Ap, 1:200), α‐Tubulin (Abclonal, AC012, 1:200) and Integrin‐β1 (Abclonal, A23497, 1:200).

Techniques: Protein-Protein interactions, Immunofluorescence, Control

Mechanistic analysis of YOD1-mediated regulation by Y-Exos in macrophage polarization and osteogenic differentiation. (A) PCA analysis of transcriptomic profiles of LPS-stimulated BMMs treated with or without YOD1. (B) Number of differentially expressed genes identified after YOD1 treatment (P < 0.05, |log₂(FC)| > 1). (C) KEGG pathway enrichment analysis of differentially expressed genes. (D) Western blot analysis of Hippo/YAP signaling-related proteins and macrophage polarization markers in BMMs treated with YOD1 or Y-Exos under LPS stimulation. (E) Effects of YAP1 nuclear translocation inhibition by Verteporfin on ARG1 and iNOS expression in BMMs. (F-G) Quantification of protein expression in (D-E). (H) Western blot analysis of AKT/mTOR signaling-related proteins in BMMs after YOD1 or Y-Exos treatment. (I) Quantification of AKT/mTOR-related protein expression. (J) Effects of AKT and mTOR inhibition by MK2206 and Rapamycin on macrophage polarization-related proteins. (K) Western blot analysis of Hippo/YAP signaling-related proteins and osteogenic markers in BMSCs after YOD1 or Y-Exos treatment during osteogenic induction. (L-M) Quantification of protein expression in (J-K). (N) F-actin ring staining showing the effects of Rapamycin on the indirect regulation of osteoclast differentiation by YOD1 and Y-Exos (scale bar = 100 μm). (O-P) Western blot analysis and quantification of NFATC1 expression after Rapamycin treatment. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.

Journal: International Journal of Biological Sciences

Article Title: Young plasma-derived exosomes deliver YOD1 to induce M2 polarization and ameliorate osteoporosis via mTOR signaling pathways

doi: 10.7150/ijbs.138620

Figure Lengend Snippet: Mechanistic analysis of YOD1-mediated regulation by Y-Exos in macrophage polarization and osteogenic differentiation. (A) PCA analysis of transcriptomic profiles of LPS-stimulated BMMs treated with or without YOD1. (B) Number of differentially expressed genes identified after YOD1 treatment (P < 0.05, |log₂(FC)| > 1). (C) KEGG pathway enrichment analysis of differentially expressed genes. (D) Western blot analysis of Hippo/YAP signaling-related proteins and macrophage polarization markers in BMMs treated with YOD1 or Y-Exos under LPS stimulation. (E) Effects of YAP1 nuclear translocation inhibition by Verteporfin on ARG1 and iNOS expression in BMMs. (F-G) Quantification of protein expression in (D-E). (H) Western blot analysis of AKT/mTOR signaling-related proteins in BMMs after YOD1 or Y-Exos treatment. (I) Quantification of AKT/mTOR-related protein expression. (J) Effects of AKT and mTOR inhibition by MK2206 and Rapamycin on macrophage polarization-related proteins. (K) Western blot analysis of Hippo/YAP signaling-related proteins and osteogenic markers in BMSCs after YOD1 or Y-Exos treatment during osteogenic induction. (L-M) Quantification of protein expression in (J-K). (N) F-actin ring staining showing the effects of Rapamycin on the indirect regulation of osteoclast differentiation by YOD1 and Y-Exos (scale bar = 100 μm). (O-P) Western blot analysis and quantification of NFATC1 expression after Rapamycin treatment. Data are presented as mean ± SD. *P < 0.05; NS, no significant difference.

Article Snippet: The primary and secondary antibodies are listed as follows: TSG101 Rabbit antibody (Proteintech, China, 28283-1-AP), CD63 Rabbit antibody (Proteintech, China, 25682-1-AP), CD9 Rabbit antibody (Proteintech, China, 20597-1-AP), Calnexin Rabbit antibody (Proteintech, China, 10427-2-AP), CD86 Rabbit antibody(Immunoway, USA, YM8023), CD206 Rabbit antibody (Immunoway, USA, YM8349), iNOS Rabbit antibody(Proteintech, China, 22226-1-AP), ARG1 Rabbit antibody (Abcam, China, ab96183), RUNX2 Rabbit antibody (Proteintech, China, 20700-1-AP), Osteocalcin Rabbit antibody(Servicebio, China, GB11233-100), ACTIN Mouse antibody(Proteintech, China, 66009-1-Ig), YOD1 Rabbit antibody (Proteintech, China, 25370-1-AP), IDE Rabbit antibody (Proteintech, China, 21728-1-AP), VCL Rabbit antibody (Proteintech, China, 26520-1-AP), GAPDH Rabbit antibody (BOSTER, China, A00227-1), ITCH Rabbit antibody (Proteintech, China, 20920-1-AP), LATS1 Rabbit antibody (Proteintech, China, 17049-1-AP), Phospho-YAP1 (Ser127) Rabbit antibody (Proteintech, China, 80694-2-RR), YAP1 Rabbit antibody (Proteintech, China, 13584-1-AP), Phospho-AKT Rabbit antibody (Proteintech, China, 29163-1-AP), AKT Rabbit antibody (Proteintech, China, 10176-2-AP), Phospho-mTOR Rabbit antibody(ZenBio, China, 381557), mTOR Rabbit antibody (HUA BIO, China, ET1608-5), NFATC1 Mouse antibody (Proteintech, China, 66963-1-Ig).

Techniques: Analysis, Western Blot, Translocation Assay, Inhibition, Expressing, Staining, Cell Differentiation