Anderly C. Chüeh
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View article: Activation of CAMK2 by pseudokinase PEAK1 represents a targetable pathway in triple negative breast cancer
Activation of CAMK2 by pseudokinase PEAK1 represents a targetable pathway in triple negative breast cancer Open
The PEAK family of pseudokinases, comprising PEAK1-3, play oncogenic roles in several poor prognosis human cancers, including triple negative breast cancer (TNBC). However, therapeutic targeting of pseudokinases is challenging due to their…
View article: Supplementary Data from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Notes, Supplementary Figures, and Supplementary Figure Legends
View article: Supplementary Data S1 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data S1 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Data S1 - SBML model file
View article: Supplementary Data S2 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data S2 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Data S2
View article: Supplementary Data S5 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data S5 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Data S5
View article: Supplementary Data S3 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data S3 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Data S3
View article: Data from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Data from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Oncogenic FGFR4 signaling represents a potential therapeutic target in various cancer types, including triple-negative breast cancer and hepatocellular carcinoma. However, resistance to FGFR4 single-agent therapy remains a major challenge,…
View article: Supplementary Data S4 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers
Supplementary Data S4 from Integrative Modeling of Signaling Network Dynamics Identifies Cell Type–Selective Therapeutic Strategies for FGFR4-Driven Cancers Open
Supplementary Data S4
View article: Feed-forward stimulation of CAMK2 by the oncogenic pseudokinase PEAK1 generates a therapeutically ‘actionable’ signalling axis in triple negative breast cancer
Feed-forward stimulation of CAMK2 by the oncogenic pseudokinase PEAK1 generates a therapeutically ‘actionable’ signalling axis in triple negative breast cancer Open
Summary The PEAK family of pseudokinases, comprising PEAK1-3, are signalling scaffolds that play oncogenic roles in several poor prognosis human cancers, including triple negative breast cancer (TNBC). However, therapeutic targeting of pse…
View article: Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies
Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies Open
View article: Correction: ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors Across Tumor Types
Correction: ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors Across Tumor Types Open
In the original version of this article (1), Fig. 3A used the same b-tubulin control for FOS and JUN, and the legend for Fig. 4 did not clarify that the same HCT116 b-
View article: Discovery of a highly potent, selective, orally bioavailable inhibitor of KAT6A/B histone acetyltransferases with efficacy against KAT6A-high ER+ breast cancer
Discovery of a highly potent, selective, orally bioavailable inhibitor of KAT6A/B histone acetyltransferases with efficacy against KAT6A-high ER+ breast cancer Open
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Supplementary Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Supplementary Data from ATF3 Repression of BCL-XL Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
View article: Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types
Data from ATF3 Repression of BCL-X<sub>L</sub> Determines Apoptotic Sensitivity to HDAC Inhibitors across Tumor Types Open
Purpose:Histone deacetylase inhibitors (HDACi) are epigenome-targeting small molecules approved for the treatment of cutaneous T-cell lymphoma and multiple myeloma. They have also demonstrated clinical activity in acute myelogenous leukemi…
View article: Supplementary Figure 4 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 4 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Basal MYC (A) mRNA and (B) protein expression in 20 CRC cell lines. Correlation of c-MYC (C) mRNA and (D) protein with JQ1 response.
View article: Supplementary Figure 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
BET protein expression in primary colorectal cancers.
View article: Data from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Data from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Inhibitors of the bromodomain and extraterminal domain (BET) protein family attenuate the proliferation of several tumor cell lines. These effects are mediated, at least in part, through repression of c-MYC. In colorectal cancer, overexpre…
View article: Supplementary Figure legends from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure legends from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Legends to supplementary Figures
View article: Supplementary Figure 3 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 3 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Biomarkers of response to JQ1 in colorectal cancer cell lines.
View article: Supplementary Figure 3 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 3 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Biomarkers of response to JQ1 in colorectal cancer cell lines.
View article: Supplementary Figure 1 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 1 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
BET protein expression in 20 colon cancer cell lines.
View article: Supplementary Figure legends from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure legends from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Legends to supplementary Figures
View article: Supplementary Table 1 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Table 1 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Sequences of primers used.
View article: Supplementary Figure 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Figure 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
BET protein expression in primary colorectal cancers.
View article: Supplementary Table 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells
Supplementary Table 2 from Dual Targeting of Bromodomain and Extraterminal Domain Proteins, and WNT or MAPK Signaling, Inhibits c-MYC Expression and Proliferation of Colorectal Cancer Cells Open
Genotypes of colorectal cancer cell lines.