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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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    Modification of ocular defects in mouse developmental glaucoma models by tyrosinase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: Mutations in the cytochrome P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene are a common cause of human primary congenital glaucoma (PCG). Here we show that Cyp1b1-/- mice have ocular drainage structure abnormalities resembling those reported in human PCG patients. Using Cyp1b1-/- mice, we identified the tyrosinase gene (Tyr) as a modifier of the drainage structure phenotype, with Tyr deficiency increasing the magnitude of dysgenesis. The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Tyr also modified the drainage structure dysgenesis in mice with a mutant Foxc1 gene, which is also involved in PCG. These experiments raise the possibility that a tyrosinase/l-dopa pathway modifies human PCG, which could open new therapeutic avenues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Libby, Richard T -- Smith, Richard S -- Savinova, Olga V -- Zabaleta, Adriana -- Martin, Janice E -- Gonzalez, Frank J -- John, Simon W M -- CA34196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624268" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism, Ocular/genetics/pathology ; Animals ; Anterior Eye Segment/*abnormalities ; Aryl Hydrocarbon Hydroxylases/deficiency/genetics ; Cornea/abnormalities ; Cytochrome P-450 CYP1B1 ; *DNA-Binding Proteins ; Disease Models, Animal ; Female ; Forkhead Transcription Factors ; Glaucoma/*congenital/enzymology/*genetics/pathology ; Intraocular Pressure ; Iris/abnormalities ; Levodopa/administration & dosage/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Monophenol Monooxygenase/deficiency/*genetics/metabolism ; Mutation ; Phenotype ; Pregnancy ; Trabecular Meshwork/abnormalities ; Transcription Factors/genetics
    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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    Purkinje cell degeneration (pcd) phenotypes caused by mutations in the axotomy-induced gene, Nna1 (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-09
    Description: The classical recessive mouse mutant, Purkinje cell degeneration (pcd), exhibits adult-onset degeneration of cerebellar Purkinje neurons, retinal photoreceptors, olfactory bulb mitral neurons, and selected thalamic neurons, and has defective spermatogenesis. Here we identify Nna1 as the gene mutated in the original pcd and two additional pcd alleles (pcd2J and pcd3J). Nna1 encodes a putative nuclear protein containing a zinc carboxypeptidase domain initially identified by its induction in spinal motor neurons during axonal regeneration. The present study suggests an unexpected molecular link between neuronal degeneration and regeneration, and its results have potential implications for neurodegenerative diseases and male infertility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez-Gonzalez, Angeles -- La Spada, Albert R -- Treadaway, Jason -- Higdon, Jason C -- Harris, Belinda S -- Sidman, Richard L -- Morgan, James I -- Zuo, Jian -- CA 23944/CA/NCI NIH HHS/ -- CA21765/CA/NCI NIH HHS/ -- DC 04761/DC/NIDCD NIH HHS/ -- ES 10772/ES/NIEHS NIH HHS/ -- EY 12950/EY/NEI NIH HHS/ -- NS 40361/NS/NINDS NIH HHS/ -- RR 01183/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 8;295(5561):1904-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11884758" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Axotomy ; Blotting, Northern ; Brain/metabolism ; *Carboxypeptidases ; Chromosome Mapping ; Crosses, Genetic ; Female ; GTP-Binding Proteins/chemistry/*genetics/*physiology ; Gene Expression ; Genes ; In Situ Hybridization ; Male ; Mice ; Mice, Neurologic Mutants ; Molecular Sequence Data ; *Mutation ; Nerve Degeneration/*genetics ; Nerve Regeneration ; Neurons/metabolism ; Phenotype ; Purkinje Cells/cytology/*physiology ; RNA, Messenger/genetics/metabolism ; Retina/metabolism ; *Serine-Type D-Ala-D-Ala Carboxypeptidase ; Spermatogenesis ; Testis/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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  • 4
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    Nonsteroidal anti-inflammatory drugs can lower amyloidogenic Abeta42 by inhibiting Rho (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: A subset of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to preferentially reduce the secretion of the highly amyloidogenic, 42-residue amyloid-beta peptide Abeta42. We found that Rho and its effector, Rho-associated kinase, preferentially regulated the amount of Abeta42 produced in vitro and that only those NSAIDs effective as Rho inhibitors lowered Abeta42. Administration of Y-27632, a selective Rock inhibitor, also preferentially lowered brain levels of Abeta42 in a transgenic mouse model of Alzheimer's disease. Thus, the Rho-Rock pathway may regulate amyloid precursor protein processing, and a subset of NSAIDs can reduce Abeta42 through inhibition of Rho activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Yan -- Su, Yuan -- Li, Baolin -- Liu, Feng -- Ryder, John W -- Wu, Xin -- Gonzalez-DeWhitt, Patricia A -- Gelfanova, Valentina -- Hale, John E -- May, Patrick C -- Paul, Steven M -- Ni, Binhui -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Discovery Research and Bioresearch Technologies and Proteins, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA. zhou_yan_yz@lilly.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615541" target="_blank"〉PubMed〈/a〉
    Keywords: Amides/pharmacology ; Amyloid Precursor Protein Secretases ; Amyloid beta-Peptides/*metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/*pharmacology ; Aspartic Acid Endopeptidases ; Brain/drug effects/metabolism ; Cell Line, Tumor ; Endopeptidases/metabolism ; Enzyme Inhibitors/pharmacology ; Guanosine Triphosphate/metabolism ; Humans ; Ibuprofen/pharmacology ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Transgenic ; Peptide Fragments/*metabolism ; Polyisoprenyl Phosphates/pharmacology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Pyridines/pharmacology ; Sesquiterpenes ; Signal Transduction ; Sulindac/*analogs & derivatives/pharmacology ; Transfection ; rho GTP-Binding Proteins/*antagonists & inhibitors/metabolism ; rho-Associated Kinases ; rhoA GTP-Binding Protein/genetics/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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