Michael Giarrizzo
YOU?
Author Swipe
View article: A graded neonatal mouse model of necrotizing enterocolitis demonstrates that mild enterocolitis is sufficient to activate microglia and increase cerebral cytokine expression
A graded neonatal mouse model of necrotizing enterocolitis demonstrates that mild enterocolitis is sufficient to activate microglia and increase cerebral cytokine expression Open
Necrotizing enterocolitis (NEC) is an inflammatory gastrointestinal process that afflicts approximately 10% of preterm infants born in the United States each year, with a mortality rate of 30%. NEC severity is graded using Bell’s classific…
View article: Paired primary-metastasis patient-derived organoids and mouse models identify phenotypic evolution and druggable dependencies of peritoneal metastasis from appendiceal cancer
Paired primary-metastasis patient-derived organoids and mouse models identify phenotypic evolution and druggable dependencies of peritoneal metastasis from appendiceal cancer Open
Summary Peritoneal carcinomatosis is a common yet deadly manifestation of gastrointestinal cancers, with few effective treatments. To identify targetable determinants of peritoneal metastasis, we focused on appendiceal adenocarcinoma (AC),…
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: Activin A signaling stimulates neutrophil activation and macrophage migration in pancreatitis
Activin A signaling stimulates neutrophil activation and macrophage migration in pancreatitis Open
Acute Pancreatitis (AP) is associated with high mortality and current treatment options are limited to supportive care. We found that blockade of activin A (activin) in mice improves outcomes in two murine models of AP. To test the hypothe…
View article: FABP5 Inhibition against PTEN-Mutant Therapy Resistant Prostate Cancer
FABP5 Inhibition against PTEN-Mutant Therapy Resistant Prostate Cancer Open
Resistance to standard of care taxane and androgen deprivation therapy (ADT) causes the vast majority of prostate cancer (PC) deaths worldwide. We have developed RapidCaP, an autochthonous genetically engineered mouse model of PC. It is dr…
View article: A graded neonatal mouse model of necrotizing enterocolitis demonstrates that mild enterocolitis is sufficient to activate microglia and increase cerebral cytokine expression
A graded neonatal mouse model of necrotizing enterocolitis demonstrates that mild enterocolitis is sufficient to activate microglia and increase cerebral cytokine expression Open
Background Necrotizing enterocolitis (NEC) is an inflammatory gastrointestinal process that afflicts approximately 10% of preterm infants born in the United States each year, with a mortality rate of 30%. NEC severity is graded using Bell’…
View article: The Role of Krüppel-like Factors in Pancreatic Physiology and Pathophysiology
The Role of Krüppel-like Factors in Pancreatic Physiology and Pathophysiology Open
Krüppel-like factors (KLFs) belong to the family of transcription factors with three highly conserved zinc finger domains in the C-terminus. They regulate homeostasis, development, and disease progression in many tissues. It has been shown…
View article: Intestinal Epithelial Regeneration in Response to Ionizing Irradiation
Intestinal Epithelial Regeneration in Response to Ionizing Irradiation Open
The intestinal epithelium consists of a single layer of cells yet contains multiple types of terminally differentiated cells, which are generated by the active proliferation of intestinal stem cells located at the bottom of intestinal cryp…