Ron A. Hoebe
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View article: Senolytic treatment to rescue hallmarks of senescence in lymph node fibroblasts from patients with rheumatoid arthritis: Implications for premature aging and potential therapeutic intervention in early rheumatoid arthritis
Senolytic treatment to rescue hallmarks of senescence in lymph node fibroblasts from patients with rheumatoid arthritis: Implications for premature aging and potential therapeutic intervention in early rheumatoid arthritis Open
Cellular senescence, a state of proliferation arrest, is implicated in the pathogenesis of age-related diseases such as rheumatoid arthritis (RA). The pathogenesis of RA, characterized by immune dysregulation and systemic autoimmunity prec…
View article: Super-resolution GSDIM microscopy unveils distinct nanoscale characteristics of DNA repair foci under diverse genotoxic stress
Super-resolution GSDIM microscopy unveils distinct nanoscale characteristics of DNA repair foci under diverse genotoxic stress Open
DNA double-strand breaks initiate the DNA damage response (DDR), leading to the accumulation of repair proteins at break sites and the formation of the-so-called foci. Various microscopy methods, such as wide-field, confocal, electron, and…
View article: Perturbation of Copper Homeostasis Sensitizes Cancer Cells to Elevated Temperature
Perturbation of Copper Homeostasis Sensitizes Cancer Cells to Elevated Temperature Open
Temporary elevation of tumor temperature, also known as hyperthermia, is a safe and well-tolerated treatment modality. The efficacy of hyperthermia can be improved by efficient thermosensitizers, and various candidate drugs, including inhi…
View article: Senescence phenotype of lymph node stromal cells from patients with rheumatoid arthritis is partly restored by dasatinib treatment
Senescence phenotype of lymph node stromal cells from patients with rheumatoid arthritis is partly restored by dasatinib treatment Open
Objective Cellular senescence is a state of proliferation arrest of cells occurring during aging. The persistence and accumulation of senescent cells has been implicated in the pathogenesis of age-related diseases like rheumatoid arthritis…
View article: High-Content and High-Throughput Clonogenic Survival Assay Using Fluorescence Barcoding
High-Content and High-Throughput Clonogenic Survival Assay Using Fluorescence Barcoding Open
The Clonogenic Survival Assay (CSA) is a fundamental tool employed to assess cell survival and proliferative potential in cancer research. Despite its importance, CSA faces limitations, primarily its time- and labor-intensive nature and it…
View article: Levamisole suppresses activation and proliferation of human T cells by the induction of a p53-dependent DNA damage response
Levamisole suppresses activation and proliferation of human T cells by the induction of a p53-dependent DNA damage response Open
Levamisole (LMS) is a small molecule used in the treatment of idiopathic nephrotic syndrome (INS). The pathogenesis of INS remains unknown, but most evidence points towards an immunological basis of the disease. Recently, LMS has been show…
View article: Supplementary Figure S5 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S5 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1WT/R132H cells are sensitized to metformin, compared with IDH1WT/WT cells.
View article: Supplementary Figure S3 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S3 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
The IDH1-mutant inhibitor AGI-5198 increases IDH-mediated NAPDH production capacity in IDH1-mutated cells.
View article: Supplementary Table S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Table S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
SPSS output statistics for comparisons between survival curves from colony-formation assays.
View article: Supplementary Figure S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1R132H mutations reduce IDH-mediated NADPH production and radioresistance.
View article: Supplementary Figure S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1R132H mutations reduce IDH-mediated NADPH production and radioresistance.
View article: Supplementary Figure S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
D-2HG inhibits IDH-mediated NADPH production capacity, but not G6PD-mediated NADPH production capacity or IDH-mediated NADH production capacity.
View article: Supplementary Table S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Table S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
D0, n and Dq values for survival curves from colony-formation assays after IR.
View article: Supplementary Figure S5 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S5 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1WT/R132H cells are sensitized to metformin, compared with IDH1WT/WT cells.
View article: Supplementary Table S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Table S1 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
SPSS output statistics for comparisons between survival curves from colony-formation assays.
View article: Supplementary Figure S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
D-2HG inhibits IDH-mediated NADPH production capacity, but not G6PD-mediated NADPH production capacity or IDH-mediated NADH production capacity.
View article: Data from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Data from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
Isocitrate dehydrogenase 1 (IDH1) is mutated in various types of human cancer to IDH1R132H, a structural alteration that leads to catalysis of α-ketoglutarate to the oncometabolite D-2-hydroxyglutarate. In this study, we present evidence t…
View article: Supplementary Figure S4 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S4 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1MT increase ROS levels and AGI-5198 attenuates this effect.
View article: Supplementary Figure S4 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S4 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
IDH1MT increase ROS levels and AGI-5198 attenuates this effect.
View article: Data from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Data from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
Isocitrate dehydrogenase 1 (IDH1) is mutated in various types of human cancer to IDH1R132H, a structural alteration that leads to catalysis of α-ketoglutarate to the oncometabolite D-2-hydroxyglutarate. In this study, we present evidence t…
View article: Supplementary Table S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Table S2 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
D0, n and Dq values for survival curves from colony-formation assays after IR.
View article: Supplementary Figure S3 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198
Supplementary Figure S3 from Radioprotection of <i>IDH1</i>-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198 Open
The IDH1-mutant inhibitor AGI-5198 increases IDH-mediated NAPDH production capacity in IDH1-mutated cells.
View article: Reduction in PA28αβ activation in HD mouse brain correlates to increased mHTT aggregation in cell models
Reduction in PA28αβ activation in HD mouse brain correlates to increased mHTT aggregation in cell models Open
Huntington’s disease is an autosomal dominant heritable disorder caused by an expanded CAG trinucleotide repeat at the N-terminus of the Huntingtin ( HTT ) gene. Lowering the levels of soluble mutant HTT protein prior to aggregation throug…
View article: Evaluation of the Heat Shock Protein 90 Inhibitor Ganetespib as a Sensitizer to Hyperthermia-Based Cancer Treatments
Evaluation of the Heat Shock Protein 90 Inhibitor Ganetespib as a Sensitizer to Hyperthermia-Based Cancer Treatments Open
Hyperthermia is being used as a radio- and chemotherapy sensitizer for a growing range of tumor subtypes in the clinic. Its potential is limited, however, by the ability of cancer cells to activate a protective mechanism known as the heat …