Lee M. Graves
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View article: Multi-omics signature of healthy versus unhealthy lifestyles reveals associations with diseases
Multi-omics signature of healthy versus unhealthy lifestyles reveals associations with diseases Open
This multi-omics cross-sectional study investigated differences in metabolomics, proteomics, and epigenomics profiles between two groups of adults matched for age but differing in lifestyle factors such as body composition, diet, and physi…
View article: Chemoproteomic Profiling of <i>C. albicans</i> for Characterization of Antifungal Kinase Inhibitors
Chemoproteomic Profiling of <i>C. albicans</i> for Characterization of Antifungal Kinase Inhibitors Open
Candida albicans is a major cause of systemic candidiasis, a severe fungal infection with a ∼40% mortality rate. Yck2, a casein kinase 1 (CK1) in C. albicans, is targeted by antifungal inhibitors YK-I-02 (YK) and MN-I-157 (MN…
View article: Chemoproteomic Profiling of <i>C. albicans</i> for Characterization of Anti-fungal Kinase Inhibitors
Chemoproteomic Profiling of <i>C. albicans</i> for Characterization of Anti-fungal Kinase Inhibitors Open
Candida albicans is a growing health concern as the leading causal agent of systemic candidiasis, a life-threatening fungal infection with a mortality rate of ∼40% despite best available therapy. Yck2, a fungal casein kinase 1 (CK1) family…
View article: A multi-kinase inhibitor screen identifies inhibitors preserving stem-cell-like chimeric antigen receptor T cells
A multi-kinase inhibitor screen identifies inhibitors preserving stem-cell-like chimeric antigen receptor T cells Open
Chimeric antigen receptor T cells (CAR T cells) with T stem (TSCM) cell-like phenotypic characteristics promote sustained antitumor effects. We performed an unbiased and automated high-throughput screen of a kinase-focused compo…
View article: Supplementary Table S1 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Table S1 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Table S1. Proteomics data
View article: Supplementary Figure S13 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S13 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S13. TR-107 treatment impacts the transcriptomic profile of HCT116 cells. (A) Downregulated pathway analysis in HCT116 cells identified related transcripts, which were grouped by pathway and filtered by significance an…
View article: Supplementary Figure S11 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S11 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S11. TR-107 treatment reduces integrated stress response and antioxidant protein expression in CRC cells. Immunoblotting of ATF3 and ATF4 and densitometry analysis of colorectal cancer cells (A) DLD-1, (B) LS 1034, (C)…
View article: Supplementary Figure S5 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S5 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S5. TR-107 treatment dysregulates the cell cycle and leads to cytostatic arrest of CRC cells. Colorectal cancer cells (A) LoVo, (B) NCI-H508, (C) LS 174T, and (D) RKO were treated with vehicle control (0.1% DMSO) or in…
View article: Supplementary Figure S3 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S3 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S3. Cell confluence images confirm a dose- and time-dependent inhibition of CRC cell proliferation. Colorectal cancer cells (A) LoVo, (B) NCI-H508, (C) LS 174T, and (D) RKO were treated in a 6-well plate format with ve…
View article: Supplementary Figure S8 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S8 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S8. TR-107 reduces total ATP production confirming an inactivation of OXPHOS and suppressed glycolytic compensatory response. Colorectal cancer cells (A) DLD-1, (B) LS1034, (C) HT29, and (D) HCT116 were treated with ve…
View article: Supplementary Figure S9 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S9 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S9. TR-107 reduces total ATP production confirming an inactivation of OXPHOS and suppressed glycolytic compensatory response. Colorectal cancer cells (A) LoVo, (B) NCI-H508, (C) LS 174T, and (D) RKO were treated with v…
View article: Supplementary Figure S4 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S4 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S4. TR-107 treatment dysregulates the cell cycle and leads to cytostatic arrest of CRC cells. Colorectal cancer cells (A) DLD-1, (B) LS1034, (C) HT29, and (D) HCT116 were treated with vehicle control (0.1% DMSO) or ind…
View article: Supplementary Figure S6 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S6 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S6. Washout of TR-107 treatment suggests an irreversible inhibition of CRC cell viability. (A) HCT116 cells were treated in a 96-well plate format with vehicle control (0.1% DMSO) or indicated concentrations of TR-107 …
View article: Supplementary Figure S7 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S7 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S7. TR-107 reduces mitochondrial metabolic function in CRC cells. (A-D) Mitochondrial oxygen consumption rate (OCR) and (E-H) glycolytic proton efflux rate (PER) were evaluated in colorectal cancer cells LoVo, NCI-H508…
View article: Supplementary Table S2 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Table S2 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Table S2. Analysis of downregulated proteins upon TR-107 treatment.
View article: Supplementary Figure S15 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S15 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S15. TR-107 increases cellular and mitochondrial ROS, leading to mitochondrial membrane permeabilization and lipid peroxidation. MITOSOX Red levels were measured in HCT116 (A) and DLD-1 cells (B) over a three-day perio…
View article: Supplementary Figure Legends from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure Legends from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure Legends
View article: Supplementary Figure S16 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S16 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S16. Co-treatment with TR-107 and Erastin leads to the synergistic inhibition of CRC cell viability. (A-D) Dose response matrices were generated for the CRC cell lines LoVo, NCI-H508, LS 174T, and RKO from each CMS cla…
View article: Supplementary Figure S1 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S1 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S1. Assessment of IC50 of TR-107 in NIH 3T3 cells. (A) NIH 3T3 cells were treated with vehicle control (0.1% DMSO) or various log-fold concentrations of TR-107 as described in Materials and Methods. CellTiter-Glo cell …
View article: Supplementary Figure S10 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S10 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S10. TR-107 downregulates the expression of essential mitochondrial proteins. Colorectal cancer cells (A) LoVo, (B) NCI-H508, (C) LS 174T, and (D) RKO were treated with vehicle control (0.1% DMSO) or TR-107 (50 nmol/L)…
View article: Supplementary Figure S14 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S14 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S14. TR-107 treatment impacts the transcriptomic profile of DLD-1 cells. (A) and (B) RT-PCR analysis of components of ISR and ferroptosis pathways in DLD-1 after 24 and 72 hours of TR-107 treatment, respectively. The g…
View article: Supplementary Figure S12 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S12 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S12. TR-107 treatment reduces integrated stress response and antioxidant protein expression in CRC cells. Immunoblotting of ATF3 and ATF4 and densitometry analysis of colorectal cancer cells (A) LoVo, (B) NCI-H508, (C)…
View article: Supplementary Figure S2 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Figure S2 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Figure S2. Cell confluence images confirm a dose- and time-dependent inhibition of CRC cell proliferation. Colorectal cancer cells (A) DLD-1, (B) LS1034, (C) HT29, and (D) HCT116 were treated in a 6-well plate format with veh…
View article: Supplementary Table S3 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Supplementary Table S3 from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Supplementary Table S3. Transcriptomic and proteomic data analysis.
View article: Data from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
Data from TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Oxidative phosphorylation is an essential metabolic process for cancer proliferation and therapy resistance. The ClpXP complex maintains mitochondrial proteostasis by degrading misfolded proteins. Madera Therapeutics has developed a class …
View article: TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells
TR-107, an Agonist of Caseinolytic Peptidase Proteolytic Subunit, Disrupts Mitochondrial Metabolism and Inhibits the Growth of Human Colorectal Cancer Cells Open
Oxidative phosphorylation is an essential metabolic process for cancer proliferation and therapy resistance. The ClpXP complex maintains mitochondrial proteostasis by degrading misfolded proteins. Madera Therapeutics has developed a class …
View article: Combining the constitutive TRAIL-secreting induced neural stem cell therapy with the novel anti-cancer drug TR-107 in glioblastoma
Combining the constitutive TRAIL-secreting induced neural stem cell therapy with the novel anti-cancer drug TR-107 in glioblastoma Open
View article: Combining the constitutive TRAIL-secreting induced neural stem cell therapy with the novel anti-cancer drug TR-107 in glioblastoma
Combining the constitutive TRAIL-secreting induced neural stem cell therapy with the novel anti-cancer drug TR-107 in glioblastoma Open
Tumor-homing neural stem cell (NSC) therapy is emerging as a promising treatment for aggressive cancers of the brain. Despite their success, developing tumor-homing NSC therapy therapies that maintain durable tumor suppression remains a ch…
View article: Defining the KRAS- and ERK-dependent transcriptome in KRAS-mutant cancers
Defining the KRAS- and ERK-dependent transcriptome in KRAS-mutant cancers Open
How the KRAS oncogene drives cancer growth remains poorly understood. Therefore, we established a systemwide portrait of KRAS- and extracellular signal-regulated kinase (ERK)-dependent gene transcription in KRAS-mutant cancer to delineate …
View article: Determining the ERK-regulated phosphoproteome driving KRAS-mutant cancer
Determining the ERK-regulated phosphoproteome driving KRAS-mutant cancer Open
To delineate the mechanisms by which the ERK1 and ERK2 mitogen-activated protein kinases support mutant KRAS-driven cancer growth, we determined the ERK-dependent phosphoproteome in KRAS-mutant pancreatic cancer. We determined that ERK1 an…