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Full-Text Articles in Life Sciences
Pyruvate Kinase Isoform M2 Influences Autophagy And Related Processes In Hepatocellular Carcinoma Cells, Matthew Lin
Pyruvate Kinase Isoform M2 Influences Autophagy And Related Processes In Hepatocellular Carcinoma Cells, Matthew Lin
University Scholar Projects
Hepatocellular carcinoma (HCC) is the most common form of liver cancer that affects ~14 million people in the world. Like all cancers, HCC is a disease that arises from unstinted cellular growth initiated by genetic alterations, metabolic changes, and dysregulation in key cellular pathways. Of interest is the relationship between metabolism and cell proliferation/degradation for therapeutic targeting. Pyruvate kinase M2 is a dimeric, glycolytically inactive isoform of the final enzyme involved in glycolysis, that is often upregulated in cancerous tissue. It is thought that the enzymatic function of PKM2 outside of glycolysis contributes to the biosynthesis of anabolic intermediates used …
The Scaffolding Protein Iqgap1 Promotes Hepatic Proliferation And Protects The Liver From Injury, Hanna Erickson, Sayeepriyadarshini Anakk
The Scaffolding Protein Iqgap1 Promotes Hepatic Proliferation And Protects The Liver From Injury, Hanna Erickson, Sayeepriyadarshini Anakk
Hepatobiliary Cancers: Pathobiology and Translational Advances
No abstract provided.
Maintenance Of Mitochondrial Genomic Integrity In The Absence Of Manganese Superoxide Dismutase In Mouse Liver Hepatocytes., Anthony R. Cyr, Kyle E. Brown, Michael L. Mccormick, Mitchell C. Coleman, Adam J. Case, George S. Watts, Bernard W. Futscher, Douglas R. Spitz, Frederick E. Domann
Maintenance Of Mitochondrial Genomic Integrity In The Absence Of Manganese Superoxide Dismutase In Mouse Liver Hepatocytes., Anthony R. Cyr, Kyle E. Brown, Michael L. Mccormick, Mitchell C. Coleman, Adam J. Case, George S. Watts, Bernard W. Futscher, Douglas R. Spitz, Frederick E. Domann
Journal Articles: Cellular & Integrative Physiology
Manganese superoxide dismutase, encoded by the Sod2 gene, is a ubiquitously expressed mitochondrial antioxidant enzyme that is essential for mammalian life. Mice born with constitutive genetic knockout of Sod2 do not survive the neonatal stage, which renders the longitudinal study of the biochemical and metabolic effects of Sod2 loss difficult. However, multiple studies have demonstrated that tissue-specific knockout of Sod2 in murine liver yields no observable gross pathology or injury to the mouse. We hypothesized that Sod2 loss may have sub-pathologic effects on liver biology, including the acquisition of reactive oxygen species-mediated mitochondrial DNA mutations. To evaluate this, we established …