HY-139400 Search Results


mrtx849  (MedChemExpress)
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MedChemExpress mrtx849
( A ) Heatmap displaying the resistance index of ARS1620, AMG510, and <t>MRTX849</t> across various KRAS G12C–mutant cancer cell lines. ( B ) Venn diagram illustrating the overlapping relationships among 3 gene sets associated with resistance to KRAS G12C inhibitors as in . ( C ) Bar chart presenting the top 10 regulatory factors involved in modulating a set of 134 genes highlighted with white font in B . ( D ) Network graph visualizing the interplay between these 10 regulatory factors. ( E ) Quantification of immunofluorescence depicting the subcellular localization of YAP/TAZ in the indicated cells as in . ( F ) Box-and-whisker plots (bulk RNA-seq) presenting YAP Lisa scores in parental cells and KRAS G12C inhibitor–resistant cells. ( G ) Box-and-whisker plot (left, bulk RNA-seq) and ridge plot (right, scRNA-seq) displaying YAP UP scores in H358 cells treated with ARS1620 for the indicated duration. ( H ) tSNE plots showing single-cell clustering (left) and YAP UP scores (right) in H358 cells treated with ARS1620 for indicated durations. ( I ) Immunoblots demonstrating changes in YAP/TAZ and ERK phosphorylation levels in intrinsically resistant cells (H2030, SW1573) before and after AMG510 treatment, and following the withdrawal of the drug. ( J and K ) Immunoblots ( J ) and line graph ( K ) illustrating the temporal dynamics of YAP phosphorylation in sensitive cells (H358) and resistant cells (SW1573) in response to AMG510 treatment. Data were analyzed using Student’s t test ( F ) or 1-way ANOVA followed by Tukey’s test for multiple comparisons ( G ). Blots provided together were set up in parallel at the same time ( I and J ).
Mrtx849, supplied by MedChemExpress, 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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Image Search Results


( A ) Heatmap displaying the resistance index of ARS1620, AMG510, and MRTX849 across various KRAS G12C–mutant cancer cell lines. ( B ) Venn diagram illustrating the overlapping relationships among 3 gene sets associated with resistance to KRAS G12C inhibitors as in . ( C ) Bar chart presenting the top 10 regulatory factors involved in modulating a set of 134 genes highlighted with white font in B . ( D ) Network graph visualizing the interplay between these 10 regulatory factors. ( E ) Quantification of immunofluorescence depicting the subcellular localization of YAP/TAZ in the indicated cells as in . ( F ) Box-and-whisker plots (bulk RNA-seq) presenting YAP Lisa scores in parental cells and KRAS G12C inhibitor–resistant cells. ( G ) Box-and-whisker plot (left, bulk RNA-seq) and ridge plot (right, scRNA-seq) displaying YAP UP scores in H358 cells treated with ARS1620 for the indicated duration. ( H ) tSNE plots showing single-cell clustering (left) and YAP UP scores (right) in H358 cells treated with ARS1620 for indicated durations. ( I ) Immunoblots demonstrating changes in YAP/TAZ and ERK phosphorylation levels in intrinsically resistant cells (H2030, SW1573) before and after AMG510 treatment, and following the withdrawal of the drug. ( J and K ) Immunoblots ( J ) and line graph ( K ) illustrating the temporal dynamics of YAP phosphorylation in sensitive cells (H358) and resistant cells (SW1573) in response to AMG510 treatment. Data were analyzed using Student’s t test ( F ) or 1-way ANOVA followed by Tukey’s test for multiple comparisons ( G ). Blots provided together were set up in parallel at the same time ( I and J ).

Journal: JCI Insight

Article Title: YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis

doi: 10.1172/jci.insight.178535

Figure Lengend Snippet: ( A ) Heatmap displaying the resistance index of ARS1620, AMG510, and MRTX849 across various KRAS G12C–mutant cancer cell lines. ( B ) Venn diagram illustrating the overlapping relationships among 3 gene sets associated with resistance to KRAS G12C inhibitors as in . ( C ) Bar chart presenting the top 10 regulatory factors involved in modulating a set of 134 genes highlighted with white font in B . ( D ) Network graph visualizing the interplay between these 10 regulatory factors. ( E ) Quantification of immunofluorescence depicting the subcellular localization of YAP/TAZ in the indicated cells as in . ( F ) Box-and-whisker plots (bulk RNA-seq) presenting YAP Lisa scores in parental cells and KRAS G12C inhibitor–resistant cells. ( G ) Box-and-whisker plot (left, bulk RNA-seq) and ridge plot (right, scRNA-seq) displaying YAP UP scores in H358 cells treated with ARS1620 for the indicated duration. ( H ) tSNE plots showing single-cell clustering (left) and YAP UP scores (right) in H358 cells treated with ARS1620 for indicated durations. ( I ) Immunoblots demonstrating changes in YAP/TAZ and ERK phosphorylation levels in intrinsically resistant cells (H2030, SW1573) before and after AMG510 treatment, and following the withdrawal of the drug. ( J and K ) Immunoblots ( J ) and line graph ( K ) illustrating the temporal dynamics of YAP phosphorylation in sensitive cells (H358) and resistant cells (SW1573) in response to AMG510 treatment. Data were analyzed using Student’s t test ( F ) or 1-way ANOVA followed by Tukey’s test for multiple comparisons ( G ). Blots provided together were set up in parallel at the same time ( I and J ).

Article Snippet: Verteporfin, MRTX849, and buparlisib were supplied by MedChemExpress.

Techniques: Mutagenesis, Immunofluorescence, Whisker Assay, RNA Sequencing Assay, Western Blot

( A ) Dose-response curves depicting the relative viability of H358, H1373, and MIAPACA2 cells with or without ectopic expression of constantly activated YAP or TAZ under treatment with ARS1620, AMG510, or MRTX849 for 5 days. ( B ) Dot plots displaying the quantification of clonogenic assay showing the growth of H358 and MIAPACA2 cells with or without ectopic expression of constantly activated YAP or TAZ upon treatment with KRAS G12C inhibitors as in . ( C ) Dose-response curves presenting the relative viability of KYSE410, H2030, and SW1573 cells with or without knockdown of YAP/TAZ or TEADs under treatment with ARS1620, AMG510, or MRTX849 for 5 days. ( D ) Dot plots depicting the IC 50 values (median of at least triplicate experiments) of different cell lines with or without knockdown of YAP/TAZ or TEADs under treatment with the indicated KRAS G12C inhibitors for 5 days. ( E and F ) Dot plots displaying the quantification of clonogenic assay showing the growth of SW1573 and H2030 cells with or without knockdown of YAP/TAZ upon treatment with KRAS G12C inhibitors as in . Data are presented as mean ± SEM ( A and C ) or mean ± SD ( B , E , and F ).

Journal: JCI Insight

Article Title: YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis

doi: 10.1172/jci.insight.178535

Figure Lengend Snippet: ( A ) Dose-response curves depicting the relative viability of H358, H1373, and MIAPACA2 cells with or without ectopic expression of constantly activated YAP or TAZ under treatment with ARS1620, AMG510, or MRTX849 for 5 days. ( B ) Dot plots displaying the quantification of clonogenic assay showing the growth of H358 and MIAPACA2 cells with or without ectopic expression of constantly activated YAP or TAZ upon treatment with KRAS G12C inhibitors as in . ( C ) Dose-response curves presenting the relative viability of KYSE410, H2030, and SW1573 cells with or without knockdown of YAP/TAZ or TEADs under treatment with ARS1620, AMG510, or MRTX849 for 5 days. ( D ) Dot plots depicting the IC 50 values (median of at least triplicate experiments) of different cell lines with or without knockdown of YAP/TAZ or TEADs under treatment with the indicated KRAS G12C inhibitors for 5 days. ( E and F ) Dot plots displaying the quantification of clonogenic assay showing the growth of SW1573 and H2030 cells with or without knockdown of YAP/TAZ upon treatment with KRAS G12C inhibitors as in . Data are presented as mean ± SEM ( A and C ) or mean ± SD ( B , E , and F ).

Article Snippet: Verteporfin, MRTX849, and buparlisib were supplied by MedChemExpress.

Techniques: Expressing, Clonogenic Assay, Knockdown

( A ) Immunoblots revealing the expression levels and phosphorylation status of MEK, ERK, RSK, and S6 in H358, H358R, and H358R N20 cells after treatment with AMG510 (1 μM) for 3 days. ( B – D ) Immunoblots displaying the levels of p-S6 and S6 in H358, KYSE410, and SW1573 cells with or without knockdown of YAP/TAZ under treatment with ARS1620 ( B ), AMG510 ( C ), or MRTX849 ( D ) as indicated. This panel was excerpted from . Blots provided together were set up in parallel at the same time ( A – D ).

Journal: JCI Insight

Article Title: YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis

doi: 10.1172/jci.insight.178535

Figure Lengend Snippet: ( A ) Immunoblots revealing the expression levels and phosphorylation status of MEK, ERK, RSK, and S6 in H358, H358R, and H358R N20 cells after treatment with AMG510 (1 μM) for 3 days. ( B – D ) Immunoblots displaying the levels of p-S6 and S6 in H358, KYSE410, and SW1573 cells with or without knockdown of YAP/TAZ under treatment with ARS1620 ( B ), AMG510 ( C ), or MRTX849 ( D ) as indicated. This panel was excerpted from . Blots provided together were set up in parallel at the same time ( A – D ).

Article Snippet: Verteporfin, MRTX849, and buparlisib were supplied by MedChemExpress.

Techniques: Western Blot, Expressing, Knockdown