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MedChemExpress yap agonist
<t>ITGB1/FAK/YAP</t> mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.
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MedChemExpress yap
<t>ITGB1/FAK/YAP</t> mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.
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Cell Signaling Technology Inc yap1 phosphorylated on serine 127
Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Cell Signaling Technology Inc yap d8h1x xp rabbit mab
Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Cell Signaling Technology Inc rabbit monoclonal anti yap
Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Cell Signaling Technology Inc yap
Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Santa Cruz Biotechnology anti yap
Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or <t>phospho-YAP1,</t> respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.
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Image Search Results


ITGB1/FAK/YAP mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.

Journal: Bioactive Materials

Article Title: From disease model to therapeutic insight: An engineered hydrogel reveals the role of matrix viscous dissipation in intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.021

Figure Lengend Snippet: ITGB1/FAK/YAP mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.

Article Snippet: During this period, in accordance with a previous study, 10 μL of FAK agonist (ZINC40099027, 10 μM, MCE, HY-134570) or YAP agonist (PY-60, 10 μM, MCE, HY-141644) were injected into the compressed IVDs every other day using a 31G needle.

Techniques: Cell Culture, Immunofluorescence, Expressing, Western Blot

Pharmacological activating of YAP alleviates NPCs senescence and IVDD progression. a, Schematic illustration of the in vivo experiments design. Rats received a FAK agonist or a YAP agonist every other day to indirectly or directly activate YAP. b, Images of rats IVDD model c, Representative MRI and X-ray images of the IVDs after injection of FAK agonist and YAP agonist with the corresponding quantitative analysis (n = 5). d, Representative H&E and S. O. staining of IVDs. Scale bars = 1 mm. e, Representative IF images of ACAN and COL II. Scale bars = 100 μm. f, Representative IF images of p16INK4a and YAP. g, Representative IHC images of cGAS with the corresponding quantitative analysis. Scale bars = 100 μm (n = 5). All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference compared to the control group, and the symbol “#” represents a statistical difference compared to the compression group.

Journal: Bioactive Materials

Article Title: From disease model to therapeutic insight: An engineered hydrogel reveals the role of matrix viscous dissipation in intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.021

Figure Lengend Snippet: Pharmacological activating of YAP alleviates NPCs senescence and IVDD progression. a, Schematic illustration of the in vivo experiments design. Rats received a FAK agonist or a YAP agonist every other day to indirectly or directly activate YAP. b, Images of rats IVDD model c, Representative MRI and X-ray images of the IVDs after injection of FAK agonist and YAP agonist with the corresponding quantitative analysis (n = 5). d, Representative H&E and S. O. staining of IVDs. Scale bars = 1 mm. e, Representative IF images of ACAN and COL II. Scale bars = 100 μm. f, Representative IF images of p16INK4a and YAP. g, Representative IHC images of cGAS with the corresponding quantitative analysis. Scale bars = 100 μm (n = 5). All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference compared to the control group, and the symbol “#” represents a statistical difference compared to the compression group.

Article Snippet: During this period, in accordance with a previous study, 10 μL of FAK agonist (ZINC40099027, 10 μM, MCE, HY-134570) or YAP agonist (PY-60, 10 μM, MCE, HY-141644) were injected into the compressed IVDs every other day using a 31G needle.

Techniques: In Vivo, Injection, Staining, Control

Viscous dissipation biomimetic hydrogel alleviates ECM remodeling and NPCs senescence during IVDD. a, Schematic diagram of the mechanical testing procedures. Axial tension-compression and stress-relaxation tests were conducted to evaluate the mechanical properties of IVDs at 12 weeks b, Representative force-displacement curves of all groups. c, Representative stress-relaxation curves of all groups. d, Quantitative analysis of compressive stiffness, tensile stiffness (n = 5). e, Quantitative analysis of normalized NZ and τ 1/2 (n = 5). h, Representative IF images of p16INK4a and YAP at 12 weeks. Scale bars = 50 μm and 20 μm, respectively. i, Representative IHC images of cGAS in NP tissues at 12 weeks. Scale bars = 100 μm (n = 5). The symbol “∗” represents a statistical difference compared to the sham group, and the symbol “#” represents a statistical difference compared to the defect group.

Journal: Bioactive Materials

Article Title: From disease model to therapeutic insight: An engineered hydrogel reveals the role of matrix viscous dissipation in intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.021

Figure Lengend Snippet: Viscous dissipation biomimetic hydrogel alleviates ECM remodeling and NPCs senescence during IVDD. a, Schematic diagram of the mechanical testing procedures. Axial tension-compression and stress-relaxation tests were conducted to evaluate the mechanical properties of IVDs at 12 weeks b, Representative force-displacement curves of all groups. c, Representative stress-relaxation curves of all groups. d, Quantitative analysis of compressive stiffness, tensile stiffness (n = 5). e, Quantitative analysis of normalized NZ and τ 1/2 (n = 5). h, Representative IF images of p16INK4a and YAP at 12 weeks. Scale bars = 50 μm and 20 μm, respectively. i, Representative IHC images of cGAS in NP tissues at 12 weeks. Scale bars = 100 μm (n = 5). The symbol “∗” represents a statistical difference compared to the sham group, and the symbol “#” represents a statistical difference compared to the defect group.

Article Snippet: During this period, in accordance with a previous study, 10 μL of FAK agonist (ZINC40099027, 10 μM, MCE, HY-134570) or YAP agonist (PY-60, 10 μM, MCE, HY-141644) were injected into the compressed IVDs every other day using a 31G needle.

Techniques:

ITGB1/FAK/YAP mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.

Journal: Bioactive Materials

Article Title: From disease model to therapeutic insight: An engineered hydrogel reveals the role of matrix viscous dissipation in intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.021

Figure Lengend Snippet: ITGB1/FAK/YAP mechanotransduction axis mediates the regulation of ECM viscous dissipation on YAP. a, GSEA revealed that “Reactome integrin signaling”, “Gobo focal adhesion assembly”, “Gobo regulation of cytoskeleton” and “Kegg regulation of actin cytoskeleton” were upregulated in the NPCs cultured on V-gel compared with the NPCs cultured on E-gel. b, Heatmap of the series of DEGs related to mechanotransduction. c, Representative IF images of ITGB1 and YAP in NPCs with corresponding quantitative analysis, Scale bars = 50 μm d, Representative immunofluorescence images of p-FAK, Vinculin, YAP, and F-actin with quantitative analysis of cell areas, p-FAK expression and the ratio of nuclear YAP. Relative cell areas and nuclear YAP ratios were quantified across 50 cells from three independent biological replicates (n = 50). Relative fluorescent intensity of p-FAK was quantified from three independent biological replicates (n = 3). e, Western blotting analysis of YAP and p-YAP. All data are presented as means ± SD. Statistical significance was determined by one-way ANOVA with Tukey's multiple-comparisons test. p < 0.05 was considered statistically significant. The symbol “∗” represents a statistical difference.

Article Snippet: Agonists in cell culture were used at the following concertation: 1.5 μM PY-60 to activate YAP (MCE, China, HY-141644), 0.8 μM Pyrintegrin to activate ITGB1 (MCE, China, HY-13306) and 10 nM ZINC40099027 to activate FAK (MCE, China, HY-134570).

Techniques: Cell Culture, Immunofluorescence, Expressing, Western Blot

Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or phospho-YAP1, respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.

Journal: iScience

Article Title: Promotion of breast cancer by the DNPH1 enzyme

doi: 10.1016/j.isci.2026.115227

Figure Lengend Snippet: Alterations in mammary tumors upon Dnph1 knockout (A) Examples of CD31 staining in mammary tumors from a MMTV-Her2/Dnph1 +/+ and a MMTV-Her2/Dnph1 −/− mouse. Right panels show ImageJ-mediated image modulation to enhance vessel structures, allowing the computer-mediated quantification of blood vessel density. Scale bars, 0.4 mm. (B) Corresponding quantification of vessel density. Tumors were age- and weight-matched; two-tailed, unpaired t test. (C) Tumor vessel density plotted against the weight of the tumor. These tumors were not weight- or age-matched, yet include those shown in panel B. Shown are linear regressions; while the slopes were not significantly different, the Y-intercepts were significantly different ( p = 0.0007). (D) Relative levels of AMP, GMP, and UMP in mammary tumors from MMTV-Her2/Dnph1 +/+ and MMTV-Her2/Dnph1 −/− mice; two-tailed, unpaired t test. (E and F) Immunohistochemical staining for phospho-AMPKα or phospho-YAP1, respectively, on age- and weight-matched tumors as in panel B. Examples of immunohistochemical staining are shown at the bottom. Scale bars, 0.4 mm. Means with standard deviation are shown in panels B and D-F.

Article Snippet: YAP1 phosphorylated on serine 127 , Cell Signaling , Cat# 4911.

Techniques: Knock-Out, Staining, Two Tailed Test, Immunohistochemical staining, Standard Deviation

Model how DNPH1 promotes breast tumor development and progression This model is centered around a DNPH1-YAP1 axis, yet DNPH1 may utilize to-be-identified effectors other than YAP1 to stimulate, e.g., stem cells or angiogenesis.

Journal: iScience

Article Title: Promotion of breast cancer by the DNPH1 enzyme

doi: 10.1016/j.isci.2026.115227

Figure Lengend Snippet: Model how DNPH1 promotes breast tumor development and progression This model is centered around a DNPH1-YAP1 axis, yet DNPH1 may utilize to-be-identified effectors other than YAP1 to stimulate, e.g., stem cells or angiogenesis.

Article Snippet: YAP1 phosphorylated on serine 127 , Cell Signaling , Cat# 4911.

Techniques: