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by Zhao, S and Xu, W and Jiang, W and Yu, W and Lin, Y and Zhang, T and Yao, J and Zhou, L and Zeng, Y and Li, H and Li, Y and Shi, J and An, W and Hancock, S. M and He, F and Qin, L and Chin, J and Yang, P and Chen, X and Lei, Q and Xiong, Y and Guan, K.-L
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2010, Volume 327, Issue 5968, pp. 1000 - 1004
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 09/2009, Volume 284, Issue 38, pp. 25593 - 25601
.... The occupied glucocorticoid receptor (GR) is a transcription factor. However, those genes regulating lipid metabolism under GR control are not fully known... 
OBESITY | PLASMA | GENE | CHROMATIN | ANGIOGENESIS | DIET | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPERLIPIDEMIA | MICE | TRANSCRIPTIONAL REGULATION | PROTEIN-4 | Transcription, Genetic - drug effects | Hypertriglyceridemia - genetics | Humans | Dexamethasone - adverse effects | Receptors, Glucocorticoid - metabolism | Hepatocytes - metabolism | Fatty Liver - chemically induced | Adipose Tissue - metabolism | Angiopoietin-like 4 Protein | Dexamethasone - pharmacology | Glucocorticoids - genetics | Glucocorticoids - metabolism | Response Elements - genetics | Lipoprotein Lipase - metabolism | Glucocorticoids - adverse effects | Fatty Liver - genetics | Angiopoietins - metabolism | Fatty Liver - metabolism | Lipoprotein Lipase - genetics | Liver - metabolism | Rats | Hypertriglyceridemia - metabolism | Mice, Knockout | Triglycerides - metabolism | Adipose Tissue, White | Hypertriglyceridemia - chemically induced | Animals | Receptors, Glucocorticoid - genetics | Cell Line, Tumor | Dexamethasone - metabolism | Glucocorticoids - pharmacology | Mice | Transcription, Genetic - genetics | Triglycerides - genetics | Angiopoietins - genetics | Index Medicus | Lipids and Lipoproteins | Metabolism, Regulation, and Signaling | Transcription | Dermatologi och venereologi | Dermatology and Venereal Diseases | Dexamethasone/adverse effects/metabolism/pharmacology | Hypertriglyceridemia/chemically induced/genetics/metabolism | Receptors | Adipose Tissue/metabolism | Liver/metabolism | Tumor | Adipose Tissue | Cell Line | Fatty Liver/chemically induced/genetics/metabolism | Triglycerides/genetics/ metabolism | Response Elements/genetics | Angiopoietins/genetics/ metabolism | Knockout | Lipoprotein Lipase/genetics/metabolism | White | Hepatocytes/metabolism | Genetic/drug effects/genetics | Glucocorticoids/adverse effects/genetics/ metabolism/pharmacology | Glucocorticoid/genetics/ metabolism
Journal Article
Journal of Gastroenterology and Hepatology, ISSN 0815-9319, 03/2009, Volume 24, Issue 3, pp. 443 - 452
Background and Aims:  We examined extrinsic and intrinsic (endogenous) mitochondrial apoptosis pathways in experimental non‐alcoholic steatohepatitis (NASH).... 
mitochondria | methionine and choline deficiency | insulin‐like growth factor‐1 | TRAIL‐R killer/DR5 | TNF receptors | cell death pathways | p53 | Cell death pathways | TRAIL-R killer/DR5 | Methionine and choline deficiency | Mitochondria | Insulin-like growth factor-1 | P53 | HEPATOCYTE APOPTOSIS | ACIDS | DR5 | insulin-like growth factor-1 | NONALCOHOLIC STEATOHEPATITIS | LIVER-DISEASE | PATHOGENESIS | NECROSIS | TNF-ALPHA | LIGAND | GASTROENTEROLOGY & HEPATOLOGY | TRAIL-R killer | NF-KAPPA-B | HEPATIC STEATOSIS | Liver - pathology | Liver - enzymology | Fatty Liver - pathology | Mitochondria, Liver - metabolism | Caspase 3 - metabolism | Choline Deficiency - complications | Male | Alanine Transaminase - blood | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | fas Receptor - metabolism | Tumor Suppressor Protein p53 - genetics | Time Factors | Receptors, Tumor Necrosis Factor, Type II - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Nutritional Status | Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics | BH3 Interacting Domain Death Agonist Protein - metabolism | Disease Models, Animal | Methionine - deficiency | Receptors, Tumor Necrosis Factor - metabolism | Fatty Liver - metabolism | Mitochondria, Liver - pathology | Liver - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Mitochondria, Liver - enzymology | Animals | Mice | bcl-X Protein - metabolism | Insulin-Like Growth Factor I - metabolism | Apoptosis | Fatty Liver - etiology | BH3 Interacting Domain Death Agonist Protein, metabolism | Receptors, Tumor Necrosis Factor, Type II, metabolism | Fatty Liver, pathology | Mitochondria, Liver, metabolism | Receptors, Tumor Necrosis Factor, metabolism | Cyclin-Dependent Kinase Inhibitor p21, metabolism | Insulin-Like Growth Factor I, metabolism | Caspase 3, metabolism | Antigens, CD95, metabolism | RNA, Messenger, metabolism | Tumor Suppressor Protein p53, metabolism | Methionine, deficiency | Choline Deficiency, complications | Tumor Suppressor Protein p53, genetics | bcl-X Protein, metabolism | Mitochondria, Liver, pathology | Liver, pathology | Alanine Transaminase, blood | Liver, metabolism | Fatty Liver, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, metabolism | Liver, enzymology | Fatty Liver, etiology | Mitochondria, Liver, enzymology | Receptors, Tumor Necrosis Factor, Type I, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, genetics | Messenger RNA | Choline | Methionine | Mitochondrial DNA | Tumor proteins | Peptide hormones | Growth factors
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2013, Volume 123, Issue 4, pp. 1662 - 1676
Journal Article
Hepatology (Baltimore, Md.), ISSN 0270-9139, 2012, Volume 56, Issue 6, pp. 2255 - 2267
Liver cirrhosis is a predominant risk factor for hepatocellular carcinoma (HCC). However, the mechanism underlying the progression from cirrhosis to HCC... 
PROGENITOR CELLS | STEM-CELLS | HEPATOCELLULAR-CARCINOMA | HEPATOCYTES | TGF-BETA | EPIGENETIC REGULATION | PTEN | SELF-RENEWAL | TUMORIGENICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Rats, Wistar | TOR Serine-Threonine Kinases - metabolism | Humans | Glycoproteins - metabolism | Liver Neoplasms, Experimental - chemically induced | Male | MicroRNAs - metabolism | Proto-Oncogene Proteins c-akt - genetics | Antigens, CD - metabolism | Epithelial Cell Adhesion Molecule | Pluripotent Stem Cells - pathology | Liver Neoplasms, Experimental - metabolism | Peptides - metabolism | Neoplastic Stem Cells - metabolism | Diethylnitrosamine | Liver Cirrhosis - metabolism | Antigens, Neoplasm - metabolism | Biomarkers, Tumor - metabolism | Antigens, Differentiation - metabolism | Liver Neoplasms, Experimental - pathology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - metabolism | Liver - metabolism | Mice, Inbred C57BL | PTEN Phosphohydrolase - metabolism | Rats | Mice, SCID | AC133 Antigen | Cell Adhesion Molecules - metabolism | Cell Transformation, Neoplastic - metabolism | Pluripotent Stem Cells - metabolism | Thy-1 Antigens - metabolism | Transforming Growth Factor beta - pharmacology | Animals | Pluripotent Stem Cells - drug effects | Liver Cirrhosis - pathology | Mice, Inbred NOD | Mice | Cell Transformation, Neoplastic - pathology | Transforming Growth Factor beta - metabolism | Proteins | Liver cancer | Liver cirrhosis | Hepatology
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 535, Issue 7611, pp. 303 - 307
Cellular mechanisms that mediate steatohepatitis, an increasingly prevalent condition in the Western world for which no therapies are available, are poorly... 
Fatty Liver/genetics | Cholesterol, HDL/metabolism | Atherosclerosis/genetics | Male | Lipoproteins, HDL/deficiency | Ubiquitination | Proteolysis | Diet, High-Fat | Liver X Receptors | Female | Protein Stability | Cholesterol, Dietary/metabolism | Lipogenesis/genetics | Orphan Nuclear Receptors/genetics | Receptors, LDL/deficiency | Gene Expression Regulation | Lipoproteins, LDL/metabolism | ATP Binding Cassette Transporter, Subfamily G, Member 5 | ATP-Binding Cassette Transporters/metabolism | ATP Binding Cassette Transporter, Subfamily G, Member 8 | Sterol Regulatory Element Binding Protein 1/metabolism | Lipoproteins/metabolism | Phosphatidylcholines/biosynthesis | Animals | Hepatocytes/metabolism | Fatty Acids, Unsaturated/metabolism | Ligands | ATP Binding Cassette Transporter 1/metabolism | Mice | Bile Acids and Salts/metabolism | FATTY LIVER-DISEASE | REVERSE CHOLESTEROL TRANSPORT | ER STRESS | MULTIDISCIPLINARY SCIENCES | ELEMENT-BINDING PROTEIN-1C | IN-VIVO | ALPHA | X-RECEPTOR | MICE | OXIDATION-PRODUCTS | INTESTINAL EPITHELIAL-CELLS | Lipoproteins, HDL - genetics | Atherosclerosis - genetics | Cholesterol, Dietary - metabolism | Phosphatidylcholines - biosynthesis | Lipoproteins, HDL - metabolism | Fatty Liver - therapy | Hepatocytes - metabolism | Orphan Nuclear Receptors - metabolism | Phosphatidylcholines - metabolism | ATP Binding Cassette Transporter 1 - metabolism | Atherosclerosis - therapy | Lipogenesis - genetics | Lipoproteins - metabolism | Receptors, LDL - deficiency | ATP-Binding Cassette Transporters - metabolism | Lipoproteins, HDL - deficiency | Lipoproteins, LDL - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Fatty Liver - genetics | Receptors, LDL - genetics | Cholesterol, HDL - metabolism | Fatty Liver - prevention & control | Bile Acids and Salts - metabolism | Fatty Acids, Unsaturated - metabolism | Orphan Nuclear Receptors - genetics | ATP Binding Cassette Transporter, Sub-Family G, Member 8 | Atherosclerosis - prevention & control | ATP Binding Cassette Transporter, Sub-Family G, Member 5 | Proteolipids | Transcription factors | Lipoproteins | Liver diseases | Atherosclerosis | Genetic aspects | Blood lipoproteins | Properties | Ubiquitin-proteasome system | Health aspects | Risk factors | Proteins | Diet | Liver | Gene expression | Cholesterol
Journal Article
Nature communications, ISSN 2041-1723, 2013, Volume 4, Issue 1, p. 1829
Journal Article
Nature (London), ISSN 1476-4687, 2015, Volume 527, Issue 7578, pp. 329 - 335
Ever since Stephen Paget's 1889 hypothesis, metastatic organotropism has remained one of cancer's greatest mysteries. Here we demonstrate that exosomes from... 
CELLS | BONE METASTASES | VESICLES | BREAST-CANCER METASTASIS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | GROWTH | NICHE | MICROVESICLES | PROTEINS | PROTEOMICS | Exosomes - metabolism | Tropism | Phosphorylation | Epithelial Cells - metabolism | Receptors, Vitronectin - antagonists & inhibitors | Humans | Lung - cytology | Integrin beta4 - metabolism | Integrins - metabolism | Brain - metabolism | Integrin alpha6beta1 - metabolism | S100 Proteins - genetics | Neoplasm Metastasis - prevention & control | Female | Kupffer Cells - metabolism | Lung - metabolism | Receptors, Vitronectin - metabolism | Epithelial Cells - cytology | Integrin alpha6beta4 - metabolism | Fibroblasts - metabolism | Biomarkers - metabolism | Brain - cytology | Kupffer Cells - cytology | Endothelial Cells - metabolism | Liver - metabolism | Mice, Inbred C57BL | Integrin alpha6beta4 - antagonists & inhibitors | Organ Specificity | Animals | Endothelial Cells - cytology | Neoplasm Metastasis - pathology | Cell Line, Tumor | Integrin beta Chains - metabolism | Fibroblasts - cytology | Liver - cytology | Mice | Genes, src | Integrins - antagonists & inhibitors | Complications and side effects | Development and progression | Cell organelles | Metastasis | Health aspects | Integrins | Tumors | Studies | Microscopy | Liver | Melanoma | Fibroblasts | Breast cancer | Chemokines | mechanisms of disease | cancer microenvironment | BASIC BIOLOGICAL SCIENCES | metastasis | 60 APPLIED LIFE SCIENCES
Journal Article