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  • Mice  (164)
  • Meteorology and Climatology
  • 2005-2009  (194)
  • 1950-1954
  • 2008  (194)
  • 1
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    Neurokinin 1 receptor antagonism as a possible therapy for alcoholism (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: Alcohol dependence is a major public health challenge in need of new treatments. As alcoholism evolves, stress systems in the brain play an increasing role in motivating continued alcohol use and relapse. We investigated the role of the neurokinin 1 receptor (NK1R), a mediator of behavioral stress responses, in alcohol dependence and treatment. In preclinical studies, mice genetically deficient in NK1R showed a marked decrease in voluntary alcohol consumption and had an increased sensitivity to the sedative effects of alcohol. In a randomized controlled experimental study, we treated recently detoxified alcoholic inpatients with an NK1R antagonist (LY686017; n = 25) or placebo (n = 25). LY686017 suppressed spontaneous alcohol cravings, improved overall well-being, blunted cravings induced by a challenge procedure, and attenuated concomitant cortisol responses. Brain functional magnetic resonance imaging responses to affective stimuli likewise suggested beneficial LY686017 effects. Thus, as assessed by these surrogate markers of efficacy, NK1R antagonism warrants further investigation as a treatment in alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉George, David T -- Gilman, Jodi -- Hersh, Jacqueline -- Thorsell, Annika -- Herion, David -- Geyer, Christopher -- Peng, Xiaomei -- Kielbasa, William -- Rawlings, Robert -- Brandt, John E -- Gehlert, Donald R -- Tauscher, Johannes T -- Hunt, Stephen P -- Hommer, Daniel -- Heilig, Markus -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1536-9. doi: 10.1126/science.1153813. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276852" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; *Alcohol Drinking/drug therapy ; Alcoholism/*drug therapy ; Animals ; Behavior, Addictive/drug therapy ; Brain/drug effects/physiology ; Emotions/drug effects ; Ethanol/administration & dosage/pharmacology ; Female ; Humans ; Hydrocortisone/blood ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; *Neurokinin-1 Receptor Antagonists ; Pyridines/administration & dosage/pharmacology/*therapeutic use ; Receptors, Neurokinin-1/deficiency/genetics/*physiology ; Triazoles/administration & dosage/pharmacology/*therapeutic use
    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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    Cutaneous cancer stem cell maintenance is dependent on beta-catenin signalling (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-04
    Description: Continuous turnover of epithelia is ensured by the extensive self-renewal capacity of tissue-specific stem cells. Similarly, epithelial tumour maintenance relies on cancer stem cells (CSCs), which co-opt stem cell properties. For most tumours, the cellular origin of these CSCs and regulatory pathways essential for sustaining stemness have not been identified. In murine skin, follicular morphogenesis is driven by bulge stem cells that specifically express CD34. Here we identify a population of cells in early epidermal tumours characterized by phenotypic and functional similarities to normal bulge skin stem cells. This population contains CSCs, which are the only cells with tumour initiation properties. Transplants derived from these CSCs preserve the hierarchical organization of the primary tumour. We describe beta-catenin signalling as being essential in sustaining the CSC phenotype. Ablation of the beta-catenin gene results in the loss of CSCs and complete tumour regression. In addition, we provide evidence for the involvement of increased beta-catenin signalling in malignant human squamous cell carcinomas. Because Wnt/beta-catenin signalling is not essential for normal epidermal homeostasis, such a mechanistic difference may thus be targeted to eliminate CSCs and consequently eradicate squamous cell carcinomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Peinado, Hector -- Kassen, Deepika -- Hussenet, Thomas -- Metzger, Daniel -- Chambon, Pierre -- Huber, Marcel -- Hohl, Daniel -- Cano, Amparo -- Birchmeier, Walter -- Huelsken, Joerg -- England -- Nature. 2008 Apr 3;452(7187):650-3. doi: 10.1038/nature06835.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne/ISREC (Swiss Institute for Experimental Cancer Research) and National Center of Competence in Research Molecular Oncology, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/metabolism ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Epidermis/pathology ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplastic Stem Cells/*metabolism/*pathology ; *Signal Transduction ; Skin Neoplasms/*pathology ; beta Catenin/*metabolism
    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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  • 3
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    Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-02-19
    Description: Understanding the neuropathology of multiple sclerosis (MS) is essential for improved therapies. Therefore, identification of targets specific to pathological types of MS may have therapeutic benefits. Here we identify, by laser-capture microdissection and proteomics, proteins unique to three major types of MS lesions: acute plaque, chronic active plaque and chronic plaque. Comparative proteomic profiles identified tissue factor and protein C inhibitor within chronic active plaque samples, suggesting dysregulation of molecules associated with coagulation. In vivo administration of hirudin or recombinant activated protein C reduced disease severity in experimental autoimmune encephalomyelitis and suppressed Th1 and Th17 cytokines in astrocytes and immune cells. Administration of mutant forms of recombinant activated protein C showed that both its anticoagulant and its signalling functions were essential for optimal amelioration of experimental autoimmune encephalomyelitis. A proteomic approach illuminated potential therapeutic targets selective for specific pathological stages of MS and implicated participation of the coagulation cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, May H -- Hwang, Sun-Il -- Roy, Dolly B -- Lundgren, Deborah H -- Price, Jordan V -- Ousman, Shalina S -- Fernald, Guy Haskin -- Gerlitz, Bruce -- Robinson, William H -- Baranzini, Sergio E -- Grinnell, Brian W -- Raine, Cedric S -- Sobel, Raymond A -- Han, David K -- Steinman, Lawrence -- T32 AI007290/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Feb 28;451(7182):1076-81. doi: 10.1038/nature06559. Epub 2008 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18278032" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Blood Coagulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/metabolism/pathology ; Female ; *Gene Expression Profiling ; Humans ; Inflammation/metabolism/pathology ; Male ; Mice ; Middle Aged ; Multiple Sclerosis/classification/drug therapy/*metabolism/*pathology ; Protein C/genetics/metabolism/pharmacology ; *Proteomics ; Th1 Cells/immunology ; Th2 Cells/immunology ; Thrombin/antagonists & inhibitors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    The impact of microRNAs on protein output (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-01
    Description: MicroRNAs are endogenous approximately 23-nucleotide RNAs that can pair to sites in the messenger RNAs of protein-coding genes to downregulate the expression from these messages. MicroRNAs are known to influence the evolution and stability of many mRNAs, but their global impact on protein output had not been examined. Here we use quantitative mass spectrometry to measure the response of thousands of proteins after introducing microRNAs into cultured cells and after deleting mir-223 in mouse neutrophils. The identities of the responsive proteins indicate that targeting is primarily through seed-matched sites located within favourable predicted contexts in 3' untranslated regions. Hundreds of genes were directly repressed, albeit each to a modest degree, by individual microRNAs. Although some targets were repressed without detectable changes in mRNA levels, those translationally repressed by more than a third also displayed detectable mRNA destabilization, and, for the more highly repressed targets, mRNA destabilization usually comprised the major component of repression. The impact of microRNAs on the proteome indicated that for most interactions microRNAs act as rheostats to make fine-scale adjustments to protein output.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745094/" 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/PMC2745094/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baek, Daehyun -- Villen, Judit -- Shin, Chanseok -- Camargo, Fernando D -- Gygi, Steven P -- Bartel, David P -- R01 GM067031/GM/NIGMS NIH HHS/ -- R01 HG003456/HG/NHGRI NIH HHS/ -- R01 HG003456-04A1/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Sep 4;455(7209):64-71. doi: 10.1038/nature07242. Epub 2008 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18668037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; HeLa Cells ; Humans ; Isotope Labeling ; Male ; Mice ; MicroRNAs/*genetics/*metabolism ; Neutrophils/metabolism ; Oligonucleotide Array Sequence Analysis ; *Protein Biosynthesis ; Proteomics ; Transfection
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Live-animal tracking of individual haematopoietic stem/progenitor cells in their niche (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-05
    Description: Stem cells reside in a specialized, regulatory environment termed the niche that dictates how they generate, maintain and repair tissues. We have previously documented that transplanted haematopoietic stem and progenitor cell populations localize to subdomains of bone-marrow microvessels where the chemokine CXCL12 is particularly abundant. Using a combination of high-resolution confocal microscopy and two-photon video imaging of individual haematopoietic cells in the calvarium bone marrow of living mice over time, we examine the relationship of haematopoietic stem and progenitor cells to blood vessels, osteoblasts and endosteal surface as they home and engraft in irradiated and c-Kit-receptor-deficient recipient mice. Osteoblasts were enmeshed in microvessels and relative positioning of stem/progenitor cells within this complex tissue was nonrandom and dynamic. Both cell autonomous and non-autonomous factors influenced primitive cell localization. Different haematopoietic cell subsets localized to distinct locations according to the stage of differentiation. When physiological challenges drove either engraftment or expansion, bone-marrow stem/progenitor cells assumed positions in close proximity to bone and osteoblasts. Our analysis permits observing in real time, at a single cell level, processes that previously have been studied only by their long-term outcome at the organismal level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820276/" 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/PMC2820276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo Celso, Cristina -- Fleming, Heather E -- Wu, Juwell W -- Zhao, Cher X -- Miake-Lye, Sam -- Fujisaki, Joji -- Cote, Daniel -- Rowe, David W -- Lin, Charles P -- Scadden, David T -- R01 EY014106/EY/NEI NIH HHS/ -- R01 EY014106-05/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jan 1;457(7225):92-6. doi: 10.1038/nature07434. Epub 2008 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19052546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology ; Bone Marrow ; Cell Division ; Cell Separation ; Hematopoietic Stem Cells/*cytology ; Mice ; Mice, Inbred C57BL ; Osteoblasts/cytology ; Proto-Oncogene Proteins c-kit/genetics/metabolism ; Skull/cytology ; Stem Cell Niche/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    WSTF regulates the H2A.X DNA damage response via a novel tyrosine kinase activity (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-19
    Description: DNA double-stranded breaks present a serious challenge for eukaryotic cells. The inability to repair breaks leads to genomic instability, carcinogenesis and cell death. During the double-strand break response, mammalian chromatin undergoes reorganization demarcated by H2A.X Ser 139 phosphorylation (gamma-H2A.X). However, the regulation of gamma-H2A.X phosphorylation and its precise role in chromatin remodelling during the repair process remain unclear. Here we report a new regulatory mechanism mediated by WSTF (Williams-Beuren syndrome transcription factor, also known as BAZ1B)-a component of the WICH complex (WSTF-ISWI ATP-dependent chromatin-remodelling complex). We show that WSTF has intrinsic tyrosine kinase activity by means of a domain that shares no sequence homology to any known kinase fold. We show that WSTF phosphorylates Tyr 142 of H2A.X, and that WSTF activity has an important role in regulating several events that are critical for the DNA damage response. Our work demonstrates a new mechanism that regulates the DNA damage response and expands our knowledge of domains that contain intrinsic tyrosine kinase activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854499/" 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/PMC2854499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, Andrew -- Li, Haitao -- Shechter, David -- Ahn, Sung Hee -- Fabrizio, Laura A -- Erdjument-Bromage, Hediye -- Ishibe-Murakami, Satoko -- Wang, Bin -- Tempst, Paul -- Hofmann, Kay -- Patel, Dinshaw J -- Elledge, Stephen J -- Allis, C David -- F32 GM075486/GM/NIGMS NIH HHS/ -- P30 CA08748/CA/NCI NIH HHS/ -- R01 GM040922/GM/NIGMS NIH HHS/ -- R01 GM040922-24/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jan 1;457(7225):57-62. doi: 10.1038/nature07668. Epub 2008 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromatin Biology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092802" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/metabolism ; *DNA Damage ; Histones/genetics/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Nucleosomes/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/*metabolism ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-08
    Description: We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its own receptor TrkA in mouse and rat neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain-derived neurotrophic factor and neurotrophin-4, which, through the receptor p75, can kill neighboring neurons with low retrograde NGF-TrkA signaling whereas neurons with high NGF-TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" 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/PMC3612357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deppmann, Christopher D -- Mihalas, Stefan -- Sharma, Nikhil -- Lonze, Bonnie E -- Niebur, Ernst -- Ginty, David D -- EY016281/EY/NEI NIH HHS/ -- F32 NS053187/NS/NINDS NIH HHS/ -- NS053187/NS/NINDS NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):369-73. doi: 10.1126/science.1152677. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Survival ; Cells, Cultured ; Computer Simulation ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Mathematics ; Mice ; *Models, Neurological ; Nerve Growth Factor/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/cytology/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Receptor, trkA/genetics/*metabolism ; Receptors, Nerve Growth Factor/genetics/metabolism ; Signal Transduction ; Superior Cervical Ganglion/*cytology
    Print ISSN: 0036-8075
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  • 8
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    Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-21
    Description: The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kravchenko, Vladimir V -- Kaufmann, Gunnar F -- Mathison, John C -- Scott, David A -- Katz, Alexander Z -- Grauer, David C -- Lehmann, Mandy -- Meijler, Michael M -- Janda, Kim D -- Ulevitch, Richard J -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):259-63. doi: 10.1126/science.1156499. Epub 2008 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Sciences, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566250" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/physiology ; Adult ; Animals ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cystic Fibrosis/microbiology ; Female ; *Gene Expression Regulation ; Homoserine/*analogs & derivatives/physiology ; Humans ; I-kappa B Kinase/metabolism ; I-kappa B Proteins/metabolism ; Immunity, Innate ; Interferon-gamma/immunology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; NF-kappa B/*metabolism ; Phosphorylation ; Pseudomonas Infections/immunology/microbiology ; Pseudomonas aeruginosa/immunology/*pathogenicity/physiology ; *Signal Transduction ; Toll-Like Receptors/metabolism ; Transcription Factor RelA/metabolism
    Print ISSN: 0036-8075
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  • 9
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    White fat progenitor cells reside in the adipose vasculature (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-09-20
    Description: White adipose (fat) tissues regulate metabolism, reproduction, and life span. Adipocytes form throughout life, with the most marked expansion of the lineage occurring during the postnatal period. Adipocytes develop in coordination with the vasculature, but the identity and location of white adipocyte progenitor cells in vivo are unknown. We used genetically marked mice to isolate proliferating and renewing adipogenic progenitors. We found that most adipocytes descend from a pool of these proliferating progenitors that are already committed, either prenatally or early in postnatal life. These progenitors reside in the mural cell compartment of the adipose vasculature, but not in the vasculature of other tissues. Thus, the adipose vasculature appears to function as a progenitor niche and may provide signals for adipocyte development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597101/" 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/PMC2597101/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Zeve, Daniel -- Suh, Jae Myoung -- Bosnakovski, Darko -- Kyba, Michael -- Hammer, Robert E -- Tallquist, Michelle D -- Graff, Jonathan M -- 1R01DK064261/DK/NIDDK NIH HHS/ -- 1R01DK066556/DK/NIDDK NIH HHS/ -- R01 DK064261/DK/NIDDK NIH HHS/ -- R01 DK064261-01/DK/NIDDK NIH HHS/ -- R01 DK064261-02/DK/NIDDK NIH HHS/ -- R01 DK064261-03/DK/NIDDK NIH HHS/ -- R01 DK064261-04/DK/NIDDK NIH HHS/ -- R01 DK064261-05/DK/NIDDK NIH HHS/ -- R01 DK066556/DK/NIDDK NIH HHS/ -- R01 DK066556-01/DK/NIDDK NIH HHS/ -- R01 DK066556-02/DK/NIDDK NIH HHS/ -- R01 DK066556-03/DK/NIDDK NIH HHS/ -- R01 DK066556-04/DK/NIDDK NIH HHS/ -- R01 DK066556-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):583-6. doi: 10.1126/science.1156232. Epub 2008 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801968" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, White/*cytology/metabolism ; Adipogenesis ; Adipose Tissue/*blood supply/cytology ; Animals ; Antigens, CD/metabolism ; Blood Vessels/*cytology ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Doxycycline/pharmacology ; Gene Expression Profiling ; Mice ; Mice, Transgenic ; Multipotent Stem Cells/*cytology/metabolism ; PPAR gamma/genetics/metabolism ; Stromal Cells/*cytology/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    An inhibitor of FtsZ with potent and selective anti-staphylococcal activity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: FtsZ is an essential bacterial guanosine triphosphatase and homolog of mammalian beta-tubulin that polymerizes and assembles into a ring to initiate cell division. We have created a class of small synthetic antibacterials, exemplified by PC190723, which inhibits FtsZ and prevents cell division. PC190723 has potent and selective in vitro bactericidal activity against staphylococci, including methicillin- and multi-drug-resistant Staphylococcus aureus. The putative inhibitor-binding site of PC190723 was mapped to a region of FtsZ that is analogous to the Taxol-binding site of tubulin. PC190723 was efficacious in an in vivo model of infection, curing mice infected with a lethal dose of S. aureus. The data validate FtsZ as a target for antibacterial intervention and identify PC190723 as suitable for optimization into a new anti-staphylococcal therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haydon, David J -- Stokes, Neil R -- Ure, Rebecca -- Galbraith, Greta -- Bennett, James M -- Brown, David R -- Baker, Patrick J -- Barynin, Vladimir V -- Rice, David W -- Sedelnikova, Sveta E -- Heal, Jonathan R -- Sheridan, Joseph M -- Aiwale, Sachin T -- Chauhan, Pramod K -- Srivastava, Anil -- Taneja, Amit -- Collins, Ian -- Errington, Jeff -- Czaplewski, Lloyd G -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1673-5. doi: 10.1126/science.1159961.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Prolysis, Begbroke Science Park, Oxfordshire OX5 1PF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801997" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Bacterial Agents/*pharmacology/therapeutic use ; Bacillus subtilis/chemistry/*drug effects/genetics ; Bacterial Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Binding Sites ; Cell Division/drug effects ; Crystallography, X-Ray ; Cytoskeletal Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Drug Resistance, Bacterial/genetics ; Drug Resistance, Multiple, Bacterial ; Ligands ; Methicillin Resistance ; Mice ; Microbial Sensitivity Tests ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Pyridines/chemistry/metabolism/*pharmacology/therapeutic use ; Staphylococcal Infections/*drug therapy ; Staphylococcus aureus/chemistry/*drug effects ; Thiazoles/chemistry/metabolism/*pharmacology/therapeutic use ; Tubulin/chemistry/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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