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  • 1
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    A natural product that lowers cholesterol as an antagonist ligand for FXR (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: Extracts of the resin of the guggul tree (Commiphora mukul) lower LDL (low-density lipoprotein) cholesterol levels in humans. The plant sterol guggulsterone [4,17(20)-pregnadiene-3,16-dione] is the active agent in this extract. We show that guggulsterone is a highly efficacious antagonist of the farnesoid X receptor (FXR), a nuclear hormone receptor that is activated by bile acids. Guggulsterone treatment decreases hepatic cholesterol in wild-type mice fed a high-cholesterol diet but is not effective in FXR-null mice. Thus, we propose that inhibition of FXR activation is the basis for the cholesterol-lowering activity of guggulsterone. Other natural products with specific biologic effects may modulate the activity of FXR or other relatively promiscuous nuclear hormone receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Urizar, Nancy L -- Liverman, Amy B -- Dodds, D'Nette T -- Silva, Frank Valentin -- Ordentlich, Peter -- Yan, Yingzhuo -- Gonzalez, Frank J -- Heyman, Richard A -- Mangelsdorf, David J -- Moore, David D -- New York, N.Y. -- Science. 2002 May 31;296(5573):1703-6. Epub 2002 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Caco-2 Cells ; Carrier Proteins/genetics/metabolism ; Cells, Cultured ; Chenodeoxycholic Acid/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Hepatocytes/metabolism ; Histone Acetyltransferases ; Humans ; *Hydroxysteroid Dehydrogenases ; Hypolipidemic Agents/metabolism/*pharmacology ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; Pregnenediones/metabolism/*pharmacology ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/metabolism ; Receptors, Steroid/antagonists & inhibitors/metabolism ; Transcription Factors/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    A cellular striptease act (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werb, Z -- Yan, Y -- CA72006/CA/NCI NIH HHS/ -- HD26732/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1279-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, CA 94143-0452, USA. zena@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867633" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Animals ; Catalytic Domain ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Growth Substances/metabolism ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/*metabolism ; Mice ; Models, Biological ; Receptor, Epidermal Growth Factor/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Production of p53 gene knockout rats by homologous recombination in embryonic stem cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-13
    Description: The use of homologous recombination to modify genes in embryonic stem (ES) cells provides a powerful means to elucidate gene function and create disease models. Application of this technology to engineer genes in rats has not previously been possible because of the absence of germline-competent ES cells in this species. We have recently established authentic rat ES cells. Here we report the generation of gene knockout rats using the ES-cell-based gene targeting technology. We designed a targeting vector to disrupt the tumour suppressor gene p53 (also known as Tp53) in rat ES cells by means of homologous recombination. p53 gene-targeted rat ES cells can be routinely generated. Furthermore, the p53 gene-targeted mutation in the rat ES-cell genome can transmit through the germ line via ES-cell rat chimaeras to create p53 gene knockout rats. The rat is the most widely used animal model in biological research. The establishment of gene targeting technology in rat ES cells, in combination with advances in genomics and the vast amount of research data on physiology and pharmacology in this species, now provide a powerful new platform for the study of human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937076/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937076/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tong, Chang -- Li, Ping -- Wu, Nancy L -- Yan, Youzhen -- Ying, Qi-Long -- 1R01 RR025881/RR/NCRR NIH HHS/ -- R01 OD010926/OD/NIH HHS/ -- R01 RR025881/RR/NCRR NIH HHS/ -- R01 RR025881-01A2/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Sep 9;467(7312):211-3. doi: 10.1038/nature09368. Epub 2010 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Culture Techniques ; Embryo, Mammalian/cytology ; Embryonic Stem Cells/*cytology ; Female ; Gene Knockout Techniques/*methods ; *Genes, p53 ; Germ-Line Mutation ; Male ; Mice ; Molecular Sequence Data ; Rats/*genetics ; Rats, Inbred F344 ; Rats, Sprague-Dawley ; Recombination, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Protection from experimental asthma by an endogenous bronchodilator (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-28
    Description: Mechanisms that protect against asthma remain poorly understood. S-nitrosoglutathione (GSNO), an endogenous bronchodilator, is depleted from asthmatic airways, suggesting a protective role. We report that, following allergen challenge, wild-type mice exhibiting airway hyperresponsivity have increased airway levels of the enzyme GSNO reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs). In contrast, mice with genetic deletion of GSNOR exhibit increases in lung SNOs and are protected from airway hyperresponsivity. Our results indicate that endogenous SNOs, governed by GSNOR, are critical regulators of airway responsivity and may provide new therapeutic approaches to asthma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2128762/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2128762/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Que, Loretta G -- Liu, Limin -- Yan, Yun -- Whitehead, Gregory S -- Gavett, Stephen H -- Schwartz, David A -- Stamler, Jonathan S -- ES012496/ES/NIEHS NIH HHS/ -- HL004171/HL/NHLBI NIH HHS/ -- K08 HL004171/HL/NHLBI NIH HHS/ -- K08 HL004171-05/HL/NHLBI NIH HHS/ -- P01 ES012496/ES/NIEHS NIH HHS/ -- P01 ES012496-010004/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1618-21. Epub 2005 May 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15919956" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Alcohol Dehydrogenase ; Allergens ; Animals ; Asthma/drug therapy/*physiopathology ; Bronchi ; Bronchial Hyperreactivity/drug therapy/physiopathology ; Bronchodilator Agents ; Female ; Glutathione Reductase/genetics/*metabolism ; Homeostasis ; Imines/pharmacology ; Isoproterenol/pharmacology ; Lung/metabolism/*physiopathology ; Male ; Methacholine Chloride/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitric Oxide ; Nitric Oxide Synthase/antagonists & inhibitors/metabolism ; Nitric Oxide Synthase Type II ; Ovalbumin ; S-Nitrosoglutathione/*metabolism/pharmacology ; S-Nitrosothiols/*metabolism ; Trachea/drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Vessel formation. De novo formation of a distinct coronary vascular population in neonatal heart (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-07-06
    Description: The postnatal coronary vessels have been viewed as developing through expansion of vessels formed during the fetal period. Using genetic lineage tracing, we found that a substantial portion of postnatal coronary vessels arise de novo in the neonatal mouse heart, rather than expanding from preexisting embryonic vasculature. Our data show that lineage conversion of neonatal endocardial cells during trabecular compaction generates a distinct compartment of the coronary circulation located within the inner half of the ventricular wall. This lineage conversion occurs within a brief period after birth and provides an efficient means of rapidly augmenting the coronary vasculature. This mechanism of postnatal coronary vascular growth provides avenues for understanding and stimulating cardiovascular regeneration following injury and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275002/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275002/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Xueying -- Hu, Tianyuan -- Zhang, Hui -- He, Lingjuan -- Huang, Xiuzhen -- Liu, Qiaozhen -- Yu, Wei -- He, Liang -- Yang, Zhen -- Yan, Yan -- Yang, Xiao -- Zhong, Tao P -- Pu, William T -- Zhou, Bin -- 2 R01 HL094683/HL/NHLBI NIH HHS/ -- R01 HL094683/HL/NHLBI NIH HHS/ -- R01 HL116461/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 4;345(6192):90-4. doi: 10.1126/science.1251487.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. ; Zhongshan Hospital, Fudan University, Shanghai 200032, China. ; State Key Laboratory of Proteomics, Institute of Biotechnology, Beijing 100071, China. ; State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, China. ; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. Department of Cardiology, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA. ; Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. zhoubin@sibs.ac.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24994653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage/genetics ; Coronary Vessels/*growth & development/physiology ; Endocardium/cytology/physiology ; Heart/*growth & development/physiology ; Mice ; Myocardium/cytology ; Neovascularization, Physiologic/genetics/*physiology ; Regeneration
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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