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Mst1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sirnas for taz  (Santa Cruz Biotechnology)
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(A-C) Depletion of YAP1 using two different <t>siRNAs</t> abrogated angiogenic tubule formation on matrigel compared to the control siRNA transfected HUVECs, HAECs and HMEC-Ls (scale 500 μm). Quantification of the fold change in number of junctions formed upon YAP1 depletion is presented graphically on the right. (D) Depletion of YAP1 eliminated angiogenic tubule formation in HUVECs, even under hypoxic conditions. The suppression of tubule formation is quantified in the adjacent charts. (E) A proximity ligation assay (PLA) showed increased interaction of YAP1 with HIF1α in A549 and H1650 cells subjected to hypoxia (1% O2) for 24h. Scale bar 25 μm; Blue –DAPI, Red – YAP1/HIF1α PLA foci. (F) Co-immunoprecipitation-western blot assays on A549 and H1650 cells indicate that YAP1 directly associates with HIF1α protein. A reverse immunoprecipitation confirmed the same result with HIF1α IP and YAP1 western blot (lower panel); 20% of the input was loaded in the lysate lanes. A normal IgG control IP showed minimal interaction in the co-immunoprecipitations. (G-H) Elevated interaction of YAP1 and HIF1α is detected in human lung tumor tissues as compared to normal lung by PLA performed on a lung tissue microarray (H). Scale bar 25 μm; Blue –DAPI, Red – foci of YAP1/HIF1α interaction, Green - Pan-cytokeratin. The quantitation of the PLA is represented graphically (G). The bar graph represents mean ± SD of the indicated number of cores, representing each tumor type. * p <0.05, ** p<0.01 and *** p< 0.005 derived by Student’s t-test.
Sirnas For Taz, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 92 stars, based on 1 article reviews
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92/100 stars
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(A-C) Depletion of YAP1 using two different siRNAs abrogated angiogenic tubule formation on matrigel compared to the control siRNA transfected HUVECs, HAECs and HMEC-Ls (scale 500 μm). Quantification of the fold change in number of junctions formed upon YAP1 depletion is presented graphically on the right. (D) Depletion of YAP1 eliminated angiogenic tubule formation in HUVECs, even under hypoxic conditions. The suppression of tubule formation is quantified in the adjacent charts. (E) A proximity ligation assay (PLA) showed increased interaction of YAP1 with HIF1α in A549 and H1650 cells subjected to hypoxia (1% O2) for 24h. Scale bar 25 μm; Blue –DAPI, Red – YAP1/HIF1α PLA foci. (F) Co-immunoprecipitation-western blot assays on A549 and H1650 cells indicate that YAP1 directly associates with HIF1α protein. A reverse immunoprecipitation confirmed the same result with HIF1α IP and YAP1 western blot (lower panel); 20% of the input was loaded in the lysate lanes. A normal IgG control IP showed minimal interaction in the co-immunoprecipitations. (G-H) Elevated interaction of YAP1 and HIF1α is detected in human lung tumor tissues as compared to normal lung by PLA performed on a lung tissue microarray (H). Scale bar 25 μm; Blue –DAPI, Red – foci of YAP1/HIF1α interaction, Green - Pan-cytokeratin. The quantitation of the PLA is represented graphically (G). The bar graph represents mean ± SD of the indicated number of cores, representing each tumor type. * p <0.05, ** p<0.01 and *** p< 0.005 derived by Student’s t-test.

Journal: Cancer research communications

Article Title: A Novel PHD2/VHL-mediated Regulation of YAP1 Contributes to VEGF Expression and Angiogenesis

doi: 10.1158/2767-9764.crc-21-0084

Figure Lengend Snippet: (A-C) Depletion of YAP1 using two different siRNAs abrogated angiogenic tubule formation on matrigel compared to the control siRNA transfected HUVECs, HAECs and HMEC-Ls (scale 500 μm). Quantification of the fold change in number of junctions formed upon YAP1 depletion is presented graphically on the right. (D) Depletion of YAP1 eliminated angiogenic tubule formation in HUVECs, even under hypoxic conditions. The suppression of tubule formation is quantified in the adjacent charts. (E) A proximity ligation assay (PLA) showed increased interaction of YAP1 with HIF1α in A549 and H1650 cells subjected to hypoxia (1% O2) for 24h. Scale bar 25 μm; Blue –DAPI, Red – YAP1/HIF1α PLA foci. (F) Co-immunoprecipitation-western blot assays on A549 and H1650 cells indicate that YAP1 directly associates with HIF1α protein. A reverse immunoprecipitation confirmed the same result with HIF1α IP and YAP1 western blot (lower panel); 20% of the input was loaded in the lysate lanes. A normal IgG control IP showed minimal interaction in the co-immunoprecipitations. (G-H) Elevated interaction of YAP1 and HIF1α is detected in human lung tumor tissues as compared to normal lung by PLA performed on a lung tissue microarray (H). Scale bar 25 μm; Blue –DAPI, Red – foci of YAP1/HIF1α interaction, Green - Pan-cytokeratin. The quantitation of the PLA is represented graphically (G). The bar graph represents mean ± SD of the indicated number of cores, representing each tumor type. * p <0.05, ** p<0.01 and *** p< 0.005 derived by Student’s t-test.

Article Snippet: The two different siRNAs for YAP1 were purchased from Santa Cruz Biotechnologies (sc-38637) and ThermoFisher Scientific (107951) respectively. siRNAs For TAZ (sc-45232), MST1 (sc-39249), MST2 (sc-39247), LATS2 (sc-37444), HIF1α (sc-35561), PHD2 (sc-45537), PHD3 (sc-45799), TEAD2 (sc-45232) and TEAD4 (sc-96187) were purchased from Santa Cruz Biotechnologies. siRNAs for LATS1 (137593), HIF1α (106498), TAZ (122501), TEAD2 (107179), TEAD4 (115367), PHD2 (133478) and PHD3 (128749) were purchased from ThermoFisher Scientific.

Techniques: Control, Transfection, Proximity Ligation Assay, Immunoprecipitation, Western Blot, Microarray, Quantitation Assay, Derivative Assay

(A) Depletion of YAP1, but not TAZ, resulted in decreased VEGF promoter luciferase activity in hypoxic A549 and H1650 cells in a transient transfection assay. (B) RT-qPCRs showed decreased expression of endogenous VEGF mRNA in A549 cells transfected with YAP1 siRNA and subjected to hypoxia. Such a change was not observed when TAZ was depleted in the A549 cells. (C) Similarly, depletion of YAP1, but not TAZ, decreased VEGF promoter luciferase activity in A549 and H1650 cells treated with 1mM DMOG as compared to control vehicle treated cells. (D) The expression of endogenous VEGF mRNA was reduced when A549 cells were transfected with YAP1 siRNA but not TAZ siRNA; cells treated with 1mM DMOG showed the same result. (E) YAP1 and HIF1α overexpression showed an increased effect on VEGF promoter luciferase activity in transient transfections in A549 and H1650 cells. (F) Loss of VEGF-luc promoter luciferase activity in transient transfection assays upon HIF1α depletion when YAP1 was overexpressed; no significant change was observed with the depletion of TEAD2 or TEAD4 using two different siRNAs for each. (G) RT-qPCRs showed an increase in endogenous VEGF mRNA expression in A549 cells when YAP1 was overexpressed. However, this increase in endogenous VEGF mRNA was less when HIF1α was depleted in the presence of YAP1. The depletion of TEAD2 or TEAD4 did not affect the expression of endogenous VEGF mRNA expression, when YAP1 was overexpressed. (H) ChIP-qPCR analysis performed in normoxic and hypoxic A549 cells with the indicated antibodies showed increased presence of YAP1 at the HIF1α binding sites on VEGF promoter at position −866 to −987 bp, upstream of transcription start site in the hypoxic A549 cells. (I) A site-directed mutation in the HIF1α binding site on the VEGF promoter (mutVEGF-Luc) abrogated promoter luciferase activity induced by YAP1. The bar graphs in this panel represents mean ± SEM of three independent experiments. * p <0.05 and ** p<0.01 derived by two-way ANOVA with post-hoc test.

Journal: Cancer research communications

Article Title: A Novel PHD2/VHL-mediated Regulation of YAP1 Contributes to VEGF Expression and Angiogenesis

doi: 10.1158/2767-9764.crc-21-0084

Figure Lengend Snippet: (A) Depletion of YAP1, but not TAZ, resulted in decreased VEGF promoter luciferase activity in hypoxic A549 and H1650 cells in a transient transfection assay. (B) RT-qPCRs showed decreased expression of endogenous VEGF mRNA in A549 cells transfected with YAP1 siRNA and subjected to hypoxia. Such a change was not observed when TAZ was depleted in the A549 cells. (C) Similarly, depletion of YAP1, but not TAZ, decreased VEGF promoter luciferase activity in A549 and H1650 cells treated with 1mM DMOG as compared to control vehicle treated cells. (D) The expression of endogenous VEGF mRNA was reduced when A549 cells were transfected with YAP1 siRNA but not TAZ siRNA; cells treated with 1mM DMOG showed the same result. (E) YAP1 and HIF1α overexpression showed an increased effect on VEGF promoter luciferase activity in transient transfections in A549 and H1650 cells. (F) Loss of VEGF-luc promoter luciferase activity in transient transfection assays upon HIF1α depletion when YAP1 was overexpressed; no significant change was observed with the depletion of TEAD2 or TEAD4 using two different siRNAs for each. (G) RT-qPCRs showed an increase in endogenous VEGF mRNA expression in A549 cells when YAP1 was overexpressed. However, this increase in endogenous VEGF mRNA was less when HIF1α was depleted in the presence of YAP1. The depletion of TEAD2 or TEAD4 did not affect the expression of endogenous VEGF mRNA expression, when YAP1 was overexpressed. (H) ChIP-qPCR analysis performed in normoxic and hypoxic A549 cells with the indicated antibodies showed increased presence of YAP1 at the HIF1α binding sites on VEGF promoter at position −866 to −987 bp, upstream of transcription start site in the hypoxic A549 cells. (I) A site-directed mutation in the HIF1α binding site on the VEGF promoter (mutVEGF-Luc) abrogated promoter luciferase activity induced by YAP1. The bar graphs in this panel represents mean ± SEM of three independent experiments. * p <0.05 and ** p<0.01 derived by two-way ANOVA with post-hoc test.

Article Snippet: The two different siRNAs for YAP1 were purchased from Santa Cruz Biotechnologies (sc-38637) and ThermoFisher Scientific (107951) respectively. siRNAs For TAZ (sc-45232), MST1 (sc-39249), MST2 (sc-39247), LATS2 (sc-37444), HIF1α (sc-35561), PHD2 (sc-45537), PHD3 (sc-45799), TEAD2 (sc-45232) and TEAD4 (sc-96187) were purchased from Santa Cruz Biotechnologies. siRNAs for LATS1 (137593), HIF1α (106498), TAZ (122501), TEAD2 (107179), TEAD4 (115367), PHD2 (133478) and PHD3 (128749) were purchased from ThermoFisher Scientific.

Techniques: Luciferase, Activity Assay, Transient Transfection Assay, Expressing, Transfection, Control, Over Expression, ChIP-qPCR, Binding Assay, Mutagenesis, Derivative Assay

(A) Treatment with 1mM DMOG for 24h elevated YAP1 protein levels in A549 and H1650 cells as compared to control vehicle treated cells, as seen by western blotting. There was no notable change in YAP1 phosphorylation (B) Depletion of PHD2, but not PHD3, with two different siRNAs in A549 cells showed an increase in YAP1 protein levels as compared to control siRNA transfected cells. (C) Depletion of PHD2, but not HIF1α, elevates the levels of total YAP1 in A549 cells. Depleting HIF1α along with PHD2 also elevated YAP1 levels under normoxic conditions. (D) Proximity ligation assay revealed that YAP1 associates with PHD2 and this interaction decreases upon hypoxia (1% O2) exposure for 24h in both A549 and H1650 cells. Scale bar 10 μm, Blue –DAPI, Red – YAP1/PHD2 PLA foci. (E) Single YAP1 or PHD2 antibody used as negative controls in the above PLA experiment. (F) Co-immunoprecipitation assay in normoxic and hypoxic cells further confirmed that YAP1 directly interacts with PHD2 and the association is decreased in hypoxic cells. TAZ was also found to associate with PHD2 but no significant difference was observed in its levels between normoxic and hypoxic conditions. (G) Depletion of PHD2 by two different siRNAs eliminate the prolyl hydroxylation of YAP1, as seen in an IP-Western blot experiment on A549 cells. (H) A ubiquitin immunoprecipitation in PHD2-depleted A549 cells showed a decrease in ubiquitination of YAP1 proteins compared to the control siRNA treated cells.

Journal: Cancer research communications

Article Title: A Novel PHD2/VHL-mediated Regulation of YAP1 Contributes to VEGF Expression and Angiogenesis

doi: 10.1158/2767-9764.crc-21-0084

Figure Lengend Snippet: (A) Treatment with 1mM DMOG for 24h elevated YAP1 protein levels in A549 and H1650 cells as compared to control vehicle treated cells, as seen by western blotting. There was no notable change in YAP1 phosphorylation (B) Depletion of PHD2, but not PHD3, with two different siRNAs in A549 cells showed an increase in YAP1 protein levels as compared to control siRNA transfected cells. (C) Depletion of PHD2, but not HIF1α, elevates the levels of total YAP1 in A549 cells. Depleting HIF1α along with PHD2 also elevated YAP1 levels under normoxic conditions. (D) Proximity ligation assay revealed that YAP1 associates with PHD2 and this interaction decreases upon hypoxia (1% O2) exposure for 24h in both A549 and H1650 cells. Scale bar 10 μm, Blue –DAPI, Red – YAP1/PHD2 PLA foci. (E) Single YAP1 or PHD2 antibody used as negative controls in the above PLA experiment. (F) Co-immunoprecipitation assay in normoxic and hypoxic cells further confirmed that YAP1 directly interacts with PHD2 and the association is decreased in hypoxic cells. TAZ was also found to associate with PHD2 but no significant difference was observed in its levels between normoxic and hypoxic conditions. (G) Depletion of PHD2 by two different siRNAs eliminate the prolyl hydroxylation of YAP1, as seen in an IP-Western blot experiment on A549 cells. (H) A ubiquitin immunoprecipitation in PHD2-depleted A549 cells showed a decrease in ubiquitination of YAP1 proteins compared to the control siRNA treated cells.

Article Snippet: The two different siRNAs for YAP1 were purchased from Santa Cruz Biotechnologies (sc-38637) and ThermoFisher Scientific (107951) respectively. siRNAs For TAZ (sc-45232), MST1 (sc-39249), MST2 (sc-39247), LATS2 (sc-37444), HIF1α (sc-35561), PHD2 (sc-45537), PHD3 (sc-45799), TEAD2 (sc-45232) and TEAD4 (sc-96187) were purchased from Santa Cruz Biotechnologies. siRNAs for LATS1 (137593), HIF1α (106498), TAZ (122501), TEAD2 (107179), TEAD4 (115367), PHD2 (133478) and PHD3 (128749) were purchased from ThermoFisher Scientific.

Techniques: Control, Western Blot, Phospho-proteomics, Transfection, Proximity Ligation Assay, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Immunoprecipitation