Christian M. Metallo

ORCID: 0000-0003-2404-3040
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About
Contact & Profiles
Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Lung Cancer Treatments and Mutations
  • Mitochondrial Function and Pathology
  • Metabolomics and Mass Spectrometry Studies
  • Metabolism and Genetic Disorders
  • Pancreatic and Hepatic Oncology Research
  • Epigenetics and DNA Methylation
  • Adipose Tissue and Metabolism
  • Metabolism, Diabetes, and Cancer
  • RNA modifications and cancer
  • Gastrointestinal Tumor Research and Treatment
  • Lung Cancer Research Studies
  • Amino Acid Enzymes and Metabolism
  • Pancreatic function and diabetes
  • Diet and metabolism studies
  • Cancer Genomics and Diagnostics
  • Pluripotent Stem Cells Research
  • Lipid metabolism and biosynthesis
  • Cancer, Lipids, and Metabolism
  • Sphingolipid Metabolism and Signaling
  • Peroxisome Proliferator-Activated Receptors
  • Endoplasmic Reticulum Stress and Disease
  • Microbial Metabolic Engineering and Bioproduction
  • Liver Disease Diagnosis and Treatment
  • Autophagy in Disease and Therapy

Salk Institute for Biological Studies
2020-2025

University of California, San Diego
2016-2025

Torrey Pines Institute For Molecular Studies
2023-2024

Massachusetts Institute of Technology
2009-2023

La Jolla Bioengineering Institute
2016-2023

Moores Cancer Center
2015-2020

La Jolla Alcohol Research
2014-2019

Sanford Consortium for Regenerative Medicine
2018

Jacobs (United States)
2018

University of Birmingham
2015

Metabolic reprogramming is emerging as a hallmark of the innate immune response, and dynamic control metabolites such succinate serves to facilitate execution inflammatory responses in macrophages other cells. Immunoresponsive gene 1 (Irg1) expression induced by stimuli, its enzyme product cis-aconitate decarboxylase catalyzes production itaconate from tricarboxylic acid cycle. Here we identify an immunometabolic regulatory pathway that links Irg1 accumulation occurs context responses....

10.1074/jbc.m115.685792 article EN cc-by Journal of Biological Chemistry 2016-05-10

Unchecked growth and proliferation is a hallmark of cancer, numerous oncogenic mutations reprogram cellular metabolism to fuel these processes. As central metabolic organelle, mitochondria execute critical biochemical functions for the synthesis fundamental components, including fatty acids, amino nucleotides. Despite extensive interest in glycolytic phenotype many cancer cells, tumors contain fully functional that support survival. Furthermore, tumor cells commonly increase flux through one...

10.1186/s40170-015-0128-2 article EN cc-by Cancer & Metabolism 2015-01-23

Mechanisms of metabolic flexibility enable cells to survive under stressful conditions and can thwart therapeutic responses. Acetyl-coenzyme A (CoA) plays central roles in energy production, lipid metabolism, epigenomic modifications. Here, we show that, upon genetic deletion Acly, the gene coding for ATP-citrate lyase (ACLY), remain viable proliferate, although at an impaired rate. In absence ACLY, upregulate ACSS2 utilize exogenous acetate provide acetyl-CoA de novo lipogenesis (DNL)...

10.1016/j.celrep.2016.09.069 article EN cc-by-nc-nd Cell Reports 2016-10-01

Induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) have enormous potential for the study of human cardiac disorders. However, their physiological immaturity severely limits utility as a model system and adoption drug discovery. Here, we describe maturation media designed to provide oxidative substrates adapted metabolic needs iPSC (hiPSC)-CMs. Compared with conventionally cultured hiPSC-CMs, metabolically matured hiPSC-CMs contract greater force show an increased reliance on...

10.1016/j.celrep.2020.107925 article EN cc-by-nc-nd Cell Reports 2020-07-01

Abstract Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur several types of cancer, but the metabolic consequences these genetic changes are not fully understood. In this study, we performed 13C flux analysis on a panel isogenic cell lines containing heterozygous IDH1/2 mutations. We observed that under hypoxic conditions, IDH1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reductive glutamine metabolism, IDH2-mutant cells....

10.1158/0008-5472.can-14-0772-t article EN Cancer Research 2014-04-23

The AMP-activated protein kinase (AMPK) is a highly conserved master regulator of metabolism, whose activation has been proposed to be therapeutically beneficial for the treatment several metabolic diseases, including nonalcoholic fatty liver disease (NAFLD). NAFLD, characterized by excessive accumulation hepatic lipids, most common chronic and major risk factor development steatohepatitis, type 2 diabetes, other conditions. To assess therapeutic potential AMPK activation, we have generated...

10.1016/j.celrep.2018.12.036 article EN cc-by-nc-nd Cell Reports 2019-01-01
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