0000000000402909

AUTHOR

M. Victoria García-mediavilla

showing 2 related works from this author

The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulati…

2013

Liver fatty acid binding protein (FABP1) prevents lipotoxicity of free fatty acids and regulates fatty acid trafficking and partition. Our objective is to investigate the transcription factors controlling the human FABP1 gene and their regulation in nonalcoholic fatty liver disease (NAFLD). Adenovirus-mediated expression of multiple transcription factors in HepG2 cells and cultured human hepatocytes demonstrated that FOXA1 and PPARα are among the most effective activators of human FABP1, whereas C/EBPα is a major dominant repressor. Moreover, FOXA1 and PPARα induced re-distribution of FABP1 protein and increased cytoplasmic expression. Reporter assays demonstrated that the major basal activ…

Hepatocyte Nuclear Factor 3-alphaMaleRepressorBiologyFatty Acid-Binding ProteinsFatty acid-binding proteinMiceTransactivationNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCCAAT-Enhancer-Binding Protein-alphamedicineAnimalsHumansPPAR alphaadipocyte protein 2Molecular BiologyTranscription factorCells Culturedchemistry.chemical_classificationFatty acidHep G2 CellsCell Biologymedicine.diseaseMolecular biologyFatty LiverMice Inbred C57BLLipotoxicitychemistrybiology.proteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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Repression of the nuclear receptor small heterodimer partner by steatotic drugs and in advanced nonalcoholic fatty liver disease.

2015

The small heterodimer partner (SHP) (NR0B2) is an atypical nuclear receptor that lacks a DNA-binding domain. It interacts with and inhibits many transcription factors, affecting key metabolic processes, including bile acid, cholesterol, fatty acid, and drug metabolism. Our aim was to determine the influence of steatotic drugs and nonalcoholic fatty liver disease (NAFLD) on SHP expression and investigate the potential mechanisms. SHP was found to be repressed by steatotic drugs (valproate, doxycycline, tetracycline, and cyclosporin A) in cultured hepatic cells and the livers of different animal models of NAFLD: iatrogenic (tetracycline-treated rats), genetic (glycine N-methyltransferase-defi…

MaleTranscription GeneticThiazepinesResponse elementReceptors Cytoplasmic and NuclearBiologyMiceNon-alcoholic Fatty Liver DiseaseCyclosporin amedicineCCAAT-Enhancer-Binding Protein-alphaAnimalsHumansProtein kinase APromoter Regions GeneticTranscription factorCells CulturedPharmacologyMitogen-Activated Protein Kinase 1KinaseValproic AcidFatty liverTetracyclinemedicine.diseaseFatty LiverDoxycyclineCancer researchSmall heterodimer partnerCyclosporineMolecular MedicineSignal transductionSignal TransductionMolecular pharmacology
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