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( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of <t>CGRP</t> in the supernatant <t>of</t> <t>DRGn</t> with and without ES. n = 8. n.s., not significant.
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( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of <t>CGRP</t> in the supernatant <t>of</t> <t>DRGn</t> with and without ES. n = 8. n.s., not significant.
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( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of <t>CGRP</t> in the supernatant <t>of</t> <t>DRGn</t> with and without ES. n = 8. n.s., not significant.
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( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of <t>CGRP</t> in the supernatant <t>of</t> <t>DRGn</t> with and without ES. n = 8. n.s., not significant.
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( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of <t>CGRP</t> in the supernatant <t>of</t> <t>DRGn</t> with and without ES. n = 8. n.s., not significant.
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Image Search Results


( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of CGRP in the supernatant of DRGn with and without ES. n = 8. n.s., not significant.

Journal: Science Advances

Article Title: Activation of the YAP1/pSTAT3/NRP1 axis in peritendinous sensory nerves promotes tendon healing

doi: 10.1126/sciadv.aec1272

Figure Lengend Snippet: ( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of CGRP in the supernatant of DRGn with and without ES. n = 8. n.s., not significant.

Article Snippet: Culture supernatants from treated DRGn were collected, and concentrations of CGRP (lot no. E-EL-R0135, Elabscience, China) were quantified using ELISA kits according to the manufacturer’s protocols.

Techniques: Control, Quantitative RT-PCR, Expressing, Binding Assay, Sequencing, Luciferase

( A ) Schematic diagram of DRGn treatment and detection. ( B and C ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 and NRP1 in vitro in the absence or presence of shSTAT3 and ES. β-actin was used as an internal control. n = 3. ( D and E ) Protein expression levels and quantitative results of YAP1 and NRP1 in vitro in the absence or presence of shYAP1 and ES. β-actin was used as an internal control. n = 3. ( F to I ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 , YAP1, and NRP1 in the absence or presence of shSTAT3, shYAP1, and ES. n = 3. ( J ) Schematic illustration of the cross-talk between DRGn and HUVECs. ( K and L ) Expression levels of CGRP in the supernatant of DRGn under different treatments. n = 8. ( M ) Wound scratch assay in HUVECs under different treatments. n = 3. Ctrl, control.

Journal: Science Advances

Article Title: Activation of the YAP1/pSTAT3/NRP1 axis in peritendinous sensory nerves promotes tendon healing

doi: 10.1126/sciadv.aec1272

Figure Lengend Snippet: ( A ) Schematic diagram of DRGn treatment and detection. ( B and C ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 and NRP1 in vitro in the absence or presence of shSTAT3 and ES. β-actin was used as an internal control. n = 3. ( D and E ) Protein expression levels and quantitative results of YAP1 and NRP1 in vitro in the absence or presence of shYAP1 and ES. β-actin was used as an internal control. n = 3. ( F to I ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 , YAP1, and NRP1 in the absence or presence of shSTAT3, shYAP1, and ES. n = 3. ( J ) Schematic illustration of the cross-talk between DRGn and HUVECs. ( K and L ) Expression levels of CGRP in the supernatant of DRGn under different treatments. n = 8. ( M ) Wound scratch assay in HUVECs under different treatments. n = 3. Ctrl, control.

Article Snippet: Culture supernatants from treated DRGn were collected, and concentrations of CGRP (lot no. E-EL-R0135, Elabscience, China) were quantified using ELISA kits according to the manufacturer’s protocols.

Techniques: Expressing, In Vitro, Control, Wound Healing Assay