Seth J. Parker
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View article: Metabolomics analysis of SNAT2-deficient cells: Implications for the discovery of selective small-molecule inhibitors of an amino acid transporter
Metabolomics analysis of SNAT2-deficient cells: Implications for the discovery of selective small-molecule inhibitors of an amino acid transporter Open
Amino acid uptake by the solute carrier family of transporter proteins is critical to support cell metabolism, and inhibition of transporter activity represents a tractable strategy to restrict nutrient availability to cancer cells. A smal…
View article: Restricting lysine normalizes toxic catabolites associated with ALDH7A1 deficiency in cells and mice
Restricting lysine normalizes toxic catabolites associated with ALDH7A1 deficiency in cells and mice Open
Lysine metabolism converges at α-aminoadipic semialdehyde dehydrogenase (ALDH7A1). Rare loss-of-function mutations in ALDH7A1 cause a toxic accumulation of lysine catabolites, including piperideine-6-carboxylate (P6C), that are thought to …
View article: Proteomics and personalized patient-derived xenograft models identify treatment opportunities for a progressive malignancy within a clinically actionable timeframe and change care
Proteomics and personalized patient-derived xenograft models identify treatment opportunities for a progressive malignancy within a clinically actionable timeframe and change care Open
Increased access to high-throughput DNA sequencing platforms has transformed the diagnostic landscape of pediatric malignancies by identifying and integrating actionable genomic or transcriptional features that refine diagnosis, classifica…
View article: Targeting pancreatic cancer metabolic dependencies through glutamine antagonism
Targeting pancreatic cancer metabolic dependencies through glutamine antagonism Open
Pancreatic ductal adenocarcinoma (PDAC) cells use glutamine (Gln) to support proliferation and redox balance. Early attempts to inhibit Gln metabolism using glutaminase inhibitors resulted in rapid metabolic reprogramming and therapeutic r…
View article: A Peptidisc-Based Survey of the Plasma Membrane Proteome of a Mammalian Cell
A Peptidisc-Based Survey of the Plasma Membrane Proteome of a Mammalian Cell Open
Membrane proteins play critical roles at the cell surface and their misfunction is a hallmark of many human diseases. A precise evaluation of the plasma membrane proteome is therefore essential for cell biology and for discovering novel bi…
View article: Table S2. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S2. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S2. Patient Cohort Characteristics
View article: Supplementary Figures from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Supplementary Figures from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Supplementary.Figures 1-8
View article: Supplemental Information from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Supplemental Information from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Supplemental Methods and Supplemental Figure Legends
View article: Table S3. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S3. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S3.FPKM values for all genes identified through RNA-sequencing
View article: Table S5. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S5. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S5: Results of RNA sequencing in PDA cell lines (HS-766T and MiaPaCa2) with each modulated by CRISPR/Cas9 to delete HuR expression.
View article: Table S1. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S1. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S1: Nomenclature used throughout manuscript to describe genetically modified cell lines.
View article: Supplementary Figures from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Supplementary Figures from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Supplementary.Figures 1-8
View article: Supplemental Information from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Supplemental Information from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Supplemental Methods and Supplemental Figure Legends
View article: Table S4. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S4. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S4. List of Enzymes directly involved in the anti-oxidant defense response.
View article: Table S5. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S5. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S5: Results of RNA sequencing in PDA cell lines (HS-766T and MiaPaCa2) with each modulated by CRISPR/Cas9 to delete HuR expression.
View article: Data from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Data from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Cancer aggressiveness may result from the selective pressure of a harsh nutrient-deprived microenvironment. Here we illustrate how such conditions promote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Glucose or gluta…
View article: Table S1. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S1. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S1: Nomenclature used throughout manuscript to describe genetically modified cell lines.
View article: Table S2. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S2. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S2. Patient Cohort Characteristics
View article: Table S4. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S4. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S4. List of Enzymes directly involved in the anti-oxidant defense response.
View article: Table S3. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Table S3. from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Table S3.FPKM values for all genes identified through RNA-sequencing
View article: Data from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells
Data from Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells Open
Cancer aggressiveness may result from the selective pressure of a harsh nutrient-deprived microenvironment. Here we illustrate how such conditions promote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Glucose or gluta…
View article: Supplementary Figures 1 - 6 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Supplementary Figures 1 - 6 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
PDF file - 348KB, Figure S1: Isogenic IDH1 mutation compromises metabolic reprogramming under hypoxia. Figure S2: Simulated and measured uncorrected MIDs. Figure S3: Compromised Reductive TCA Metabolism is specific to cells with mutant IDH…
View article: Supplementary Methods, Figure Legends from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Supplementary Methods, Figure Legends from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
PDF file - 136KB
View article: Data from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Data from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in several types of cancer, but the metabolic consequences of these genetic changes are not fully understood. In this study, we performed 13C metabolic flux analysis on…
View article: Supplementary Methods, Figure Legends from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Supplementary Methods, Figure Legends from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
PDF file - 136KB
View article: Supplementary Figures 1 - 6 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Supplementary Figures 1 - 6 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
PDF file - 348KB, Figure S1: Isogenic IDH1 mutation compromises metabolic reprogramming under hypoxia. Figure S2: Simulated and measured uncorrected MIDs. Figure S3: Compromised Reductive TCA Metabolism is specific to cells with mutant IDH…
View article: Data from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism
Data from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism Open
Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in several types of cancer, but the metabolic consequences of these genetic changes are not fully understood. In this study, we performed 13C metabolic flux analysis on…