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  • 1
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    Mouse brain organization revealed through direct genome-scale TF expression analysis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-25
    Description: In the developing brain, transcription factors (TFs) direct the formation of a diverse array of neurons and glia. We identifed 1445 putative TFs in the mouse genome. We used in situ hybridization to map the expression of over 1000 of these TFs and TF-coregulator genes in the brains of developing mice. We found that 349 of these genes showed restricted expression patterns that were adequate to describe the anatomical organization of the brain. We provide a comprehensive inventory of murine TFs and their expression patterns in a searchable brain atlas database.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, Paul A -- Fu, Hui -- Luo, Ping -- Zhao, Qing -- Yu, Jing -- Ferrari, Annette -- Tenzen, Toyoaki -- Yuk, Dong-In -- Tsung, Eric F -- Cai, Zhaohui -- Alberta, John A -- Cheng, Le-Ping -- Liu, Yang -- Stenman, Jan M -- Valerius, M Todd -- Billings, Nathan -- Kim, Haesun A -- Greenberg, Michael E -- McMahon, Andrew P -- Rowitch, David H -- Stiles, Charles D -- Ma, Qiufu -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2255-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/anatomy & histology/embryology/*growth & development/*metabolism ; Cloning, Molecular ; Corpus Striatum/anatomy & histology/embryology/growth & development/metabolism ; DNA Primers ; Databases, Factual ; *Gene Expression Profiling ; *Genome ; Hypothalamus/anatomy & histology/embryology/growth & development/metabolism ; In Situ Hybridization ; Mesencephalon/anatomy & histology/embryology/growth & development/metabolism ; Mice ; Neocortex/anatomy & histology/embryology/growth & development/metabolism ; Polymerase Chain Reaction ; Rhombencephalon/anatomy & histology/embryology/growth & development/metabolism ; Spinal Cord/anatomy & histology/embryology/growth & development/metabolism ; Thalamus/anatomy & histology/embryology/growth & development/metabolism ; Transcription Factors/*genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Role of the kinase MST2 in suppression of apoptosis by the proto-oncogene product Raf-1 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-25
    Description: The ablation of the protein kinase Raf-1 renders cells hypersensitive to apoptosis despite normal regulation of extracellular signal-regulated kinases, which suggests that apoptosis protection is mediated by a distinct pathway. We used proteomic analysis of Raf-1 signaling complexes to show that Raf-1 counteracts apoptosis by suppressing the activation of mammalian sterile 20-like kinase (MST2). Raf-1 prevents dimerization and phosphorylation of the activation loop of MST2 independently of its protein kinase activity. Depletion of MST2 from Raf-1-/- mouse or human cells abrogated sensitivity to apoptosis, whereas overexpression of MST2 induced apoptosis. Conversely, depletion of Raf-1 from Raf-1+/+ mouse or human cells led to MST2 activation and apoptosis. The concomitant depletion of both Raf-1 and MST2 prevented apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, Eric -- Rushworth, Linda -- Baccarini, Manuela -- Kolch, Walter -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; *Apoptosis ; COS Cells ; Cell Line, Tumor ; Dimerization ; Humans ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proteomics ; Proto-Oncogene Proteins c-raf/genetics/*metabolism ; RNA, Small Interfering ; Signal Transduction ; Staurosporine/pharmacology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Mechanisms of hair graying: incomplete melanocyte stem cell maintenance in the niche (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-25
    Description: Hair graying is the most obvious sign of aging in humans, yet its mechanism is largely unknown. Here, we used melanocyte-tagged transgenic mice and aging human hair follicles to demonstrate that hair graying is caused by defective self-maintenance of melanocyte stem cells. This process is accelerated dramatically with Bcl2 deficiency, which causes selective apoptosis of melanocyte stem cells, but not of differentiated melanocytes, within the niche at their entry into the dormant state. Furthermore, physiologic aging of melanocyte stem cells was associated with ectopic pigmentation or differentiation within the niche, a process accelerated by mutation of the melanocyte master transcriptional regulator Mitf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, Emi K -- Granter, Scott R -- Fisher, David E -- AR43369/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):720-4. Epub 2004 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Hematology/Oncology, Melanoma Program in Medical Oncology, Dana-Farber Cancer Institute, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. emi_k_nishimura@yahoo.co.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618488" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Aging/*physiology ; Animals ; Apoptosis ; Cell Differentiation ; Cell Shape ; DNA-Binding Proteins/genetics/metabolism ; *Hair Color ; Hair Follicle/cytology/*physiology ; Humans ; Melanins/biosynthesis ; Melanocytes/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microphthalmia-Associated Transcription Factor ; Middle Aged ; Morphogenesis ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Stem Cells/*physiology ; Transcription Factors/genetics/metabolism ; Vibrissae/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cell biology. "Pumping" iron: the proteins (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, Ernest -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2051-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA 92037, USA. beutler@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/*metabolism ; Biological Transport ; Cation Transport Proteins/genetics/*metabolism ; Enterocytes/metabolism ; Erythropoiesis ; Erythropoietin/genetics/metabolism ; Gene Expression Regulation ; Hemochromatosis/genetics ; Hepatocytes/metabolism ; Hepcidins ; Histocompatibility Antigens Class I/genetics ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 1/*metabolism ; Iron Regulatory Protein 2/*metabolism ; Membrane Proteins/genetics ; Mice ; Models, Biological ; Mutation ; Nitric Oxide/metabolism ; Oxygen/physiology ; Response Elements ; Signal Transduction ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Phosphorylation of proteins by inositol pyrophosphates (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: The inositol pyrophosphates IP7 and IP8 contain highly energetic pyrophosphate bonds. Although implicated in various biologic functions, their molecular sites of action have not been clarified. Using radiolabeled IP7, we detected phosphorylation of multiple eukaryotic proteins. We also observed phosphorylation of endogenous proteins by endogenous IP7 in yeast. Phosphorylation by IP7 is nonenzymatic and may represent a novel intracellular signaling mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saiardi, Adolfo -- Bhandari, Rashna -- Resnick, Adam C -- Snowman, Adele M -- Snyder, Solomon H -- DA00074/DA/NIDA NIH HHS/ -- MH068830-02/MH/NIMH NIH HHS/ -- MH18501/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2101-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University, School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604408" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Escherichia coli Proteins/metabolism ; Humans ; Inositol Phosphates/*metabolism ; Kinetics ; Magnesium/metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/chemistry/*metabolism ; Phosphates/metabolism ; Phosphorylation ; Phosphotransferases (Phosphate Group Acceptor)/metabolism ; Protein Kinases/genetics/metabolism ; Proteins/*metabolism ; RNA-Binding Proteins/chemistry/*metabolism ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/chemistry/*metabolism ; Serine/metabolism ; Signal Transduction ; Temperature
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnett, Heather A -- Fancy, Stephen P J -- Alberta, John A -- Zhao, Chao -- Plant, Sheila R -- Kaing, Sovann -- Raine, Cedric S -- Rowitch, David H -- Franklin, Robin J M -- Stiles, Charles D -- 689/Multiple Sclerosis Society/United Kingdom -- NS08952/NS/NINDS NIH HHS/ -- NS11920/NS/NINDS NIH HHS/ -- NS4051/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2111-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Basic Helix-Loop-Helix Transcription Factors ; Brain/growth & development/*physiology ; Cell Nucleus/metabolism ; Cuprizone/pharmacology ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Demyelinating Diseases/*physiopathology ; Ethidium/pharmacology ; Humans ; Lysophosphatidylcholines/pharmacology ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/physiopathology ; Myelin Sheath/*physiology ; Nerve Tissue Proteins/genetics/*metabolism/physiology ; Oligodendroglia/*physiology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/growth & development/*physiology ; Stem Cells/physiology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Medicine. Visfatin: a new adipokine (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hug, Christopher -- Lodish, Harvey F -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):366-7. Epub 2004 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604359" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Adipose Tissue/*metabolism ; Animals ; Blood Glucose/analysis ; Cytokines/blood/genetics/*metabolism ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Female ; Gene Targeting ; Glucose/metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/blood/metabolism ; Mice ; Mice, Obese ; Molecular Mimicry ; Muscle Cells/metabolism ; Nicotinamide Phosphoribosyltransferase ; Receptor, Insulin/metabolism ; Recombinant Proteins/metabolism ; Subcutaneous Tissue ; Viscera
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Nutrient availability regulates SIRT1 through a forkhead-dependent pathway (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Nutrient availability regulates life-span in a wide range of organisms. We demonstrate that in mammalian cells, acute nutrient withdrawal simultaneously augments expression of the SIRT1 deacetylase and activates the Forkhead transcription factor Foxo3a. Knockdown of Foxo3a expression inhibited the starvation-induced increase in SIRT1 expression. Stimulation of SIRT1 transcription by Foxo3a was mediated through two p53 binding sites present in the SIRT1 promoter, and a nutrient-sensitive physical interaction was observed between Foxo3a and p53. SIRT1 expression was not induced in starved p53-deficient mice. Thus, in mammalian cells, p53, Foxo3a, and SIRT1, three proteins separately implicated in aging, constitute a nutrient-sensing pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemoto, Shino -- Fergusson, Maria M -- Finkel, Toren -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2105-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604409" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Binding Sites ; Culture Media ; Culture Media, Serum-Free ; DNA-Binding Proteins/*metabolism ; Forkhead Transcription Factors ; Gene Deletion ; Genes, p53 ; Glucose ; HeLa Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; PC12 Cells ; Promoter Regions, Genetic ; RNA, Small Interfering/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Serum ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; *Starvation ; Transcription Factors/*metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Mammalian tissue oxygen levels modulate iron-regulatory protein activities in vivo (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: The iron-regulatory proteins (IRPs) posttranscriptionally regulate expression of transferrin receptor, ferritin, and other iron metabolism proteins. Although both IRPs can regulate expression of the same target genes, IRP2-/- mice significantly misregulate iron metabolism and develop neurodegeneration, whereas IRP1-/- mice are spared. We found that IRP2-/- cells misregulated iron metabolism when cultured in 3 to 6% oxygen, which is comparable to physiological tissue concentrations, but not in 21% oxygen, a concentration that activated IRP1 and allowed it to substitute for IRP2. Thus, IRP2 dominates regulation of mammalian iron homeostasis because it alone registers iron concentrations and modulates its RNA-binding activity at physiological oxygen tensions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyron-Holtz, Esther G -- Ghosh, Manik C -- Rouault, Tracey A -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2087-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604406" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Ferritins/biosynthesis/metabolism ; Gene Expression Regulation ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 1/genetics/*metabolism ; Iron Regulatory Protein 2/genetics/*metabolism ; Lymphocytes/*metabolism ; Macrophages/*metabolism ; Mice ; Oxidants/metabolism ; Oxygen/*physiology ; RNA/metabolism ; Receptors, Transferrin/biosynthesis/metabolism ; Response Elements ; Spleen/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Comment on "Uracil DNA glycosylase activity is dispensable for immunoglobulin class switch" (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stivers, James T -- GM56834-09/GM/NIGMS NIH HHS/ -- R01 GM056834/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2042; author reply 2042.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Johns Hopkins Medical School, 725 North Wolfe Street, Baltimore, MD 21205, USA. jstivers@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Catalysis ; DNA/*metabolism ; DNA Damage ; DNA Glycosylases/*metabolism ; DNA Repair ; Humans ; *Immunoglobulin Class Switching ; Mice ; Mutation ; Recombination, Genetic ; Uracil/metabolism ; Uracil-DNA Glycosidase ; Viral Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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