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    Wyświetlanie 1-13 z 13
    Tytuł:
    Elevated Nrf-2 responses are insufficient to mitigate protein carbonylation in hepatospecific PTEN deletion mice.
    Autorzy:
    Petersen DR; Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
    Saba LM; Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
    Sayin VI; Department of Pathology, New York University School of Medicine, New York, New York, United States of America.; Perlmutter Cancer Center, New York University School of Medicine, New York, New York, United States of America.
    Papagiannakopoulos T; Department of Pathology, New York University School of Medicine, New York, New York, United States of America.; Perlmutter Cancer Center, New York University School of Medicine, New York, New York, United States of America.
    Schmidt EE; Department of Microbiology and Immunology, Montana State University, Bozeman, Montana, United States of America.
    Merrill GF; Department of Biochemistry and Biophysics, Oregon State University, Corvalis, Oregon, United States of America.
    Orlicky DJ; Department of Pathology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
    Shearn CT; Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
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    Źródło:
    PloS one [PLoS One] 2018 May 25; Vol. 13 (5), pp. e0198139. Date of Electronic Publication: 2018 May 25 (Print Publication: 2018).
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural
    MeSH Terms:
    Gene Knockout Techniques*
    Liver/*metabolism
    NF-E2-Related Factor 2/*metabolism
    PTEN Phosphohydrolase/*deficiency
    PTEN Phosphohydrolase/*genetics
    Protein Carbonylation/*genetics
    Aldehydes/metabolism ; Animals ; Antioxidants/metabolism ; Autophagy/genetics ; Cell Proliferation/genetics ; Female ; Liver/cytology ; Male ; Mice ; Mice, Inbred C57BL ; Organ Specificity ; Oxidative Stress/genetics ; Proteomics
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
    Tytuł:
    Liver-Specific Deletion of Phosphatase and Tensin Homolog Deleted on Chromosome 10 Significantly Ameliorates Chronic EtOH-Induced Increases in Hepatocellular Damage.
    Autorzy:
    Shearn CT; Skaggs School of Pharmaceutical Sciences and Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    Orlicky DJ; Department of Pathology, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    McCullough RL; Skaggs School of Pharmaceutical Sciences and Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    Jiang H; Department of Pediatrics, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    Maclean KN; Department of Pediatrics, School of Medicine University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    Mercer KE; Arkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, AK, United States of America.
    Stiles BL; Department of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, United States of America.
    Saba LM; Skaggs School of Pharmaceutical Sciences and Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
    Ronis MJ; Arkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, AK, United States of America.
    Petersen DR; Skaggs School of Pharmaceutical Sciences and Pharmacy, University of Colorado Anschutz Medical Campus, Aurora, CO, United States of America.
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    Źródło:
    PloS one [PLoS One] 2016 Apr 28; Vol. 11 (4), pp. e0154152. Date of Electronic Publication: 2016 Apr 28 (Print Publication: 2016).
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural
    MeSH Terms:
    Alcohol Drinking/*metabolism
    Chemical and Drug Induced Liver Injury, Chronic/*metabolism
    Ethanol/*adverse effects
    Fatty Liver, Alcoholic/*metabolism
    Liver/*drug effects
    PTEN Phosphohydrolase/*genetics
    Alanine Transaminase/genetics ; Alanine Transaminase/metabolism ; Alcohol Drinking/genetics ; Alcohol Drinking/pathology ; Animals ; Chemical and Drug Induced Liver Injury, Chronic/genetics ; Chemical and Drug Induced Liver Injury, Chronic/pathology ; Disease Models, Animal ; Fatty Acids, Unsaturated/metabolism ; Fatty Liver, Alcoholic/genetics ; Fatty Liver, Alcoholic/pathology ; Female ; Gene Expression Regulation ; Glutathione/metabolism ; Lipogenesis/genetics ; Liver/metabolism ; Liver/pathology ; Male ; Mice ; Mice, Knockout ; Oxidative Stress ; PTEN Phosphohydrolase/deficiency ; Protein Carbonylation ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Triglycerides/metabolism
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknieSzczegóły
    Tytuł:
    Short term feeding of a high fat diet exerts an additive effect on hepatocellular damage and steatosis in liver-specific PTEN knockout mice.
    Autorzy:
    Shearn CT; Department of Pharmaceutical Sciences, University of Colorado Denver Anchutz Medical Campus, Aurora, Colorado, United States of America.
    Mercer KE; Arkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
    Orlicky DJ; Department of Pathology, University of Colorado Denver Anchutz Medical Campus, Aurora, Colorado, United States of America.
    Hennings L; Arkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
    Smathers-McCullough RL; Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
    Stiles BL; Department of Pharmaceutical Sciences, University of Southern California, Los Angeles, California, United States of America.
    Ronis MJ; Arkansas Children's Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America; Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
    Petersen DR; Department of Pharmaceutical Sciences, University of Colorado Denver Anchutz Medical Campus, Aurora, Colorado, United States of America.
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    Źródło:
    PloS one [PLoS One] 2014 May 12; Vol. 9 (5), pp. e96553. Date of Electronic Publication: 2014 May 12 (Print Publication: 2014).
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural
    MeSH Terms:
    Diet, High-Fat/*adverse effects
    Fatty Liver/*metabolism
    Fatty Liver/*pathology
    Liver/*metabolism
    Liver/*pathology
    PTEN Phosphohydrolase/*metabolism
    Animals ; CD36 Antigens/metabolism ; Cytochrome P-450 CYP4A/metabolism ; Male ; Mice ; Mice, Knockout ; Oxidative Stress/physiology ; PTEN Phosphohydrolase/genetics
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknieSzczegóły
    Tytuł:
    Deletion of GSTA4-4 results in increased mitochondrial post-translational modification of proteins by reactive aldehydes following chronic ethanol consumption in mice
    Autorzy:
    Colin T. Shearn
    Kristofer S. Fritz
    Alisabeth H. Shearn
    Laura M. Saba
    Kelly E. Mercer
    Bridgette Engi
    James J. Galligan
    Piotr Zimniak
    David J. Orlicky
    Martin J. Ronis
    Dennis R. Petersen
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    Temat:
    Ethanol
    Lipid peroxidation
    GSTA4
    Protein carbonylation
    Liver
    Oxidative stress
    Mitochondria
    Medicine (General)
    R5-920
    Biology (General)
    QH301-705.5
    Źródło:
    Redox Biology, Vol 7, Iss C, Pp 68-77 (2016)
    Opis pliku:
    electronic resource
    Relacje:
    http://www.sciencedirect.com/science/article/pii/S2213231715300148; https://doaj.org/toc/2213-2317
    Dostęp URL:
    https://doaj.org/article/a0c8a20508814e5c97a8857b03dd80be  Link otwiera się w nowym oknie
    Czasopismo naukowe
    Szczegóły
      Wyświetlanie 1-13 z 13

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