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  • Cells, Cultured  (85)
  • American Association for the Advancement of Science (AAAS)  (85)
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  • American Association for the Advancement of Science (AAAS)  (85)
  • American Geophysical Union
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  • American Physical Society (APS)
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  • 1
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    Control of synaptic strength by glial TNFalpha (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-03-23
    Beschreibung: Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity and ensheathe synapses, their influence on synaptic strength has largely been ignored. Here, we show that a protein produced by glia, tumor necrosis factor alpha (TNFalpha), enhances synaptic efficacy by increasing surface expression of AMPA receptors. Preventing the actions of endogenous TNFalpha has the opposite effects. Thus, the continual presence of TNFalpha is required for preservation of synaptic strength at excitatory synapses. Through its effects on AMPA receptor trafficking, TNFalpha may play roles in synaptic plasticity and modulating responses to neural injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beattie, Eric C -- Stellwagen, David -- Morishita, Wade -- Bresnahan, Jacqueline C -- Ha, Byeong Keun -- Von Zastrow, Mark -- Beattie, Michael S -- Malenka, Robert C -- DA00439/DA/NIDA NIH HHS/ -- MH063394/MH/NIMH NIH HHS/ -- NS 31193/NS/NINDS NIH HHS/ -- NS38079/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 22;295(5563):2282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, CA 94304, USA. beattie.2@osu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11910117" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD/pharmacology ; Astrocytes/*metabolism ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Gene Expression Regulation/drug effects ; Hippocampus/cytology/metabolism ; Neuronal Plasticity/drug effects ; Neurons/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, Tumor Necrosis Factor ; Receptors, Tumor Necrosis Factor, Type I ; Synapses/drug effects/*metabolism ; Synaptic Transmission/drug effects ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Genomic instability in mice lacking histone H2AX (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-04-06
    Beschreibung: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" 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/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/physiology ; Base Sequence ; Cell Aging ; Cell Cycle ; Cells, Cultured ; *Chromosome Aberrations ; DNA Damage ; *DNA Repair ; Female ; Gene Targeting ; Histones/chemistry/*genetics/*physiology ; Immunoglobulin Class Switching ; Infertility, Male/genetics/physiopathology ; Lymphocyte Count ; Male ; Meiosis ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Phosphorylation ; *Recombination, Genetic ; Spermatocytes/physiology ; T-Lymphocytes/immunology/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Signal transduction. History matters (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-08-10
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ingolia, Nicholas T -- Murray, Andrew W -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):948-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology and Bauer Center for Genomics Research, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12169717" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptation, Physiological ; Animals ; Biological Evolution ; *Cell Cycle Proteins ; Cells, Cultured ; Dual Specificity Phosphatase 1 ; *Feedback, Physiological ; Immediate-Early Proteins/*metabolism ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/*metabolism ; Models, Biological ; *Phosphoprotein Phosphatases ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Historical essay. The early years of HIV/AIDS (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-12-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, Robert C -- New York, N.Y. -- Science. 2002 Nov 29;298(5599):1728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Human Virology and Department of Microbiology and Immunology, University of Maryland, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12459576" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): AIDS Serodiagnosis/history ; Acquired Immunodeficiency Syndrome/diagnosis/*history/immunology/virology ; CD4-Positive T-Lymphocytes/virology ; Cell Line ; Cells, Cultured ; France ; *HIV/classification/isolation & purification/physiology ; History, 20th Century ; Human T-lymphotropic virus 1/isolation & purification/physiology ; Human T-lymphotropic virus 2/isolation & purification/physiology ; Humans ; Interleukin-2/history/isolation & purification/physiology ; Patents as Topic/history ; RNA-Directed DNA Polymerase/history/isolation & purification/metabolism ; United States ; Virus Cultivation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Discrete microdomains with high concentration of cAMP in stimulated rat neonatal cardiac myocytes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-03-02
    Beschreibung: The second messenger cyclic adenosine monophosphate (cAMP) is the most important modulator of sympathetic control over cardiac contractility. In cardiac myocytes and many other cell types, however, cAMP transduces the signal generated upon stimulation of various receptors and activates different cellular functions, raising the issue of how specificity can be achieved. In the general field of signal transduction, the view is emerging that specificity is guaranteed by tight localization of signaling events. Here, we show that in neonatal rat cardiac myocytes, beta-adrenergic stimulation generates multiple microdomains with increased concentration of cAMP in correspondence with the region of the transverse tubule/junctional sarcoplasmic reticulum membrane. The restricted pools of cAMP show a range of action as small as approximately 1 micrometer, and free diffusion of the second messenger is limited by the activity of phosphodiesterases. Furthermore, we demonstrate that such gradients of cAMP specifically activate a subset of protein kinase A molecules anchored in proximity to the T tubule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaccolo, Manuela -- Pozzan, Tullio -- TCP00089/Telethon/Italy -- New York, N.Y. -- Science. 2002 Mar 1;295(5560):1711-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences and Venetian Institute for Molecular Medicine, University of Padua, Via Orus 2, 35129 Padua, Italy. manuela.zaccolo@unipd.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11872839" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 1-Methyl-3-isobutylxanthine/pharmacology ; A Kinase Anchor Proteins ; Adaptor Proteins, Signal Transducing ; Animals ; Animals, Newborn ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Intracellular Membranes/metabolism ; Kinetics ; Luminescent Proteins ; Myocardium/*cytology/*metabolism/ultrastructure ; Norepinephrine/pharmacology ; Phosphodiesterase Inhibitors/pharmacology ; Proto-Oncogene Proteins/pharmacology ; Rats ; Receptors, Adrenergic, beta/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sarcoplasmic Reticulum/*metabolism ; Second Messenger Systems ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Contribution of human alpha-defensin 1, 2, and 3 to the anti-HIV-1 activity of CD8 antiviral factor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-09-28
    Beschreibung: It has been known since 1986 that CD8 T lymphocytes from certain HIV-1-infected individuals who are immunologically stable secrete a soluble factor, termed CAF, that suppresses HIV-1 replication. However, the identity of CAF remained elusive despite an extensive search. By means of a protein-chip technology, we identified a cluster of proteins that were secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated. These proteins were identified as alpha-defensin 1, 2, and 3 on the basis of specific antibody recognition and amino acid sequencing. CAF activity was eliminated or neutralized by an antibody specific for human alpha-defensins. Synthetic and purified preparations of alpha-defensins also inhibited the replication of HIV-1 isolates in vitro. Taken together, our results indicate that alpha-defensin 1, 2, and 3 collectively account for much of the anti-HIV-1 activity of CAF that is not attributable to beta-chemokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Linqi -- Yu, Wenjie -- He, Tian -- Yu, Jian -- Caffrey, Rebecca E -- Dalmasso, Enrique A -- Fu, Siyu -- Pham, Thang -- Mei, Jianfeng -- Ho, Jaclyn J -- Zhang, Wenyong -- Lopez, Peter -- Ho, David D -- AI-42848/AI/NIAID NIH HHS/ -- M01-RR00102/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):995-1000. Epub 2002 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, The Rockefeller University, 455 First Avenue, New York, NY 10016, USA. lzhang@adarc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351674" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Antibodies, Monoclonal ; Antiviral Agents/chemistry/isolation & purification/*pharmacology ; CD8-Positive T-Lymphocytes/chemistry/*immunology ; Cells, Cultured ; Chemokines, CC/immunology/physiology ; HIV Infections/*immunology/virology ; HIV Long-Term Survivors ; HIV-1/drug effects/*physiology ; Humans ; Mass Spectrometry ; Molecular Sequence Data ; Neutrophils/chemistry/immunology ; Protein Array Analysis ; Virus Replication ; alpha-Defensins/chemistry/isolation & purification/pharmacology/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    A heat-sensitive TRP channel expressed in keratinocytes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-05-23
    Beschreibung: Mechanical and thermal cues stimulate a specialized group of sensory neurons that terminate in the skin. Three members of the transient receptor potential (TRP) family of channels are expressed in subsets of these neurons and are activated at distinct physiological temperatures. Here, we describe the cloning and characterization of a novel thermosensitive TRP channel. TRPV3 has a unique threshold: It is activated at innocuous (warm) temperatures and shows an increased response at noxious temperatures. TRPV3 is specifically expressed in keratinocytes; hence, skin cells are capable of detecting heat via molecules similar to those in heat-sensing neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peier, Andrea M -- Reeve, Alison J -- Andersson, David A -- Moqrich, Aziz -- Earley, Taryn J -- Hergarden, Anne C -- Story, Gina M -- Colley, Sian -- Hogenesch, John B -- McIntyre, Peter -- Bevan, Stuart -- Patapoutian, Ardem -- New York, N.Y. -- Science. 2002 Jun 14;296(5575):2046-9. Epub 2002 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomics Institute of the Novartis Research Foundation, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016205" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Animals, Newborn ; Blotting, Northern ; CHO Cells ; Capsaicin/*analogs & derivatives/pharmacology ; *Cation Transport Proteins ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Cricetinae ; Epidermis/cytology/innervation/metabolism ; Ganglia, Spinal/metabolism ; *Hot Temperature ; Humans ; In Situ Hybridization ; Ion Channels/chemistry/genetics/*metabolism ; Keratinocytes/*metabolism ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Nerve Endings/physiology ; Neurons/physiology ; Patch-Clamp Techniques ; RNA, Messenger/genetics/metabolism ; Ruthenium Red/pharmacology ; Signal Transduction ; Spinal Cord/metabolism ; TRPV Cation Channels ; Temperature
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Development. Putting the brakes on regeneration (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-06-08
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKerracher, Lisa -- Ellezam, Benjamin -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1819-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Pathologie et Biologie Cellulaire, Universite de Montreal, 2900 Edouard-Montpetit, Montreal, Quebec, H3T 1J4 Canada. mckerral@patho.umontreal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12052945" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amacrine Cells/*physiology ; Animals ; Axonal Transport ; Axons/*physiology ; *Cell Communication ; Cell Differentiation ; Cell Polarity ; Cells, Cultured ; Coculture Techniques ; Dendrites/*physiology ; Embryo, Mammalian ; Nerve Crush ; *Nerve Regeneration ; Optic Nerve/cytology/physiology ; Peripheral Nerves/transplantation ; Rats ; Retinal Ganglion Cells/*physiology ; Signal Transduction ; Spinal Cord/cytology/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Abnormal vascular function and hypertension in mice deficient in estrogen receptor beta (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-01-19
    Beschreibung: Blood vessels express estrogen receptors, but their role in cardiovascular physiology is not well understood. We show that vascular smooth muscle cells and blood vessels from estrogen receptor beta (ERbeta)-deficient mice exhibit multiple functional abnormalities. In wild-type mouse blood vessels, estrogen attenuates vasoconstriction by an ERbeta-mediated increase in inducible nitric oxide synthase expression. In contrast, estrogen augments vasoconstriction in blood vessels from ERbeta-deficient mice. Vascular smooth muscle cells isolated from ERbeta-deficient mice show multiple abnormalities of ion channel function. Furthermore, ERbeta-deficient mice develop sustained systolic and diastolic hypertension as they age. These data support an essential role for ERbeta in the regulation of vascular function and blood pressure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Yan -- Bian, Zhao -- Lu, Ping -- Karas, Richard H -- Bao, Lin -- Cox, Daniel -- Hodgin, Jeffrey -- Shaul, Philip W -- Thoren, Peter -- Smithies, Oliver -- Gustafsson, Jan-Ake -- Mendelsohn, Michael E -- GM20069/GM/NIGMS NIH HHS/ -- HD30276/HD/NICHD NIH HHS/ -- HL53546/HL/NHLBI NIH HHS/ -- HL56235/HL/NHLBI NIH HHS/ -- P50 HL63494/HL/NHLBI NIH HHS/ -- R01 HL55309/HL/NHLBI NIH HHS/ -- R01 HL56069/HL/NHLBI NIH HHS/ -- R01 HL61298/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jan 18;295(5554):505-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Research Institute, New England Medical Center and Department of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11799247" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenergic alpha-Agonists/pharmacology ; Animals ; Aorta ; Blood Pressure ; Cells, Cultured ; Estradiol/*analogs & derivatives/pharmacology ; Estrogen Antagonists/pharmacology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Guanidines/pharmacology ; Humans ; Hypertension/*physiopathology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular/*physiology ; Nitric Oxide Synthase/genetics/metabolism ; Nitric Oxide Synthase Type II ; Nitroarginine/pharmacology ; Patch-Clamp Techniques ; Phenylephrine/pharmacology ; Potassium Channels/metabolism ; Receptors, Estrogen/genetics/*physiology ; *Vasoconstriction/drug effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Neurofibromas in NF1: Schwann cell origin and role of tumor environment (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-05-04
    Beschreibung: Neurofibromatosis type 1 (NF1) is one of the most prevalent dominantly inherited genetic diseases of the nervous system. NF1 encodes a tumor suppressor whose functional loss results in the development of benign neurofibromas that can progress to malignancy. Neurofibromas are complex tumors composed of axonal processes, Schwann cells, fibroblasts, perineurial cells, and mast cells. Through use of a conditional (cre/lox) allele, we show that loss of NF1 in the Schwann cell lineage is sufficient to generate tumors. In addition, complete NF1-mediated tumorigenicity requires both a loss of NF1 in cells destined to become neoplastic as well as heterozygosity in non-neoplastic cells. The requirement for a permissive haploinsufficient environment to allow tumorigenesis may have therapeutic implications for NF1 and other familial cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024710/" 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/PMC3024710/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Yuan -- Ghosh, Pritam -- Charnay, Patrick -- Burns, Dennis K -- Parada, Luis F -- R01 NS034296/NS/NINDS NIH HHS/ -- R01 NS034296-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):920-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Developmental Biology, Department of Pathology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9133, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988578" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Axons/ultrastructure ; Cell Lineage ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cranial Nerves/pathology ; Culture Techniques ; Female ; *Genes, Neurofibromatosis 1 ; Genotype ; Heterozygote ; Hyperplasia ; Loss of Heterozygosity ; Male ; Mast Cells/chemistry/pathology ; Mice ; Mice, Transgenic ; Neurofibroma/genetics/*pathology ; Neurofibromatosis 1/genetics/*pathology ; Peripheral Nerves/pathology ; Schwann Cells/chemistry/*pathology ; Spinal Nerves/pathology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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