Charles Y. Lin
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View article: Table S2 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Table S2 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Table S2: Proteogenomic fold-change data (PTPN12 normal vs deficient) (related to Figure 2).
View article: Data from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Data from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with few effective targeted therapies. Taxanes and other microtubule-targeting agents (MTA) are first-line chemotherapies for TNBC; however, the molecular mecha…
View article: Table S1 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Table S1 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Table S1: PDX proteogenomic data (related to Figure 2).
View article: Table S4 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Table S4 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Table S4: Integrated GSEA analysis (related to Figure 3).
View article: Figure S1 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S1 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S1: Integration of proteogenomics and functional genetics to reveal novel vulnerabilities in TNBC (related to Figure 1).
View article: Table S3 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Table S3 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Table S3: PTPN12-selective growth modifiers (related to Figure 3).
View article: Figure S6 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S6 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S6: PTPN12-deficient primary TNBC are sensitive to taxane chemotherapy (related to Figure 6).
View article: Figure S5 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S5 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S5: PTPN12-deficient cells exhibit mitotic defects dependent on APCFZR1 hyperactivation (related to Figure 5).
View article: Figure S2 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S2 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S2: PTPN12-deficient models exhibit downregulation of cell cycle and mitotic pathways (related to Figure 2).
View article: Figure S4 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S4 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S4: PTPN12 deficiency causes aberrant degradation of APCFZR1 substrates (related to Figure 4).
View article: Figure S3 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer
Figure S3 from Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer Open
Figure S3: PTPN12-deficient cells are vulnerable to perturbation of mitotic regulators (related to Figure 3).
View article: Recent Developments in Amber Biomolecular Simulations
Recent Developments in Amber Biomolecular Simulations Open
Amber is a molecular dynamics (MD) software package first conceived by Peter Kollman, his lab and collaborators to simulate biomolecular systems. The pmemd module is available as a serial version for central processing units (CPUs),…
View article: Data from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Data from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Upregulation of MYC is a hallmark of cancer, wherein MYC drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels cancer growth and survival, the con…
View article: Table S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S2 shows gene ontology analysis of candidate facilitator genes of MYC-induced cell death.
View article: Table S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S1 is the list of candidate facilitator genes of MYC-induced cell death. Table lists the candidate facilitators of MYC-induced cell death discovered through the MYC-specific loss of function genetic screen.
View article: Figure S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S2 shows MYC-induced cell death in MYC-ER HMECs with DIS3L, EXOSC2, EXOSC8 and DIS3 knockdown, expression of DIS3L, EXOSC2, EXOSC8 and DIS3 upon knockdown, and MYC-induced EU incorporation in MYC-hyperactivated conditions.
View article: Table S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S1 is the list of candidate facilitator genes of MYC-induced cell death. Table lists the candidate facilitators of MYC-induced cell death discovered through the MYC-specific loss of function genetic screen.
View article: Figure S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S2 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S2 shows MYC-induced cell death in MYC-ER HMECs with DIS3L, EXOSC2, EXOSC8 and DIS3 knockdown, expression of DIS3L, EXOSC2, EXOSC8 and DIS3 upon knockdown, and MYC-induced EU incorporation in MYC-hyperactivated conditions.
View article: Data from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Data from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Upregulation of MYC is a hallmark of cancer, wherein MYC drives oncogenic gene expression and elevates total RNA synthesis across cancer cell transcriptomes. Although this transcriptional anabolism fuels cancer growth and survival, the con…
View article: Figure S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S3 shows MYC-induced apoptosis and cell death in early and late timepoints, ectopic expression of BCL2 and its impact on MYC-induced RNA decay, gene expression changes upon DIS3L knockdown in MYC-hyperactivated conditions, and expre…
View article: Table S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S4 shows predictions of hypothetical purine nucleotide flux.
View article: Table S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S4 shows predictions of hypothetical purine nucleotide flux.
View article: Figure S6 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S6 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S6 shows 6-mercaptopurine dose curve in various cell lines, effect of 6-mercaptopurine on purine catabolite abundance in TNBC cells, effect of XDH knockdown on 6-mercaptopurine induced cell death, and 6-mercaptopurine- induced effec…
View article: Figure S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S4 shows DIS3L mutation in human tumors, evolutionary action score of tumor-derived mutation in DIS3L, genomic alteration of MYC and DIS3L in human breast cancer, expression of DIS3L mRNA in human breast tumors, and expression of ge…
View article: Figure S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S1 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S1 shows PCA of human breast tumors, hallmark MYC signature score for human breast tumors, expression of MYC-target NECTIN4, schematic for purine ribonucleotide catabolism, concentrations of nucleotides in physiological conditions, …
View article: Figure S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S4 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S4 shows DIS3L mutation in human tumors, evolutionary action score of tumor-derived mutation in DIS3L, genomic alteration of MYC and DIS3L in human breast cancer, expression of DIS3L mRNA in human breast tumors, and expression of ge…
View article: Table S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Table S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Table S3 shows evolutionary Action analysis of tumor-derived mutation in DIS3L.
View article: Figure S5 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S5 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S5 shows expression of MCL1 upon DIS3L knockdown, effect of XDH inhibition on MYC-induced cell death, effect of xanthosine on TNBC apoptosis, ROS and MYC-induced cell death, MYC-induced cell death upon HPRT1 knockdown, and expressio…
View article: Figure S6 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S6 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S6 shows 6-mercaptopurine dose curve in various cell lines, effect of 6-mercaptopurine on purine catabolite abundance in TNBC cells, effect of XDH knockdown on 6-mercaptopurine induced cell death, and 6-mercaptopurine- induced effec…
View article: Figure S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer
Figure S3 from MYC Induces Oncogenic Stress through RNA Decay and Ribonucleotide Catabolism in Breast Cancer Open
Figure S3 shows MYC-induced apoptosis and cell death in early and late timepoints, ectopic expression of BCL2 and its impact on MYC-induced RNA decay, gene expression changes upon DIS3L knockdown in MYC-hyperactivated conditions, and expre…