Zachary T. Schug
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View article: ACSS1-dependent acetate utilization rewires mitochondrial metabolism to support AML and melanoma tumor growth and metastasis
ACSS1-dependent acetate utilization rewires mitochondrial metabolism to support AML and melanoma tumor growth and metastasis Open
View article: Identification of Fasnall as a therapeutically effective Complex I inhibitor
Identification of Fasnall as a therapeutically effective Complex I inhibitor Open
Proliferating cancer cells actively utilize anabolic processes for biomass production, including de novo biosynthesis of amino acids, nucleotides, and fatty acids. The key enzyme of the fatty acid biosynthesis pathway, fatty acid synthase …
View article: Acetate acts as a metabolic immunomodulator by bolstering T-cell effector function and potentiating antitumor immunity in breast cancer
Acetate acts as a metabolic immunomodulator by bolstering T-cell effector function and potentiating antitumor immunity in breast cancer Open
View article: Co-Targeting FASN and mTOR Suppresses Uveal Melanoma Growth
Co-Targeting FASN and mTOR Suppresses Uveal Melanoma Growth Open
Uveal melanoma (UM) displays a high frequency of metastasis; however, effective therapies for metastatic UM are limited. Identifying unique metabolic features of UM may provide a potential targeting strategy. A lipid metabolism protein exp…
View article: Supplementary Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Supplementary Figures and Legends.
View article: Supplementary Movie 2 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Movie 2 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Aged BODIPY-C12 fibroblasts with GFP-tagged melanoma cells
View article: Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Older patients with melanoma (>50 years old) have poorer prognoses and response rates to targeted therapy compared with young patients (Significance:These data show that melanoma cells take up lipids from aged fibroblasts, via FATP2, and u…
View article: Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Older patients with melanoma (>50 years old) have poorer prognoses and response rates to targeted therapy compared with young patients (Significance:These data show that melanoma cells take up lipids from aged fibroblasts, via FATP2, and u…
View article: Supplementary Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Data from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Supplementary Figures and Legends.
View article: Supplementary Movie 1 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Movie 1 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Young BODIPY-C12 fibroblasts with GFP-Tagged melanoma cells showing lipid uptake
View article: Supplementary Movie 2 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Movie 2 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Aged BODIPY-C12 fibroblasts with GFP-tagged melanoma cells
View article: Supplementary Movie 1 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
Supplementary Movie 1 from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2 Open
Young BODIPY-C12 fibroblasts with GFP-Tagged melanoma cells showing lipid uptake
View article: Supplemental Video from Syntaphilin Regulates Neutrophil Migration in Cancer
Supplemental Video from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Supplemental Video
View article: Data from Syntaphilin Regulates Neutrophil Migration in Cancer
Data from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Pathologically activated neutrophils (PMN) with immunosuppressive activity, which are termed myeloid-derived suppressor cells (PMN-MDSC), play a critical role in regulating tumor progression. These cells have been implicated in promoting t…
View article: Supplemental Figures and Tables from Syntaphilin Regulates Neutrophil Migration in Cancer
Supplemental Figures and Tables from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Supplemental Figures, legends and tables
View article: Data from Syntaphilin Regulates Neutrophil Migration in Cancer
Data from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Pathologically activated neutrophils (PMN) with immunosuppressive activity, which are termed myeloid-derived suppressor cells (PMN-MDSC), play a critical role in regulating tumor progression. These cells have been implicated in promoting t…
View article: Supplemental Figures and Tables from Syntaphilin Regulates Neutrophil Migration in Cancer
Supplemental Figures and Tables from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Supplemental Figures, legends and tables
View article: Supplemental Video from Syntaphilin Regulates Neutrophil Migration in Cancer
Supplemental Video from Syntaphilin Regulates Neutrophil Migration in Cancer Open
Supplemental Video
View article: Supplementary Figure 7 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 7 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
Significant differential abundance analysis of lipids as a heat map. A. MDA-MB-468 and B. PC3 spheroids were treated for 4 days with inhibitors against metabolic enzymes PDHK, ACC, FASN and DGAT, and kinases PI3K, AKT and mTOR at two diffe…
View article: Figure S7 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Figure S7 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Figure S7 shows PPARg as a therapeutic target for brain metastasis.
View article: Supplementary Figure 8 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 8 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
Analysis of saturated, mono-unsaturated and poly-unsaturated phospholipids in MDA-MB-468 and PC3 spheroids. Levels of PC, PE, PI, PS, and SM in MDA-MB-468 and PC3 spheroids treated with inhibitors against metabolic enzymes PDHK, ACC, FASN …
View article: Figure S7 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Figure S7 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Figure S7 shows PPARg as a therapeutic target for brain metastasis.
View article: Supplementary Figure 3 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 3 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
GI50 calculation of spheroids treated with inhibitors. (A) MDA-MB-468 on day 8 and (B) PC3 spheroids on day 12 treated with inhibitors against metabolic enzymes PDHK, ACC, FASN and DGAT, and signalling enzymes PI3K, Akt and mTOR. Between 5…
View article: Figure S4 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Figure S4 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Figure S4 shows gene set variation analyses (GSVA) of PPAR and EIF2 pathways in WM4265.2-BrMs.
View article: Figure S4 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Figure S4 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Figure S4 shows gene set variation analyses (GSVA) of PPAR and EIF2 pathways in WM4265.2-BrMs.
View article: Figure S6 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Figure S6 from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Figure S6 shows exogenous AA, but not DHA promotes the growth of BrM cells.
View article: Supplementary Figure 3 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 3 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
GI50 calculation of spheroids treated with inhibitors. (A) MDA-MB-468 on day 8 and (B) PC3 spheroids on day 12 treated with inhibitors against metabolic enzymes PDHK, ACC, FASN and DGAT, and signalling enzymes PI3K, Akt and mTOR. Between 5…
View article: Supplementary Figure 5 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 5 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
Clustered heat map analysis of lipids in MDA-MB-468 and PC3 spheroids treated for 4 days with A. FASN and B. DGAT inhibitor at different concentrations. All Lipids were compared against DMSO control. Side covariates indicate lipid families…
View article: Supplementary Figure 6 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers
Supplementary Figure 6 from 3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers Open
Clustered heat map analysis of lipids in MDA-MB-468 and PC3 spheroids treated for 4 days with A. ACC and B. PDHK inhibitor at different concentrations. All Lipids were compared against DMSO control. Side covariates indicate lipid families,…
View article: Data from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis
Data from Polyunsaturated Fatty Acids from Astrocytes Activate PPARγ Signaling in Cancer Cells to Promote Brain Metastasis Open
Brain metastasis, the most lethal form of melanoma and carcinoma, is the consequence of favorable interactions between the invading cancer cells and the brain cells. Peroxisome proliferator–activated receptor γ (PPARγ) has ambiguous functi…