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  • Mice  (434)
  • American Association for the Advancement of Science (AAAS)  (434)
  • 2005-2009  (355)
  • 1980-1984  (79)
  • 2006  (185)
  • 2005  (170)
  • 1981  (79)
Collection
Keywords
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  • American Association for the Advancement of Science (AAAS)  (434)
  • Springer  (2)
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  • 2005-2009  (355)
  • 1980-1984  (79)
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  • 1
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    Molecular biology. Managing associations between different chromosomes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spilianakis, Charalampos G -- Flavell, Richard A -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614205" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Nucleus/genetics/metabolism ; Chromosomes, Mammalian/*genetics/metabolism ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Fluorescent Antibody Technique ; *Gene Expression Regulation ; Genomic Imprinting ; In Situ Hybridization, Fluorescence ; Insulin-Like Growth Factor II/genetics ; Mice ; Neurofibromin 1/genetics ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Regulatory Elements, Transcriptional ; Repressor Proteins/*metabolism ; Transcription, Genetic ; Transcriptional Activation ; Ubiquitin-Protein Ligases/genetics
    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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    Characterization of the piRNA complex from rat testes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Small noncoding RNAs regulate processes essential for cell growth and development, including mRNA degradation, translational repression, and transcriptional gene silencing (TGS). During a search for candidate mammalian factors for TGS, we purified a complex that contains small RNAs and Riwi, the rat homolog to human Piwi. The RNAs, frequently 29 to 30 nucleotides in length, are called Piwi-interacting RNAs (piRNAs), 94% of which map to 100 defined (〈 or = 101 kb) genomic regions. Within these regions, the piRNAs generally distribute across only one genomic strand or distribute on two strands but in a divergent, nonoverlapping manner. Preparations of piRNA complex (piRC) contain rRecQ1, which is homologous to qde-3 from Neurospora, a gene implicated in silencing pathways. Piwi has been genetically linked to TGS in flies, and slicer activity cofractionates with the purified complex. These results are consistent with a gene-silencing role for piRC in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lau, Nelson C -- Seto, Anita G -- Kim, Jinkuk -- Kuramochi-Miyagawa, Satomi -- Nakano, Toru -- Bartel, David P -- Kingston, Robert E -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):363-7. Epub 2006 Jun 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778019" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/isolation & purification/metabolism ; Animals ; Chromosomes, Mammalian ; Conserved Sequence ; DNA Helicases/isolation & purification/metabolism ; Gene Library ; Genome ; Male ; Mice ; Proteins/isolation & purification/*metabolism ; *RNA Interference ; RNA, Untranslated/chemistry/genetics/isolation & purification/*metabolism ; Rats ; Rats, Sprague-Dawley ; RecQ Helicases ; Ribonucleoproteins/chemistry/isolation & purification/*metabolism ; Testis/*chemistry ; 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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  • 3
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    Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Serotonin [5-hydroxytryptamine (5-HT)] neurotransmission in the central nervous system modulates depression and anxiety-related behaviors in humans and rodents, but the responsible downstream receptors remain poorly understood. We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of 5HT2AR signaling to the cortex normalized conflict anxiety behaviors. These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisstaub, Noelia V -- Zhou, Mingming -- Lira, Alena -- Lambe, Evelyn -- Gonzalez-Maeso, Javier -- Hornung, Jean-Pierre -- Sibille, Etienne -- Underwood, Mark -- Itohara, Shigeyoshi -- Dauer, William T -- Ansorge, Mark S -- Morelli, Emanuela -- Mann, J John -- Toth, Miklos -- Aghajanian, George -- Sealfon, Stuart C -- Hen, Rene -- Gingrich, Jay A -- KO8 MH01711/MH/NIMH NIH HHS/ -- P01 DA12923/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):536-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Columbia University and the New York State Psychiatric Institute, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*physiopathology ; Cerebral Cortex/*metabolism ; Conditioning (Psychology) ; Conflict (Psychology) ; Depression/physiopathology ; Exploratory Behavior ; Fear ; Limbic System/metabolism ; Mice ; Mice, Knockout ; Patch-Clamp Techniques ; Periaqueductal Gray/metabolism ; Prosencephalon/metabolism ; Receptor, Serotonin, 5-HT2A/genetics/*metabolism ; Receptor, Serotonin, 5-HT2C/metabolism ; Receptors, Neurotransmitter/metabolism ; Risk-Taking ; Serotonin/physiology ; *Signal Transduction ; Synaptic Transmission
    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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    A one-size-fits-all flu vaccine? (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):380-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627732" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Administration, Intranasal ; Animals ; Antibodies, Viral/biosynthesis/immunology ; Antigenic Variation ; Clinical Trials as Topic ; Drug Evaluation, Preclinical ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology ; Humans ; Influenza A virus/*immunology ; *Influenza Vaccines/administration & dosage/immunology ; Influenza, Human/*prevention & control ; Mice ; Nucleoproteins/genetics/immunology ; Orthomyxoviridae Infections/prevention & control ; RNA-Binding Proteins/genetics/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccination ; Vaccines, Attenuated/administration & dosage/immunology ; Vaccines, DNA/administration & dosage/immunology ; Viral Core Proteins/genetics/immunology ; Viral Matrix Proteins/immunology
    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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    Lhx2 maintains stem cell character in hair follicles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: During embryogenesis, stem cells are set aside to fuel the postnatal hair cycle and repair the epidermis after injury. To define how hair follicle stem cells are specified and maintained in an undifferentiated state, we developed a strategy to isolate and transcriptionally profile embryonic hair progenitors in mice. We identified Lhx2 as a transcription factor positioned downstream of signals necessary to specify hair follicle stem cells, but upstream from signals required to drive activated stem cells to terminally differentiate. Using gain- and loss-of-function studies, we uncovered a role for Lhx2 in maintaining the growth and undifferentiated properties of hair follicle progenitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2405918/" 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/PMC2405918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhee, Horace -- Polak, Lisa -- Fuchs, Elaine -- R01 AR031737/AR/NIAMS NIH HHS/ -- R01 AR031737-24/AR/NIAMS NIH HHS/ -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01 AR050452-04/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Epidermis/cytology/embryology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Hair/embryology/growth & development ; Hair Follicle/*cytology/embryology/physiology ; Homeodomain Proteins/genetics/*physiology ; LIM-Homeodomain Proteins ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; Signal Transduction ; Skin Transplantation ; Stem Cells/*physiology ; Transcription Factors/genetics/*physiology ; Up-Regulation
    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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  • 6
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    Cell biology. A metabolic push to proliferate (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brasaemle, Dawn L -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1581-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutritional Sciences, Rutgers, State University of New Jersey, New Brunswick, NJ 08901, USA. brasaemle@aesop.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973864" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Membrane/metabolism ; Cell Proliferation ; Fatty Acids/metabolism ; Glucose/administration & dosage ; Hepatocytes/cytology/*metabolism ; Hydrolysis ; *Lipid Metabolism ; *Liver Regeneration ; Mice ; Models, Biological ; Phospholipids/biosynthesis ; Triglycerides/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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    Immunology. Restless T cells sniff and go (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustelin, Tomas -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, and Program of Signal Transduction, Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA. tmustelin@burnham.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD ; Antigens, CD28/metabolism ; Antigens, CD80/metabolism ; Antigens, CD86/metabolism ; Antigens, Differentiation/genetics/*physiology ; *Autoimmunity ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/immunology ; Humans ; Integrins/physiology ; Ligands ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*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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  • 8
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    Platelet-derived serotonin mediates liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: The liver can regenerate its volume after major tissue loss. In a mouse model of liver regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5-HT2A and 2B subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5-HT2A and 2B receptors inhibited liver regeneration. Liver regeneration was also blunted in mice lacking tryptophan hydroxylase 1, which is the rate-limiting enzyme for the synthesis of peripheral serotonin. This failure of regeneration was rescued by reloading serotonin-free platelets with a serotonin precursor molecule. These results suggest that platelet-derived serotonin is involved in the initiation of liver regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lesurtel, Mickael -- Graf, Rolf -- Aleil, Boris -- Walther, Diego J -- Tian, Yinghua -- Jochum, Wolfram -- Gachet, Christian -- Bader, Michael -- Clavien, Pierre-Alain -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Visceral and Transplantation Surgery, University Hospital of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601191" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Hydroxytryptophan/pharmacology ; Amphetamines/pharmacology ; Animals ; Blood Platelets/metabolism/*physiology ; Busulfan/pharmacology ; Cell Proliferation ; Hepatectomy ; Hepatocytes/cytology ; Liver/metabolism/*physiology ; *Liver Regeneration ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Platelet Count ; Receptor, Serotonin, 5-HT2A/metabolism ; Receptor, Serotonin, 5-HT2B/metabolism ; Serotonin/blood/*physiology ; Serotonin 5-HT2 Receptor Antagonists ; Thrombocytopenia ; Ticlopidine/analogs & derivatives/pharmacology ; Tryptophan Hydroxylase/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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  • 9
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    Role of iNOS in human host defense (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, Carl -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1874-5; author reply 1874-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/enzymology/*immunology ; Cell Culture Techniques ; Cell Differentiation ; Cells, Cultured ; Humans ; Macrophages/cytology/*enzymology ; Mice ; Nitric Oxide Synthase Type II/biosynthesis/*metabolism ; Tuberculosis/enzymology/immunology
    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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    Editorial expression of concern (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Donald -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):592.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ectoderm/*physiology ; *Embryonic Development ; *Gene Expression Regulation, Developmental ; Homeodomain Proteins/*genetics/metabolism ; Mice ; Transcription Factors/*genetics/metabolism ; Trophoblasts/*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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  • 11
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    alphaE-catenin controls cerebral cortical size by regulating the hedgehog signaling pathway (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: During development, cells monitor and adjust their rates of accumulation to produce organs of predetermined size. We show here that central nervous system-specific deletion of the essential adherens junction gene, alphaE-catenin, causes abnormal activation of the hedgehog pathway, resulting in shortening of the cell cycle, decreased apoptosis, and cortical hyperplasia. We propose that alphaE-catenin connects cell-density-dependent adherens junctions with the developmental hedgehog pathway and that this connection may provide a negative feedback loop controlling the size of developing cerebral cortex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556178/" 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/PMC2556178/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lien, Wen-Hui -- Klezovitch, Olga -- Fernandez, Tania E -- Delrow, Jeff -- Vasioukhin, Valeri -- P41 RR011823/RR/NCRR NIH HHS/ -- P41 RR011823-128171/RR/NCRR NIH HHS/ -- R01 CA098161/CA/NCI NIH HHS/ -- R01 CA098161-01A1/CA/NCI NIH HHS/ -- R01 CA098161-02/CA/NCI NIH HHS/ -- R01 CA098161-03/CA/NCI NIH HHS/ -- R01 CA098161-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1609-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543460" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; Apoptosis ; Cell Adhesion ; Cell Count ; Cell Cycle ; Cell Differentiation ; Cell Polarity ; Central Nervous System/embryology ; Cerebral Cortex/cytology/*embryology/pathology/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mitosis ; Models, Biological ; Mutation ; Neurons/cytology/*physiology/ultrastructure ; Oligonucleotide Array Sequence Analysis ; *Signal Transduction ; Stem Cells/cytology/ultrastructure ; Trans-Activators/*metabolism ; Up-Regulation ; alpha Catenin/genetics/*physiology
    Print ISSN: 0036-8075
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  • 12
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    Cdx2 gene expression and trophectoderm lineage specification in mouse embryos (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Controversy exists as to whether individual blastomeres from two-cell-stage mouse embryos have identical developmental properties and fate. We show that the transcription factor Cdx2 is expressed in the nuclei of cells derived from the late-dividing but not the first-dividing blastomere of two-cell embryos and, by lineage tracing and RNA interference knock-down experiments, that this lagging cell is the precursor of trophectoderm. Cdx2 mRNA is localized toward the vegetal pole of oocytes, reorients after fertilization, and becomes concentrated in the late-dividing, two-cell-stage blastomere. The asymmetrical distribution of Cdx2 gene products in the oocyte and embryo defines the lineage to trophectoderm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deb, Kaushik -- Sivaguru, Mayandi -- Yong, Hwan Yul -- Roberts, R Michael -- R01 HD21896/HD/NICHD NIH HHS/ -- R01 HD42201/HD/NICHD NIH HHS/ -- R01 RR13438/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):992-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Sciences, Columbia, MO 65211, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; Blastomeres/*physiology ; Cell Nucleus/metabolism ; Cell Polarity ; Ectoderm/*physiology ; *Embryonic Development ; Fertilization ; *Gene Expression Regulation, Developmental ; Homeodomain Proteins/*genetics/*metabolism ; In Situ Hybridization ; Mice ; Morula/physiology ; Oocytes/physiology ; RNA Interference ; RNA, Messenger/genetics/metabolism ; RNA, Small Interfering ; Transcription Factors/*genetics/*metabolism ; Transcription, Genetic ; Trophoblasts/*physiology ; Zygote/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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  • 13
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    Cell biology. Actin discrimination (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bulinski, J Chloe -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):180-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and the Department of Pathology and Cell Biology, Columbia University, 1212 Amsterdam Avenue, New York, NY 10027-2450, USA. jcb4@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840687" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/chemistry/*metabolism ; Actins/chemistry/genetics/*metabolism ; Aminoacyltransferases/genetics/*metabolism ; Animals ; Arginine/*metabolism ; Cell Movement ; Cytoplasm/chemistry/metabolism ; Evolution, Molecular ; Fibroblasts ; Mice ; Myosins/metabolism ; Profilins/metabolism ; Protein Isoforms/genetics/metabolism ; Pseudopodia/chemistry/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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  • 14
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    Cell signaling. A new way to burn fat (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neels, Jaap G -- Olefsky, Jerrold M -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1756-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0673, USA. jolefsky@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794069" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/*metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Energy Intake ; Energy Metabolism ; Enzyme Activation ; Fasting ; Fatty Acids/metabolism ; Hepatocytes/metabolism ; Insulin/physiology ; Insulin Resistance ; *Lipid Metabolism ; Lipogenesis ; Liver/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Models, Biological ; Nuclear Proteins/*metabolism ; Obesity/therapy ; Oxidation-Reduction ; Phosphorylation ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*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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  • 15
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    Mouse genetics. NIH knocks out key mouse house (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1863.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks/economics ; Costs and Cost Analysis ; Embryo, Mammalian/cytology ; Intellectual Property ; Mice ; *Mice, Knockout ; *National Institutes of Health (U.S.) ; *Organizations, Nonprofit/economics ; Stem Cells ; Texas ; United States
    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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  • 16
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    Global control of dimorphism and virulence in fungi (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Microbial pathogens that normally inhabit our environment can adapt to thrive inside mammalian hosts. There are six dimorphic fungi that cause disease worldwide, which switch from nonpathogenic molds in soil to pathogenic yeast after spores are inhaled and exposed to elevated temperature. Mechanisms that regulate this switch remain obscure. We show that a hybrid histidine kinase senses host signals and triggers the transition from mold to yeast. The kinase also regulates cell-wall integrity, sporulation, and expression of virulence genes in vivo. This global regulator shapes how dimorphic fungal pathogens adapt to the mammalian host, which has broad implications for treating and preventing systemic fungal disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemecek, Julie C -- Wuthrich, Marcel -- Klein, Bruce S -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):583-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, WI 53792, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645097" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Coccidioides/enzymology/genetics/pathogenicity ; Fungal Proteins/genetics/physiology ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Complementation Test ; Histoplasma/enzymology/genetics/pathogenicity ; Histoplasmosis/microbiology ; Lung Diseases, Fungal/microbiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis, Insertional ; Open Reading Frames ; Protein Kinases/chemistry/*genetics/*physiology ; RNA Interference ; Saccharomyces cerevisiae/genetics ; Soil Microbiology ; Spores, Fungal/physiology ; Temperature ; Virulence/genetics
    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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  • 17
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    Mouse genetics. A mouse for every gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1862-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; Databases, Factual ; Embryo, Mammalian/cytology ; Financial Support ; Gene Targeting ; *Genes ; Genetic Techniques ; International Cooperation ; Mice ; *Mice, Knockout/genetics ; National Institutes of Health (U.S.) ; Patents as Topic ; Stem Cells ; United States
    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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  • 18
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    Ca2+ entry through plasma membrane IP3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: Inositol 1,4,5-trisphosphate receptors (IP3Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane (PM) channels in cells lacking IP3R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP3Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP3Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellis, Olivier -- Dedos, Skarlatos G -- Tovey, Stephen C -- Taufiq-Ur-Rahman -- Dubel, Stefan J -- Taylor, Colin W -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):229-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Bungarotoxins/metabolism/pharmacology ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling ; Cell Membrane/*metabolism ; Cells, Cultured ; Chickens ; Electric Conductivity ; Endoplasmic Reticulum/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; *Ion Channel Gating ; Mice ; Nuclear Envelope/metabolism ; Patch-Clamp Techniques ; Point Mutation ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Oligonucleotide-modified gold nanoparticles for intracellular gene regulation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-20
    Description: We describe the use of gold nanoparticle-oligonucleotide complexes as intracellular gene regulation agents for the control of protein expression in cells. These oligonucleotide-modified nanoparticles have affinity constants for complementary nucleic acids that are higher than their unmodified oligonucleotide counterparts, are less susceptible to degradation by nuclease activity, exhibit greater than 99% cellular uptake, can introduce oligonucleotides at a higher effective concentration than conventional transfection agents, and are nontoxic to the cells under the conditions studied. By chemically tailoring the density of DNA bound to the surface of gold nanoparticles, we demonstrated a tunable gene knockdown.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosi, Nathaniel L -- Giljohann, David A -- Thaxton, C Shad -- Lytton-Jean, Abigail K R -- Han, Min Su -- Mirkin, Chad A -- New York, N.Y. -- Science. 2006 May 19;312(5776):1027-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and International Institute for Nanotechnology, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208-3113 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Deoxyribonucleases/metabolism ; *Gene Expression Regulation ; Glutathione/metabolism ; *Gold ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; Mice ; *Nanostructures ; *Oligodeoxyribonucleotides, Antisense/metabolism ; RNA, Messenger
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Cell biology. Purinergic chemotaxis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linden, Joel -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA. jlinden@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170280" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Adenosine Monophosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Apyrase/pharmacology ; *Autocrine Communication ; Blood Platelets/metabolism ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Endothelial Cells/metabolism ; Mice ; Models, Biological ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophils/drug effects/*metabolism/physiology ; Receptor, Adenosine A3/metabolism ; Receptors, Purinergic/*metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2 ; Respiratory Burst/drug effects ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Comment on "Cell type regulates selective segregation of mouse chromosome 7 DNA strands in mitosis" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Armakolas and Klar (Reports, 24 February 2006, p. 1146) suggested that segregation of mouse chromosome 7, after induction of a site-specific crossover between homologous chromosomes, is driven by a preferential inheritance of the old Watson and the old Crick DNA strands. However, this interpretation only considered half of the possible outcomes. The conjecture fails when all possible outcomes are examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, James E -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1045; author reply 1045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel Center and Department of Biology, Brandeis University, Waltham, MA 02454-9110, USA. haber@brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Chromatids/physiology ; *Chromosome Segregation ; Chromosomes, Mammalian/*physiology ; Crossing Over, Genetic ; DNA/metabolism ; Ectoderm/cytology ; Embryo, Mammalian/cytology ; Endoderm/cytology ; G2 Phase ; Mice ; *Mitosis ; Recombination, Genetic ; Stem Cells/cytology
    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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  • 22
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    Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: Fat tissue is the most important energy depot in vertebrates. The release of free fatty acids (FFAs) from stored fat requires the enzymatic activity of lipases. We showed that genetic inactivation of adipose triglyceride lipase (ATGL) in mice increases adipose mass and leads to triacylglycerol deposition in multiple tissues. ATGL-deficient mice accumulated large amounts of lipid in the heart, causing cardiac dysfunction and premature death. Defective cold adaptation indicated that the enzyme provides FFAs to fuel thermogenesis. The reduced availability of ATGL-derived FFAs leads to increased glucose use, increased glucose tolerance, and increased insulin sensitivity. These results indicate that ATGL is rate limiting in the catabolism of cellular fat depots and plays an important role in energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haemmerle, Guenter -- Lass, Achim -- Zimmermann, Robert -- Gorkiewicz, Gregor -- Meyer, Carola -- Rozman, Jan -- Heldmaier, Gerhard -- Maier, Robert -- Theussl, Christian -- Eder, Sandra -- Kratky, Dagmar -- Wagner, Erwin F -- Klingenspor, Martin -- Hoefler, Gerald -- Zechner, Rudolf -- F 3001/Austrian Science Fund FWF/Austria -- F 3002/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 May 5;312(5774):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biosciences, University of Graz, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675698" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/metabolism ; Adipose Tissue/anatomy & histology/*enzymology/metabolism ; Adipose Tissue, Brown/enzymology ; Animals ; Blood Glucose/metabolism ; Carboxylic Ester Hydrolases/deficiency/genetics/*metabolism ; Cell Size ; *Energy Metabolism ; Fatty Acids, Nonesterified/blood/metabolism ; Female ; Heart Failure/pathology ; Homeostasis ; Insulin/blood ; Isoproterenol/pharmacology ; Kidney/metabolism ; Lipase/deficiency/genetics/*metabolism ; Lipids/blood ; *Lipolysis/drug effects ; Male ; Mice ; Myocardium/metabolism/pathology ; Myocytes, Cardiac/cytology/metabolism ; Oxygen Consumption ; Testis/metabolism ; Thermogenesis ; Triglycerides/*metabolism ; Ventricular Dysfunction, Left/physiopathology
    Print ISSN: 0036-8075
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  • 23
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    Immunology. Unraveling gut inflammation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strober, Warren -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1052-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Host Defenses, National Institutes of Health. Bethesda, MD 20892-1890. USA. wstrober@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*biosynthesis/metabolism ; Bacteria/growth & development/*immunology ; Biomarkers, Tumor/*biosynthesis/metabolism ; Crohn Disease/immunology ; Dendritic Cells/immunology/microbiology ; Gastroenteritis/*immunology ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Inflammatory Bowel Diseases/*immunology/metabolism ; Intestinal Mucosa/cytology/immunology/metabolism/microbiology ; Intestines/*microbiology ; Lectins, C-Type/*biosynthesis/metabolism ; Mice ; Paneth Cells/*metabolism ; Peptidoglycan/metabolism ; Proteins/*metabolism ; alpha-Defensins/biosynthesis/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, 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/16601194" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
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  • 25
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    Receptor activation alters inner surface potential during phagocytosis (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-22
    Description: The surface potential of biological membranes varies according to their lipid composition. We devised genetically encoded probes to assess surface potential in intact cells. These probes revealed marked, localized alterations in the charge of the inner surface of the plasma membrane of macrophages during the course of phagocytosis. Hydrolysis of phosphoinositides and displacement of phosphatidylserine accounted for the change in surface potential at the phagosomal cup. Signaling molecules such as K-Ras, Rac1, and c-Src that are targeted to the membrane by electrostatic interactions were rapidly released from membrane subdomains where the surface charge was altered by lipid remodeling during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Terebiznik, Mauricio -- Yu, Liming -- Silvius, John -- Abidi, Wasif M -- Philips, Mark -- Levine, Tim -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):347-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hepatology, and Nutrition Department, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*physiology ; Fluorescent Dyes/metabolism ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin G/immunology ; Ionomycin/pharmacology ; Lipid Bilayers/metabolism ; Liposomes/metabolism ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Molecular Probes/metabolism ; Neuropeptides/metabolism ; Opsonin Proteins ; Peptides/metabolism ; *Phagocytosis ; Phagosomes/physiology ; Phospholipids/analysis/metabolism ; Receptors, Fc/immunology/metabolism ; Static Electricity ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein ; ras Proteins/metabolism
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  • 26
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    Neuroscience. Neuron, know thy neighbor (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiCicco-Bloom, Emanuel -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Cell Biology/Pediatrics (Neurology), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA. diciccem@umdnj.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543446" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; Brain/cytology/*embryology ; *Cell Adhesion ; Cell Count ; Cell Death ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Central Nervous System/cytology/embryology ; Cytoskeleton/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mutation ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/physiology ; Trans-Activators/*metabolism ; alpha Catenin/genetics/*physiology
    Print ISSN: 0036-8075
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  • 27
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    Sequential interplay of nicotinic and GABAergic signaling guides neuronal development (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-13
    Description: GABA (gamma-aminobutyric acid), the major inhibitory transmitter in the brain, goes through a transitory phase of excitation during development. The excitatory phase promotes neuronal growth and integration into circuits. We show here that spontaneous nicotinic cholinergic activity is responsible for terminating GABAergic excitation and initiating inhibition. It does so by changing chloride transporter levels, shifting the driving force on GABA-induced currents. The timing of the transition is critical, because the two phases of GABAergic signaling provide contrasting developmental instructions. Synergistic with nicotinic excitation, GABAergic inhibition constrains neuronal morphology and innervation. The results reveal a multitiered activity-dependent strategy controlling neuronal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhaoping -- Neff, Robert A -- Berg, Darwin K -- NS012601/NS/NINDS NIH HHS/ -- NS035469/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 8;314(5805):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17158331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/pharmacology ; Calcium/metabolism ; Chick Embryo ; Chlorides/metabolism ; Ganglia, Parasympathetic/cytology/embryology ; Hippocampus/cytology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/cytology/*physiology ; Nicotine/metabolism/pharmacology ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Receptors, Nicotinic/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Symporters/genetics/metabolism ; Synaptic Transmission ; Transfection ; alpha7 Nicotinic Acetylcholine Receptor ; gamma-Aminobutyric Acid/*metabolism
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    ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosine receptors, which are recruited to the leading edge, to promote cell migration. Thus, ATP release and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling gradient sensing and migration of neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yu -- Corriden, Ross -- Inoue, Yoshiaki -- Yip, Linda -- Hashiguchi, Naoyuki -- Zinkernagel, Annelies -- Nizet, Victor -- Insel, Paul A -- Junger, Wolfgang G -- GM-60475/GM/NIGMS NIH HHS/ -- GM-66232/GM/NIGMS NIH HHS/ -- PR043034/PR/OCPHP CDC HHS/ -- R01 GM-51477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of California San Diego, San Diego, CA 92103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170310" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism/pharmacology ; Adenosine A3 Receptor Agonists ; Adenosine A3 Receptor Antagonists ; Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Animals ; *Autocrine Communication ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Cytoplasmic Granules/metabolism ; HL-60 Cells ; Humans ; Hydrolysis ; Mice ; Mice, Knockout ; Neutrophils/drug effects/metabolism/*physiology ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A3/*metabolism ; Receptors, Purinergic P2/*metabolism ; Receptors, Purinergic P2Y2 ; Signal Transduction ; Suramin/pharmacology
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    Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(Met/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. When placed in stressful settings, BDNF(Met/Met) mice exhibited increased anxiety-related behaviors that were not normalized by the antidepressant, fluoxetine. A variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880880/" 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/PMC1880880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhe-Yu -- Jing, Deqiang -- Bath, Kevin G -- Ieraci, Alessandro -- Khan, Tanvir -- Siao, Chia-Jen -- Herrera, Daniel G -- Toth, Miklos -- Yang, Chingwen -- McEwen, Bruce S -- Hempstead, Barbara L -- Lee, Francis S -- MH060478/MH/NIMH NIH HHS/ -- MH068850/MH/NIMH NIH HHS/ -- NS052819/NS/NINDS NIH HHS/ -- NS30687/NS/NINDS NIH HHS/ -- R01 NS052819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10021, USA. zheyuchen@sdu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023662" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anxiety/drug therapy/*genetics ; Behavior, Animal ; Brain-Derived Neurotrophic Factor/*genetics/*physiology ; Conditioning (Psychology) ; Dendrites/ultrastructure ; Dentate Gyrus/cytology ; Fear ; Fluoxetine/administration & dosage/pharmacology ; Hippocampus/anatomy & histology/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/cytology/metabolism ; Organ Size ; *Polymorphism, Single Nucleotide ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors/administration & dosage/pharmacology
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    A bacterial protein enhances the release and efficacy of liposomal cancer drugs (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-25
    Description: Clostridium novyi-NT is an anaerobic bacterium that can infect hypoxic regions within experimental tumors. Because C. novyi-NT lyses red blood cells, we hypothesized that its membrane-disrupting properties could be exploited to enhance the release of liposome-encapsulated drugs within tumors. Here, we show that treatment of mice bearing large, established tumors with C. novyi-NT plus a single dose of liposomal doxorubicin often led to eradication of the tumors. The bacterial factor responsible for the enhanced drug release was identified as a previously unrecognized protein termed liposomase. This protein could potentially be incorporated into diverse experimental approaches for the specific delivery of chemotherapeutic agents to tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheong, Ian -- Huang, Xin -- Bettegowda, Chetan -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Zhou, Shibin -- Vogelstein, Bert -- CA062924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Ludwig Center for Cancer Genetics and Therapeutics, Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antineoplastic Agents/*administration & dosage/pharmacokinetics/therapeutic use ; Bacterial Proteins/chemistry/genetics/*metabolism ; Base Sequence ; Camptothecin/administration & dosage/analogs & ; derivatives/pharmacokinetics/therapeutic use ; Cell Line, Tumor ; Cloning, Molecular ; Clostridium/*chemistry/genetics ; Colorectal Neoplasms/*drug therapy ; Doxorubicin/*administration & dosage/pharmacokinetics/therapeutic use ; Drug Carriers ; Humans ; Lipase/chemistry/genetics/*metabolism ; Lipid Bilayers/chemistry ; Liposomes/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Protein Structure, Tertiary
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    Neuroscience. Neurons find strength through synchrony in the brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonso, Jose-Manuel -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1604-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, State University of New York College of Optometry, New York, NY 10036, USA. jalonso@sunyopt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Excitatory Postsynaptic Potentials ; Mice ; Neural Pathways ; Neurons/*physiology ; Rats ; Somatosensory Cortex/*physiology ; Synapses/*physiology ; *Synaptic Transmission ; Thalamus/*physiology
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    A critical role for the innate immune signaling molecule IRAK-4 in T cell activation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Nobutaka -- Suzuki, Shinobu -- Millar, Douglas G -- Unno, Midori -- Hara, Hiromitsu -- Calzascia, Thomas -- Yamasaki, Sho -- Yokosuka, Tadashi -- Chen, Nien-Jung -- Elford, Alisha R -- Suzuki, Jun-Ichiro -- Takeuchi, Arata -- Mirtsos, Christine -- Bouchard, Denis -- Ohashi, Pamela S -- Yeh, Wen-Chen -- Saito, Takashi -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1927-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574867" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes/metabolism ; *Lymphocyte Activation ; Membrane Microdomains/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; ZAP-70 Protein-Tyrosine Kinase/metabolism
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    Evidence for a functional second thymus in mice (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-04
    Description: The thymus organ supports the development of T cells and is located in the thorax. Here, we report the existence of a second thymus in the mouse neck, which develops after birth and grows to the size of a small lymph node. The cervical thymus had a typical medulla-cortex structure, was found to support T cell development, and could correct T cell deficiency in athymic nude mice upon transplantation. The identification of a regular second thymus in the mouse may provide evolutionary links to thymus organogenesis in other vertebrates and suggests a need to reconsider the effect of thoracic thymectomy on de novo T cell production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terszowski, Grzegorz -- Muller, Susanna M -- Bleul, Conrad C -- Blum, Carmen -- Schirmbeck, Reinhold -- Reimann, Jorg -- Pasquier, Louis Du -- Amagai, Takashi -- Boehm, Thomas -- Rodewald, Hans-Reimer -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):284-7. Epub 2006 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Ulm, D-89081 Ulm, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Choristoma ; Forkhead Transcription Factors/genetics/physiology ; Hematopoietic Stem Cells/cytology ; Hepatitis B Antibodies/biosynthesis ; Hepatitis B Surface Antigens/immunology ; Histocompatibility Antigens Class II ; Immunocompetence ; Lymphopoiesis ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; *Neck ; Receptors, Antigen, T-Cell/analysis ; Self Tolerance ; T-Lymphocytes/*immunology ; Thymectomy ; Thymus Gland/anatomy & histology/growth & development/*immunology/transplantation
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    Alterations in 5-HT1B receptor function by p11 in depression-like states (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Chergui, Karima -- Rachleff, Ilan -- Flajolet, Marc -- Zhang, Xiaoqun -- El Yacoubi, Malika -- Vaugeois, Jean-Marie -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):77-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400147" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Electroconvulsive Therapy ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Neurons/metabolism ; Rats ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism/physiology ; Signal Transduction ; Two-Hybrid System Techniques
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    Biomedicine. Life, the universe, and body temperature (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saper, Clifford B -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):773-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Division of Sleep Medicine, and Program in Neuroscience, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. csaper@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Body Temperature ; Body Temperature Regulation ; Body Weight ; Humans ; Hypothalamus/physiology ; Ion Channels/genetics/physiology ; *Longevity ; Mice ; Mice, Transgenic ; Mitochondrial Proteins/genetics/physiology ; Preoptic Area/*physiology
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    Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Valerie G -- Heusner, Carrie L -- Bland, Ross J -- During, Matthew J -- Weinshenker, David -- Palmiter, Richard D -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Conditioning (Psychology) ; Dopamine beta-Hydroxylase/genetics/metabolism ; Droxidopa/pharmacology ; Locomotion/drug effects ; Locus Coeruleus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/*pharmacology ; Motor Activity/drug effects ; Norepinephrine/*physiology ; *Reward ; Signal Transduction ; Solitary Nucleus/*physiology ; *Synaptic Transmission
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    Combinatorial effects of odorant mixes in olfactory cortex (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-11
    Description: In mammals, each odorant is detected by a combination of different odorant receptors. Signals from different types of receptors are segregated in the nose and the olfactory bulb, but appear to be combined in individual neurons in the olfactory cortex. Here, we report that binary odorant mixes stimulate cortical neurons that are not stimulated by their individual component odorants. We propose that cortical neurons require combinations of receptor inputs for activation and that merging the receptor codes of two odorants provides novel combinations of receptor inputs that stimulate neurons beyond those activated by the single odorants. These findings may explain why odorant mixtures can elicit novel odor percepts in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Zhihua -- Buck, Linda B -- R03 DC008700-01/DC/NIDCD NIH HHS/ -- R21 DC008628-01/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1477-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Complex Mixtures ; Cytoskeletal Proteins/metabolism ; Humans ; In Situ Hybridization, Fluorescence/methods ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/metabolism ; Neurons/physiology ; *Odors ; Olfactory Pathways/cytology/*physiology ; Olfactory Receptor Neurons/physiology ; RNA, Messenger/metabolism ; Receptors, Odorant/*physiology ; Smell/*physiology
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    Developmental biology. The Turing model comes of molecular age (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383235/" 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/PMC4383235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maini, Philip K -- Baker, Ruth E -- Chuong, Cheng-Ming -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-11/AR/NIAMS NIH HHS/ -- R01 AR042177-12/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- R01 AR047364-04/AR/NIAMS NIH HHS/ -- R01 AR047364-05/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1397-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Mathematical Biology, University of Oxford, Oxford OX1 3LB, UK. maini@maths.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Diffusion ; Hair Follicle/*growth & development/metabolism ; Intercellular Signaling Peptides and Proteins/*metabolism ; Mathematics ; Mice ; *Models, Biological ; Signal Transduction ; Wnt Proteins/*metabolism
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    Immunology. When F-actin becomes too much of a good thing (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dustin, Michael L -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):767-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Progam in Molecular Pathogenesis, Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. dustin@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902113" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/antagonists & inhibitors/metabolism ; Actins/*metabolism ; Animals ; Apoptosis ; Binding Sites ; Cell Death ; Cell Movement ; *Chemotaxis, Leukocyte ; Homeostasis ; Intracellular Membranes/physiology ; Membrane Potentials ; Mice ; Microfilament Proteins/chemistry/*physiology ; Mitochondria/*physiology ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology/*physiology ; Voltage-Dependent Anion Channels/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prions in skeletal muscles of deer with chronic wasting disease (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angers, Rachel C -- Browning, Shawn R -- Seward, Tanya S -- Sigurdson, Christina J -- Miller, Michael W -- Hoover, Edward A -- Telling, Glenn C -- 2RO1 NS040334-04/NS/NINDS NIH HHS/ -- N01-AI-25491/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1117. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Chemistry ; *Deer ; Humans ; Mice ; Mice, Transgenic ; Muscle, Skeletal/*chemistry ; PrPSc Proteins/*analysis ; Prions/*analysis ; Tissue Extracts/administration & dosage ; Wasting Disease, Chronic/*metabolism/*transmission
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    New neurons follow the flow of cerebrospinal fluid in the adult brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-18
    Description: In the adult brain, neuroblasts born in the subventricular zone migrate from the walls of the lateral ventricles to the olfactory bulb. How do these cells orient over such a long distance and through complex territories? Here we show that neuroblast migration parallels cerebrospinal fluid (CSF) flow. Beating of ependymal cilia is required for normal CSF flow, concentration gradient formation of CSF guidance molecules, and directional migration of neuroblasts. Results suggest that polarized epithelial cells contribute important vectorial information for guidance of young, migrating neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawamoto, Kazunobu -- Wichterle, Hynek -- Gonzalez-Perez, Oscar -- Cholfin, Jeremy A -- Yamada, Masayuki -- Spassky, Nathalie -- Murcia, Noel S -- Garcia-Verdugo, Jose Manuel -- Marin, Oscar -- Rubenstein, John L R -- Tessier-Lavigne, Marc -- Okano, Hideyuki -- Alvarez-Buylla, Arturo -- HD 32116/HD/NICHD NIH HHS/ -- NS 28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):629-32. Epub 2006 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and Developmental and Stem Cell Biology Program, University of California San Francisco, San Francisco, CA 94143, USA. sawamoto@sc.itc.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Tissue Transplantation ; Cell Movement ; Cell Polarity ; Cerebral Ventricles/cytology/physiology ; Cerebrospinal Fluid/*physiology ; Choroid Plexus/secretion ; Cilia/physiology ; Ependyma/cytology/*physiology ; Epithelial Cells/physiology ; Intercellular Signaling Peptides and Proteins ; Mice ; Nerve Tissue Proteins/cerebrospinal fluid ; Neurons/cytology/*physiology ; Olfactory Bulb/cytology/physiology ; Recombinant Fusion Proteins/cerebrospinal fluid
    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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    Dendritic cell apoptosis in the maintenance of immune tolerance (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: Apoptosis in the immune system is critical for maintaining self-tolerance and preventing autoimmunity. Nevertheless, inhibiting apoptosis in lymphocytes is not alone sufficient to break self-tolerance, suggesting the involvement of other cell types. We investigated whether apoptosis in dendritic cells (DCs) helps regulate self-tolerance by generating transgenic mice expressing the baculoviral caspase inhibitor, p35, in DCs (DC-p35). DC-p35 mice displayed defective DC apoptosis, resulting in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestations. The observation that a defect in DC apoptosis can independently lead to autoimmunity is consistent with a central role for these cells in maintaining immune self-tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Min -- Wang, Yui-Hsi -- Wang, Yihong -- Huang, Li -- Sandoval, Hector -- Liu, Yong-Jun -- Wang, Jin -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1160-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA. minc@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497935" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Aging ; Animals ; Antibodies, Antinuclear/analysis ; *Apoptosis ; *Autoimmunity ; B-Lymphocytes/immunology ; Caspase Inhibitors ; Cell Survival ; Dendritic Cells/*immunology/*physiology ; Kidney/immunology ; Lung/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; *Self Tolerance ; Spleen/immunology ; T-Lymphocytes/immunology ; Viral Proteins/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genetic polymorphism of Fc (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandey, Janardan P -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1376-7; author reply 1376-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Immunoglobulin G/immunology ; Mice ; *Polymorphism, Genetic ; Receptors, IgG/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hoxa2- and rhombomere-dependent development of the mouse facial somatosensory map (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: In the mouse trigeminal pathway, sensory inputs from distinct facial structures, such as whiskers or lower jaw and lip, are topographically mapped onto the somatosensory cortex through relay stations in the thalamus and hindbrain. In the developing hindbrain, the mechanisms generating such maps remain elusive. We found that in the principal sensory nucleus, the whisker-related map is contributed by rhombomere 3-derived neurons, whereas the rhombomere 2-derived progeny supply the lower jaw and lip representation. Moreover, early Hoxa2 expression in neuroepithelium prevents the trigeminal nerve from ectopically projecting to the cerebellum, whereas late expression in the principal sensory nucleus promotes selective arborization of whisker-related afferents and topographic connectivity to the thalamus. Hoxa2 inactivation further results in the absence of whisker-related maps in the postnatal brain. Thus, Hoxa2- and rhombomere 3-dependent cues determine the whisker area map and are required for the assembly of the whisker-to-barrel somatosensory circuit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oury, Franck -- Murakami, Yasunori -- Renaud, Jean-Sebastien -- Pasqualetti, Massimo -- Charnay, Patrick -- Ren, Shu-Yue -- Rijli, Filippo M -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1408-13. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/Universite Louis Pasteur, UMR 7104, BP 10142, Communaute Urbaine de Strasbourg, 67404 Illkirch Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902088" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Axons/ultrastructure ; Face/innervation ; Homeodomain Proteins/genetics/*physiology ; Lip/innervation ; Mandible/embryology/innervation ; Mice ; Mice, Transgenic ; Mutation ; Neurons, Afferent/cytology ; Receptor, EphA4/metabolism ; Receptor, EphA7/metabolism ; Rhombencephalon/cytology/*embryology/metabolism ; Somatosensory Cortex/*anatomy & histology/embryology ; Thalamus/embryology/metabolism ; Trigeminal Ganglion/embryology/metabolism ; Trigeminal Nerve/*embryology/physiology ; Ventral Thalamic Nuclei/embryology ; Vibrissae/*innervation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development. Gene-suppressing proteins reveal secrets of stem cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):349.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*metabolism ; Cell Differentiation ; Chromatin/*physiology ; Embryo, Mammalian/cytology ; Gene Expression Regulation, Developmental ; *Gene Silencing ; *Genes, Regulator ; Genome, Human ; Humans ; Mice ; Nuclear Proteins ; Pluripotent Stem Cells/cytology/*physiology ; Polycomb Repressive Complex 2 ; Polycomb-Group Proteins ; Repressor Proteins/*metabolism
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    Prion-induced amyloid heart disease with high blood infectivity in transgenic mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: We investigated extraneural manifestations in scrapie-infected transgenic mice expressing prion protein lacking the glycophosphatydylinositol membrane anchor. In the brain, blood, and heart, both abnormal protease-resistant prion protein (PrPres) and prion infectivity were readily detected by immunoblot and by inoculation into nontransgenic recipients. The titer of infectious scrapie in blood plasma exceeded 10(7) 50% infectious doses per milliliter. The hearts of these transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and cardiac disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820586/" 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/PMC1820586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trifilo, Matthew J -- Yajima, Toshitaka -- Gu, Yusu -- Dalton, Nancy -- Peterson, Kirk L -- Race, Richard E -- Meade-White, Kimberly -- Portis, John L -- Masliah, Eliezer -- Knowlton, Kirk U -- Chesebro, Bruce -- Oldstone, Michael B A -- 5R01HL66424-04/HL/NHLBI NIH HHS/ -- AGO4342/PHS HHS/ -- NS041219-05/NS/NINDS NIH HHS/ -- P01 AG004342/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral-Immunobiology Laboratory, Departments of Molecular and Integrative Neurosciences and Infectology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825571" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*analysis ; Amyloidosis/blood/etiology/*pathology/physiopathology ; Animals ; Blotting, Western ; Cardiac Catheterization ; Coronary Vessels/chemistry/pathology ; Disease Models, Animal ; Glycosylphosphatidylinositols ; Heart Diseases/blood/etiology/*pathology/physiopathology ; Heart Function Tests ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microcirculation/chemistry/pathology ; Myocardial Contraction ; Myocardium/*chemistry/*pathology ; PrPC Proteins/chemistry ; PrPSc Proteins/*analysis/blood ; Scrapie/blood/*pathology/physiopathology ; Staining and Labeling ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    p53 regulates mitochondrial respiration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: The energy that sustains cancer cells is derived preferentially from glycolysis. This metabolic change, the Warburg effect, was one of the first alterations in cancer cells recognized as conferring a survival advantage. Here, we show that p53, one of the most frequently mutated genes in cancers, modulates the balance between the utilization of respiratory and glycolytic pathways. We identify Synthesis of Cytochrome c Oxidase 2 (SCO2) as the downstream mediator of this effect in mice and human cancer cell lines. SCO2 is critical for regulating the cytochrome c oxidase (COX) complex, the major site of oxygen utilization in the eukaryotic cell. Disruption of the SCO2 gene in human cancer cells with wild-type p53 recapitulated the metabolic switch toward glycolysis that is exhibited by p53-deficient cells. That SCO2 couples p53 to mitochondrial respiration provides a possible explanation for the Warburg effect and offers new clues as to how p53 might affect aging and metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matoba, Satoaki -- Kang, Ju-Gyeong -- Patino, Willmar D -- Wragg, Andrew -- Boehm, Manfred -- Gavrilova, Oksana -- Hurley, Paula J -- Bunz, Fred -- Hwang, Paul M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1650-3. Epub 2006 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Heart, Lung, and Blood Institute, 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/16728594" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins ; Cell Line, Tumor ; *Cell Respiration ; Cell Survival ; Electron Transport Complex IV/*genetics/metabolism/physiology ; Gene Expression Regulation, Neoplastic ; *Genes, p53 ; Glycolysis ; Humans ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Mitochondria, Liver/*metabolism ; Mitochondrial Proteins ; Mutation ; Oxygen Consumption ; Proteins/*genetics/physiology ; RNA, Small Interfering ; Recombination, Genetic ; Transcription, Genetic ; Transcriptional Activation ; Tumor Suppressor Protein p53/*physiology
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    Stem cells. Scientists create human stem cell line from 'dead' embryos (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1869.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology/physiology ; Cell Differentiation ; *Cell Line ; Cell Proliferation ; *Embryo Loss ; Embryo Research/economics ; Humans ; Mice ; *Pluripotent Stem Cells/cytology ; Research Support as Topic
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    Reversal of diabetes in non-obese diabetic mice without spleen cell-derived beta cell regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: Autoimmune destruction of beta cells is the predominant cause of type 1 diabetes mellitus (T1DM) in humans and is modeled in non-obese diabetic (NOD) mice. Many therapeutic interventions prevent the development of T1DM in NOD mice, but few can induce its reversal once established. Intervention with Freund's complete adjuvant, semi-allogeneic splenocytes, and temporary islet transplantation has been reported to cure NOD mice of established T1DM. Using the same approach, we report here that this treatment cured 32% of NOD mice of established diabetes (〉340 milligrams per deciliter blood glucose), although beta cells in these mice were not derived from donor splenocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chong, Anita S -- Shen, Jikun -- Tao, Jing -- Yin, Dengping -- Kuznetsov, Andrey -- Hara, Manami -- Philipson, Louis H -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1774-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Transplantation, Department of Surgery, University of Chicago, Chicago, IL 60637, USA. achong@uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556844" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Blood Glucose/analysis ; Cell Differentiation ; *Cell Transplantation ; Combined Modality Therapy ; Diabetes Mellitus, Type 1/immunology/pathology/*therapy ; Female ; Freund's Adjuvant/*therapeutic use ; Green Fluorescent Proteins/analysis ; Insulin-Secreting Cells/*cytology/physiology ; *Islets of Langerhans Transplantation ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Regeneration ; Spleen/*cytology ; Stem Cells/cytology/physiology
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    Immunology. Foiled dendritic cell suicide may lead to autoimmunity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1086.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Autoimmune Diseases/immunology ; *Autoimmunity ; Caspase 10 ; Caspase Inhibitors ; Caspases/genetics/metabolism ; Dendritic Cells/*immunology/*physiology ; Humans ; Lymphocyte Activation ; Mice ; Mutation ; Viral Proteins/genetics/metabolism
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    Cell biology. Balancing life-or-death decisions (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartek, Jiri -- Lukas, Jiri -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):261-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. jb@cancer.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BRCA2 Protein/metabolism ; Cell Cycle ; Cell Nucleus/metabolism ; Cell Survival ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/*metabolism ; *DNA Damage ; DNA Repair ; DNA Replication ; Forkhead Transcription Factors/*metabolism ; Gene Expression Regulation ; Humans ; Mice ; Models, Biological ; Phosphorylation ; RNA, Small Interfering ; Transcription, Genetic ; cdc25 Phosphatases/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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    Caveolin-1 is essential for liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Manuel A -- Albor, Cecilia -- Ingelmo-Torres, Mercedes -- Nixon, Susan J -- Ferguson, Charles -- Kurzchalia, Teymuras -- Tebar, Francesc -- Enrich, Carlos -- Parton, Robert G -- Pol, Albert -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Cellular, Facultat de Medicina, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Division ; Fatty Acids/blood/metabolism ; Glucose/administration & dosage ; Hepatectomy ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology/*metabolism ; *Lipid Metabolism ; Lipids/blood ; Liver/metabolism/ultrastructure ; *Liver Regeneration ; Male ; Mice ; Phosphorylation ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Triglycerides/blood/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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    CDK2-dependent phosphorylation of FOXO1 as an apoptotic response to DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage-induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser249) in vitro and in vivo. Phosphorylation of Ser249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage-induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser249. Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Haojie -- Regan, Kevin M -- Lou, Zhenkun -- Chen, Junjie -- Tindall, Donald J -- CA91956/CA/NCI NIH HHS/ -- DK60920/DK/NIDDK NIH HHS/ -- DK65236/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Camptothecin/pharmacology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/genetics/*metabolism ; Cytoplasm/metabolism ; *DNA Damage ; Forkhead Transcription Factors/antagonists & inhibitors/*metabolism ; Humans ; Mice ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/metabolism
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    A positive feedback loop promotes transcription surge that jump-starts Salmonella virulence circuit (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-13
    Description: The PhoP/PhoQ two-component system is a master regulator of Salmonella pathogenicity. Here we report that induction of the PhoP/PhoQ system results in an initial surge of PhoP phosphorylation; the occupancy of target promoters by the PhoP protein; and the transcription of PhoP-activated genes, which then subsides to reach new steady-state levels. This surge in PhoP activity is due to PhoP positively activating its own transcription, because a strain constitutively expressing the PhoP protein attained steady-state levels of activation asymptotically, without the surge. The strain constitutively expressing the PhoP protein was attenuated for virulence in mice, demonstrating that the surge conferred by PhoP's positive feedback loop is necessary to jump-start Salmonella's virulence program.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Dongwoo -- Lee, Eun-Jin -- Huang, Henry -- Groisman, Eduardo A -- AI49561/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 8;314(5805):1607-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Howard Hughes Medical Institute, Washington University School of Medicine, Campus Box 8230, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17158330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/*genetics/*metabolism ; *Feedback, Physiological ; Gene Expression Regulation, Bacterial ; Magnesium/metabolism ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; RNA, Bacterial/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/metabolism/*pathogenicity ; *Transcription, Genetic ; Virulence
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    B cell ligand discrimination through a spreading and contraction response (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: B cells recognize foreign antigens by virtue of cell surface immunoglobulin receptors and are most effectively activated by membrane-bound ligands. Here, we show that in the early stages of this process, B cells exhibit a two-phase response in which they first spread over the antigen-bearing membrane and then contract, thereby collecting bound antigen into a central aggregate. The extent of this response, which is both signaling- and actin-dependent, determines the quantity of antigen accumulated and hence the degree of B cell activation. Brownian dynamic simulations reproduce essential features of the antigen collection process and suggest a possible basis for affinity discrimination. We propose that dynamic spreading is an important step of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleire, S J -- Goldman, J P -- Carrasco, Y R -- Weber, M -- Bray, D -- Batista, F D -- G64713/PHS HHS/ -- New York, N.Y. -- Science. 2006 May 5;312(5774):738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675699" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Algorithms ; Animals ; Antibody Affinity ; Antigen Presentation ; Antigens, Surface/*immunology ; B-Lymphocytes/*immunology/*physiology ; Cell Shape ; Computer Simulation ; Flow Cytometry ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Models, Immunological ; Muramidase/immunology ; Receptors, Antigen, B-Cell/*immunology/metabolism ; Recombinant Fusion Proteins/immunology ; Signal Transduction ; Stochastic Processes ; T-Lymphocytes/immunology
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    Protrudin induces neurite formation by directional membrane trafficking (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: Guanosine triphosphatases of the Rab family are key regulators of membrane trafficking, with Rab11 playing a specific role in membrane recycling. We identified a mammalian protein, protrudin, that promoted neurite formation through interaction with the guanosine diphosphate (GDP)-bound form of Rab11. Phosphorylation of protrudin by extracellular signal-regulated kinase (ERK) in response to nerve growth factor promoted protrudin association with Rab11-GDP. Down-regulation of protrudin by RNA interference induced membrane extension in all directions and inhibited neurite formation. Thus, protrudin regulates Rab11-dependent membrane recycling to promote the directional membrane trafficking required for neurite formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirane, Michiko -- Nakayama, Keiichi I -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082457" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Guanosine Diphosphate/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1/metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology/physiology ; Neurites/*physiology ; PC12 Cells ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Vesicular Transport Proteins ; rab GTP-Binding Proteins/metabolism
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    A clonogenic bone marrow progenitor specific for macrophages and dendritic cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-03
    Description: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
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    Antibody class switching mediated by yeast endonuclease-generated DNA breaks (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Antibody class switching in activated B cells uses class switch recombination (CSR), which joins activation-induced cytidine deaminase (AID)-dependent double-strand breaks (DSBs) within two large immunoglobulin heavy chain (IgH) locus switch (S) regions that lie up to 200 kilobases apart. To test postulated roles of S regions and AID in CSR, we generated mutant B cells in which donor Smu and accepter Sgamma1 regions were replaced with yeast I-SceI endonuclease sites. We found that site-specific I-SceI DSBs mediate recombinational IgH locus class switching from IgM to IgG1 without S regions or AID. We propose that CSR evolved to exploit a general DNA repair process that promotes joining of widely separated DSBs within a chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zarrin, Ali A -- Del Vecchio, Catherine -- Tseng, Eva -- Gleason, Megan -- Zarin, Payam -- Tian, Ming -- Alt, Frederick W -- 2P01AI031541-15/AI/NIAID NIH HHS/ -- P01CA092625-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):377-81. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, CBR Institute for Biomedical Research, and Department of Genetics, Harvard University Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Cytidine Deaminase/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/genetics/*metabolism ; Embryonic Stem Cells ; Gene Targeting ; Genes, Immunoglobulin Heavy Chain ; Hybridomas ; *Immunoglobulin Class Switching ; Immunoglobulin G/biosynthesis/genetics ; Immunoglobulin M/biosynthesis/genetics ; *Immunoglobulin Switch Region ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins
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    Imaging of germinal center selection events during affinity maturation (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-23
    Description: The germinal center (GC) is an important site for the generation and selection of B cells bearing high-affinity antibodies, yet GC cell migration and interaction dynamics have not been directly observed. Using two-photon microscopy of mouse lymph nodes, we revealed that GC B cells are highly motile and extend long cell processes. They transited between GC dark and light zones and divided in both regions, although these B cells resided for only several hours in the light zone where antigen is displayed. GC B cells formed few stable contacts with GC T cells despite frequent encounters, and T cells were seen to carry dead B cell blebs. On the basis of these observations, we propose a model in which competition for T cell help plays a more dominant role in the selection of GC B cells than previously appreciated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, Christopher D C -- Okada, Takaharu -- Tang, H Lucy -- Cyster, Jason G -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):528-31. Epub 2006 Dec 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; B-Lymphocytes/*cytology/*immunology/physiology ; Cell Cycle ; Cell Death ; Cell Movement ; Dendritic Cells, Follicular/cytology/physiology ; Germinal Center/cytology/*immunology ; Macrophages/physiology ; Mice ; Mice, Inbred C57BL ; Microscopy/methods ; Models, Immunological ; Mutation ; T-Lymphocytes/cytology/immunology/physiology
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    Histocompatible embryonic stem cells by parthenogenesis (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-16
    Description: Genetically matched pluripotent embryonic stem (ES) cells generated via nuclear transfer or parthenogenesis (pES cells) are a potential source of histocompatible cells and tissues for transplantation. After parthenogenetic activation of murine oocytes and interruption of meiosis I or II, we isolated and genotyped pES cells and characterized those that carried the full complement of major histocompatibility complex (MHC) antigens of the oocyte donor. Differentiated tissues from these pES cells engrafted in immunocompetent MHC-matched mouse recipients, demonstrating that selected pES cells can serve as a source of histocompatible tissues for transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kitai -- Lerou, Paul -- Yabuuchi, Akiko -- Lengerke, Claudia -- Ng, Kitwa -- West, Jason -- Kirby, Andrew -- Daly, Mark J -- Daley, George Q -- T32: HD07466/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):482-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromosome Segregation ; Embryonic Stem Cells/cytology/*immunology/physiology ; Female ; Genotype ; H-2 Antigens/*genetics/*immunology ; Heterozygote ; *Histocompatibility ; Histocompatibility Antigens Class II/genetics/immunology ; *Major Histocompatibility Complex ; Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Oocytes/cytology/immunology ; *Parthenogenesis ; Pluripotent Stem Cells/cytology/*immunology/physiology ; Polymerase Chain Reaction ; Recombination, Genetic ; Stem Cell Transplantation
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    Immunology. Antibodies get a break (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhuri, Jayanta -- Jasin, Maria -- R01 GM054668/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):335-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. chaudhuj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; B-Lymphocytes/*immunology ; Cytidine Deaminase/genetics/*metabolism ; DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/*metabolism ; Genes, Immunoglobulin Heavy Chain ; *Immunoglobulin Class Switching ; *Immunoglobulin Switch Region ; Mice ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins ; Transcription, Genetic
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    Neurodegeneration. Huntington's research points to possible new therapies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
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    The functional genomics of noncoding RNA (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-09-06
    Description: Large numbers of noncoding RNA transcripts (ncRNAs) are being revealed by complementary DNA cloning and genome tiling array studies in animals. The big and as yet largely unanswered question is whether these transcripts are relevant. A paper by Willingham et al. shows the way forward by developing a strategy for large-scale functional screening of ncRNAs, involving small interfering RNA knockdowns in cell-based screens, which identified a previously unidentified ncRNA repressor of the transcription factor NFAT. It appears likely that ncRNAs constitute a critical hidden layer of gene regulation in complex organisms, the understanding of which requires new approaches in functional genomics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mattick, John S -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1527-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia. j.mattick@imb.uq.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Conserved Sequence ; DNA-Binding Proteins/antagonists & inhibitors ; *Genomics ; Humans ; Mice ; NFATC Transcription Factors ; Nuclear Proteins/antagonists & inhibitors ; *RNA Interference ; RNA, Untranslated/antagonists & inhibitors/genetics/*physiology ; Transcription Factors/antagonists & inhibitors ; beta Karyopherins/metabolism
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    Obesity and metabolic syndrome in circadian Clock mutant mice (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-04-23
    Description: The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764501/" 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/PMC3764501/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turek, Fred W -- Joshu, Corinne -- Kohsaka, Akira -- Lin, Emily -- Ivanova, Ganka -- McDearmon, Erin -- Laposky, Aaron -- Losee-Olson, Sue -- Easton, Amy -- Jensen, Dalan R -- Eckel, Robert H -- Takahashi, Joseph S -- Bass, Joseph -- AG11412/AG/NIA NIH HHS/ -- AG18200/AG/NIA NIH HHS/ -- DK02675/DK/NIDDK NIH HHS/ -- DK26356/DK/NIDDK NIH HHS/ -- HL59598/HL/NHLBI NIH HHS/ -- HL75029/HL/NHLBI NIH HHS/ -- K08 DK002675/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- R01 AG018200/AG/NIA NIH HHS/ -- R01 DK026356/DK/NIDDK NIH HHS/ -- R01 HL059598/HL/NHLBI NIH HHS/ -- R01 HL075029/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2005 May 13;308(5724):1043-5. Epub 2005 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845877" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/pathology ; Animals ; Body Weight ; Brain/metabolism ; CLOCK Proteins ; *Circadian Rhythm ; Dietary Fats/administration & dosage ; Energy Intake ; *Energy Metabolism ; *Feeding Behavior ; Hepatocytes/pathology ; Hyperglycemia ; Hyperlipidemias ; Insulin/blood ; Leptin/blood ; Metabolic Syndrome X/genetics/*physiopathology ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Neuropeptides/genetics/metabolism ; Obesity/genetics/*physiopathology ; Trans-Activators/*genetics/*physiology ; Weight Gain
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    Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-01
    Description: Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856689/" 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/PMC2856689/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGee, Aaron W -- Yang, Yupeng -- Fischer, Quentin S -- Daw, Nigel W -- Strittmatter, Stephen M -- R01 NS039962/NS/NINDS NIH HHS/ -- R01 NS039962-10/NS/NINDS NIH HHS/ -- R01 NS042304/NS/NINDS NIH HHS/ -- R01 NS042304-08/NS/NINDS NIH HHS/ -- R01 NS056485/NS/NINDS NIH HHS/ -- R01 NS056485-04/NS/NINDS NIH HHS/ -- R37 NS033020/NS/NINDS NIH HHS/ -- R37 NS033020-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chondroitin Sulfate Proteoglycans/metabolism ; Darkness ; Dominance, Ocular/*physiology ; Electrophysiology ; GPI-Linked Proteins ; Gene Targeting ; Mice ; Mice, Inbred C57BL ; Mutation ; Myelin Basic Protein/metabolism ; Myelin Proteins/genetics/metabolism/*physiology ; Myelin Sheath/*physiology ; Myelin-Associated Glycoprotein/metabolism ; Neurites/physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Photic Stimulation ; Receptors, Cell Surface/genetics/*physiology ; Signal Transduction ; Visual Cortex/cytology/growth & development/*physiology ; gamma-Aminobutyric Acid/physiology
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    Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-05
    Description: The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Koichi S -- Chamaillard, Mathias -- Ogura, Yasunori -- Henegariu, Octavian -- Inohara, Naohiro -- Nunez, Gabriel -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15692051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/*immunology ; Animals ; *Antibody Formation ; Female ; Gene Expression ; Gene Targeting ; Ileum/*immunology/microbiology ; *Immunity, Innate ; Immunity, Mucosal ; Immunoglobulins/biosynthesis ; Interleukins/biosynthesis ; Intestinal Diseases/immunology/microbiology ; Intestinal Mucosa/immunology/microbiology ; Intracellular Signaling Peptides and Proteins/*physiology ; Ligands ; Lipopolysaccharides/toxicity ; Listeria monocytogenes/growth & development/immunology/isolation & purification ; Listeriosis/*immunology/microbiology ; Liver/microbiology ; Macrophages/immunology ; Male ; Membrane Glycoproteins/physiology ; Mice ; Nod2 Signaling Adaptor Protein ; Oligonucleotide Array Sequence Analysis ; Protein Precursors/biosynthesis/genetics ; Receptors, Cell Surface/physiology ; Serum Albumin/immunology ; Signal Transduction ; Spleen/microbiology ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/biosynthesis ; alpha-Defensins/*biosynthesis/genetics
    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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    Physiology. Boosting gene extends mouse life span (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1310-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123271" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Blood Glucose/analysis ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism ; Longevity/*genetics ; Male ; Membrane Proteins/blood/*genetics/*physiology ; Mice ; Mutation ; Signal Transduction
    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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    Achieving stability of lipopolysaccharide-induced NF-kappaB activation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: The activation dynamics of the transcription factor NF-kappaB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor-alpha (TNFalpha) but stable behavior when stimulated by lipopolysaccharide (LPS). LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-kappaB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. Computational modeling of the two TLR4-dependent signaling pathways suggests that one pathway requires a time delay to establish early anti-phase activation of NF-kappaB by the two pathways. The MyD88-independent pathway required Inferon regulatory factor 3-dependent expression of TNFalpha to activate NF-kappaB, and the time required for TNFalpha synthesis established the delay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Covert, Markus W -- Leung, Thomas H -- Gaston, Jahlionais E -- Baltimore, David -- GM039458-21/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1854-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166516" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/deficiency/physiology ; Animals ; Antigens, Differentiation/physiology ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cycloheximide/pharmacology ; DNA-Binding Proteins/genetics/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/biosynthesis/genetics/metabolism ; Interferon Regulatory Factor-3 ; Kinetics ; Lipopolysaccharides/*immunology/metabolism ; Mice ; Models, Biological ; Myeloid Differentiation Factor 88 ; NF-kappa B/*metabolism ; Oligonucleotide Array Sequence Analysis ; Protein Synthesis Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Immunologic/deficiency/metabolism/physiology ; Signal Transduction ; Time Factors ; Toll-Like Receptor 4 ; Transcription Factors/genetics/physiology ; Tumor Necrosis Factor-alpha/biosynthesis/metabolism
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    Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-16
    Description: Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kujoth, G C -- Hiona, A -- Pugh, T D -- Someya, S -- Panzer, K -- Wohlgemuth, S E -- Hofer, T -- Seo, A Y -- Sullivan, R -- Jobling, W A -- Morrow, J D -- Van Remmen, H -- Sedivy, J M -- Yamasoba, T -- Tanokura, M -- Weindruch, R -- Leeuwenburgh, C -- Prolla, T A -- AG021905/AG/NIA NIH HHS/ -- AG16694/AG/NIA NIH HHS/ -- AG17994/AG/NIA NIH HHS/ -- AG18922/AG/NIA NIH HHS/ -- AG21042/AG/NIA NIH HHS/ -- DK48831/DK/NIDDK NIH HHS/ -- RR00095/RR/NCRR NIH HHS/ -- T32 AG00213/AG/NIA NIH HHS/ -- T32 GM07601/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):481-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020738" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Cloning, Molecular ; DNA Damage ; DNA Fragmentation ; DNA, Mitochondrial/*genetics ; DNA-Directed DNA Polymerase/genetics ; Gene Targeting ; Humans ; Hydrogen Peroxide/metabolism ; Lipid Peroxidation ; Liver/metabolism ; Mice ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; Muscle, Skeletal/metabolism ; *Mutation ; Myocardium/metabolism ; *Oxidative Stress ; Phenotype ; Presbycusis/etiology ; Reactive Oxygen Species/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Toll-like receptor 8-mediated reversal of CD4+ regulatory T cell function (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-27
    Description: CD4+ regulatory T (Treg) cells have a profound ability to suppress host immune responses, yet little is understood about how these cells are regulated. We describe a mechanism linking Toll-like receptor (TLR) 8 signaling to the control of Treg cell function, in which synthetic and natural ligands for human TLR8 can reverse Treg cell function. This effect was independent of dendritic cells but required functional TLR8-MyD88-IRAK4 signaling in Treg cells. Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mice enhanced anti-tumor immunity. These results suggest that TLR8 signaling could play a critical role in controlling immune responses to cancer and other diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peng, Guangyong -- Guo, Zhong -- Kiniwa, Yukiko -- Voo, Kui Shin -- Peng, Weiyi -- Fu, Tihui -- Wang, Daniel Y -- Li, Yanchun -- Wang, Helen Y -- Wang, Rong-Fu -- P01CA94237/CA/NCI NIH HHS/ -- P50 CA093459/CA/NCI NIH HHS/ -- P50CA58204/CA/NCI NIH HHS/ -- R01CA101795/CA/NCI NIH HHS/ -- R01CA90327/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1380-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell and Gene Therapy and Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123302" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adoptive Transfer ; Animals ; Antigens, Differentiation/genetics/physiology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Cell Line, Tumor ; Humans ; Immune Tolerance ; Interleukin-1 Receptor-Associated Kinases ; Killer Cells, Natural/immunology ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Myeloid Differentiation Factor 88 ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology/pathology ; Oligodeoxyribonucleotides/immunology ; Phosphotransferases (Alcohol Group Acceptor)/genetics/physiology ; Poly G/immunology ; RNA Interference ; Receptors, Cell Surface/genetics/*physiology ; Receptors, Immunologic/genetics/physiology ; *Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Toll-Like Receptor 8 ; Toll-Like Receptors
    Print ISSN: 0036-8075
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    A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-12
    Description: Most protein phosphatases have little intrinsic substrate specificity, making selective pharmacological inhibition of specific dephosphorylation reactions a challenging problem. In a screen for small molecules that protect cells from endoplasmic reticulum (ER) stress, we identified salubrinal, a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha). Salubrinal also blocks eIF2alpha dephosphorylation mediated by a herpes simplex virus protein and inhibits viral replication. These results suggest that selective chemical inhibitors of eIF2alpha dephosphorylation may be useful in diseases involving ER stress or viral infection. More broadly, salubrinal demonstrates the feasibility of selective pharmacological targeting of cellular dephosphorylation events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyce, Michael -- Bryant, Kevin F -- Jousse, Celine -- Long, Kai -- Harding, Heather P -- Scheuner, Donalyn -- Kaufman, Randal J -- Ma, Dawei -- Coen, Donald M -- Ron, David -- Yuan, Junying -- AI19838/AI/NIAID NIH HHS/ -- AI26077/AI/NIAID NIH HHS/ -- DDK42394/DK/NIDDK NIH HHS/ -- DK47119/DK/NIDDK NIH HHS/ -- ES08681/ES/NIEHS NIH HHS/ -- GM64703/GM/NIGMS NIH HHS/ -- NS35138/NS/NINDS NIH HHS/ -- R37-AG012859/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):935-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation ; Apoptosis/*drug effects ; Cell Cycle Proteins ; Cell Line ; Cinnamates/*pharmacology/toxicity ; *Cytoprotection ; Dose-Response Relationship, Drug ; Endoplasmic Reticulum/*metabolism ; Enzyme Inhibitors/pharmacology ; Eukaryotic Initiation Factor-2/*metabolism ; Genes, Reporter ; Herpesvirus 1, Human/drug effects/physiology ; Keratitis, Herpetic/drug therapy/virology ; Male ; Mice ; Oxazoles/pharmacology/toxicity ; PC12 Cells ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Protein Folding ; Protein Kinases/metabolism ; Protein Phosphatase 1 ; Proteins/metabolism ; Rats ; Thiourea/*analogs & derivatives/*pharmacology/toxicity ; Tunicamycin/pharmacology ; Viral Proteins/metabolism ; Virus Replication/drug effects
    Print ISSN: 0036-8075
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    Environmental epigenomics meeting. Supplements restore gene function via methylation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1761.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axin Protein ; Body Patterning/drug effects/genetics ; *DNA Methylation ; DNA Transposable Elements ; *Dietary Supplements ; Embryonic Development/drug effects/*genetics ; *Epigenesis, Genetic ; Female ; Folic Acid/*administration & dosage/pharmacology ; Gene Expression Regulation, Developmental/*drug effects ; Mice ; Pregnancy ; Repressor Proteins/genetics ; Tail/embryology ; Vitamin B Complex/*administration & dosage/pharmacology
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    Neuroscience. Does brain cell growth drive weight loss? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254156" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation/*drug effects ; Ciliary Neurotrophic Factor/*pharmacology ; Humans ; Hypothalamus/cytology/*drug effects ; Mice ; Neurons/cytology/*drug effects ; Weight Loss/*drug effects
    Print ISSN: 0036-8075
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    Clonal dominance of hematopoietic stem cells triggered by retroviral gene marking (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-21
    Description: Gene marking with replication-defective retroviral vectors has been used for more than 20 years to track the in vivo fate of cell clones. We demonstrate that retroviral integrations themselves may trigger nonmalignant clonal expansion in murine long-term hematopoiesis. All 29 insertions recovered from clones dominating in serially transplanted recipients affected loci with an established or potential role in the self-renewal or survival of hematopoietic stem cells. Transcriptional dysregulation occurred in all 12 insertion sites analyzed. These findings have major implications for diagnostic gene marking and the discovery of genes regulating stem cell turnover.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kustikova, Olga -- Fehse, Boris -- Modlich, Ute -- Yang, Min -- Dullmann, Jochen -- Kamino, Kenji -- von Neuhoff, Nils -- Schlegelberger, Brigitte -- Li, Zhixiong -- Baum, Christopher -- New York, N.Y. -- Science. 2005 May 20;308(5725):1171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone Marrow Transplantation, University Hospital Eppendorf, Martinistrasse 52, 20251 Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905401" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/genetics ; Bone Marrow Transplantation ; DNA-Binding Proteins/genetics ; Down-Regulation ; *Genetic Vectors ; *Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Humans ; Ligase Chain Reaction ; Mice ; Mice, Inbred C57BL ; *Mutagenesis, Insertional ; Polymerase Chain Reaction ; Proto-Oncogenes/genetics ; Retroviridae/*genetics ; Transcription Factors/genetics ; Transcription, Genetic ; Transgenes ; Up-Regulation ; *Virus Integration
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    Stem cells. Deriving 'controversy-free' ES cells is controversial (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):416-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; *Cell Line ; Embryo Implantation ; Embryo Research/economics/*ethics ; Embryo, Mammalian/*cytology ; Female ; Financing, Government ; Humans ; Mice ; Nuclear Transfer Techniques ; *Pluripotent Stem Cells ; Research Support as Topic ; *Stem Cells ; United States
    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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    SLC24A5, a putative cation exchanger, affects pigmentation in zebrafish and humans (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: Lighter variations of pigmentation in humans are associated with diminished number, size, and density of melanosomes, the pigmented organelles of melanocytes. Here we show that zebrafish golden mutants share these melanosomal changes and that golden encodes a putative cation exchanger slc24a5 (nckx5) that localizes to an intracellular membrane, likely the melanosome or its precursor. The human ortholog is highly similar in sequence and functional in zebrafish. The evolutionarily conserved ancestral allele of a human coding polymorphism predominates in African and East Asian populations. In contrast, the variant allele is nearly fixed in European populations, is associated with a substantial reduction in regional heterozygosity, and correlates with lighter skin pigmentation in admixed populations, suggesting a key role for the SLC24A5 gene in human pigmentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamason, Rebecca L -- Mohideen, Manzoor-Ali P K -- Mest, Jason R -- Wong, Andrew C -- Norton, Heather L -- Aros, Michele C -- Jurynec, Michael J -- Mao, Xianyun -- Humphreville, Vanessa R -- Humbert, Jasper E -- Sinha, Soniya -- Moore, Jessica L -- Jagadeeswaran, Pudur -- Zhao, Wei -- Ning, Gang -- Makalowska, Izabela -- McKeigue, Paul M -- O'donnell, David -- Kittles, Rick -- Parra, Esteban J -- Mangini, Nancy J -- Grunwald, David J -- Shriver, Mark D -- Canfield, Victor A -- Cheng, Keith C -- CA73935/CA/NCI NIH HHS/ -- EY11308/EY/NEI NIH HHS/ -- HD37572/HD/NICHD NIH HHS/ -- HD40179/HD/NICHD NIH HHS/ -- HG002154/HG/NHGRI NIH HHS/ -- HL077910/HL/NHLBI NIH HHS/ -- RR017441/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1782-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jake Gittlen Cancer Research Foundation, Department of Pathology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357253" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; African Continental Ancestry Group/genetics ; Alanine/genetics ; Alleles ; Amino Acid Sequence ; Animals ; Antiporters/chemistry/*genetics/physiology ; Asian Continental Ancestry Group/genetics ; Biological Evolution ; Calcium/metabolism ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genes ; Genetic Variation ; Haplotypes ; Heterozygote ; Humans ; Ion Transport ; Melanins/analysis ; Melanosomes/chemistry/ultrastructure ; Mice ; Molecular Sequence Data ; Multifactorial Inheritance ; Mutation ; Pigment Epithelium of Eye/chemistry/ultrastructure ; Polymorphism, Single Nucleotide ; Selection, Genetic ; Skin Pigmentation/*genetics ; Threonine/genetics ; Zebrafish/embryology/*genetics/metabolism ; Zebrafish Proteins/chemistry/*genetics/physiology
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    Virology. Resurrected influenza virus yields secrets of deadly 1918 pandemic (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):28-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210501" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animals ; Bioterrorism ; Chick Embryo/virology ; Containment of Biohazards ; Disease Outbreaks/history ; Editorial Policies ; *Genes, Viral ; Genome, Viral ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/*metabolism ; History, 20th Century ; Humans ; Influenza A virus/*genetics/*pathogenicity/physiology ; Influenza, Human/epidemiology/history/*virology ; Mice ; Neuraminidase/genetics/metabolism ; Publishing ; RNA Replicase/genetics/metabolism ; United States ; Virulence ; Virus Replication
    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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    Developmental biology. Bird wings really are like dinosaurs' hands (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):194.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Birds/anatomy & histology/*embryology/metabolism ; Chick Embryo ; Dinosaurs/*anatomy & histology ; Forelimb/*anatomy & histology ; Homeodomain Proteins/metabolism ; Mice ; Transcription Factors/metabolism ; Wings, Animal/anatomy & histology/*embryology/metabolism
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    PERIOD1-associated proteins modulate the negative limb of the mammalian circadian oscillator (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-30
    Description: The clock proteins PERIOD1 (PER1) and PERIOD2 (PER2) play essential roles in a negative transcriptional feedback loop that generates circadian rhythms in mammalian cells. We identified two PER1-associated factors, NONO and WDR5, that modulate PER activity. The reduction of NONO expression by RNA interference (RNAi) attenuated circadian rhythms in mammalian cells, and fruit flies carrying a hypomorphic allele were nearly arrhythmic. WDR5, a subunit of histone methyltransferase complexes, augmented PER-mediated transcriptional repression, and its reduction by RNAi diminished circadian histone methylations at the promoter of a clock gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Steven A -- Ripperger, Juergen -- Kadener, Sebastian -- Fleury-Olela, Fabienne -- Vilbois, Francis -- Rosbash, Michael -- Schibler, Ueli -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and National Centres of Competence in Research (NCCR) Frontiers in Genetics, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva-4, Switzerland. steven.brown@molbio.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860628" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; DNA-Binding Proteins/genetics/metabolism ; Drosophila/genetics/physiology ; Drosophila Proteins/genetics/physiology ; Female ; Gene Expression Regulation ; Histones/metabolism ; Immunoprecipitation ; Male ; Methylation ; Mice ; Mice, Inbred BALB C ; Nuclear Proteins/genetics/*metabolism/physiology ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Period Circadian Proteins ; Promoter Regions, Genetic ; Proteins/genetics/*metabolism ; RNA Interference ; Rats ; Receptors, Cytoplasmic and Nuclear/genetics/metabolism ; Transcription Factors ; Transcription, Genetic ; Transfection
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    Medicine. Treating neurodegenerative diseases with antibiotics (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Timothy M -- Cleveland, Don W -- R37 NS027036/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):361-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and the Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15661995" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*drug therapy ; Animals ; Anti-Bacterial Agents/pharmacology/*therapeutic use ; Brain/metabolism ; Ceftriaxone/pharmacology/*therapeutic use ; Clinical Trials as Topic ; Drug Evaluation, Preclinical ; Excitatory Amino Acid Transporter 2/genetics/metabolism ; Glutamic Acid/metabolism ; Humans ; Mice ; Motor Neurons/physiology ; Neurodegenerative Diseases/*drug therapy ; Spinal Cord/metabolism ; Synapses/physiology ; Synaptic Transmission ; beta-Lactams/pharmacology/*therapeutic use
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    Dependence of self-tolerance on TRAF6-directed development of thymic stroma (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-12
    Description: The microenvironments of the thymus are generated by thymic epithelial cells (TECs) and are essential for inducing immune self-tolerance or developing T cells. However, the molecular mechanisms that underlie the differentiation of TECs and thymic compartmentalization are not fully understood. Here we show that deficiency in the tumor necrosis factor receptor-associated factor (TRAF) 6 results in disorganized distribution of medullary TECs (mTECs) and the absence of mature mTECs. Engraftment of thymic stroma of TRAF6(-/-) embryos into athymic nude mice induced autoimmunity. Thus, TRAF6 directs the development of thymic stroma and represents a critical point of regulation for self-tolerance and autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akiyama, Taishin -- Maeda, Shiori -- Yamane, Sayaka -- Ogino, Kaori -- Kasai, Michiyuki -- Kajiura, Fumiko -- Matsumoto, Mitsuru -- Inoue, Jun-ichiro -- New York, N.Y. -- Science. 2005 Apr 8;308(5719):248-51. Epub 2005 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Biology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Cell Line ; Epithelial Cells/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Organ Culture Techniques ; Proto-Oncogene Proteins/physiology ; *Self Tolerance ; T-Lymphocytes/immunology ; TNF Receptor-Associated Factor 6/immunology/*physiology ; Thymus Gland/cytology/embryology/*immunology ; Transcription Factor RelB ; Transcription Factors/physiology
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    Microbiology. Environmentally sensitive protein proves key to making yeast pathogenic (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):515.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Fungal Proteins/genetics/physiology ; Genes, Fungal ; Lung Diseases, Fungal/microbiology ; Mice ; Mutation ; Protein Kinases/*genetics/*physiology ; RNA Interference ; Soil Microbiology ; Spores, Fungal/physiology
    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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    Gene therapy. Panel urges limits on X-SCID trials (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1544-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15761128" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animals ; *Clinical Trials as Topic ; Genetic Diseases, X-Linked/*therapy ; *Genetic Therapy/adverse effects ; Genetic Vectors ; Haplorhini ; Humans ; Infant ; Leukemia, T-Cell/etiology ; Mice ; Oncogenes ; Retroviridae/genetics ; Severe Combined Immunodeficiency/*therapy ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Circadian clock control by SUMOylation of BMAL1 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-20
    Description: The molecular machinery that governs circadian rhythmicity is based on clock proteins organized in regulatory feedback loops. Although posttranslational modification of clock proteins is likely to finely control their circadian functions, only limited information is available to date. Here, we show that BMAL1, an essential transcription factor component of the clock mechanism, is SUMOylated on a highly conserved lysine residue (Lys259) in vivo. BMAL1 shows a circadian pattern of SUMOylation that parallels its activation in the mouse liver. SUMOylation of BMAL1 requires and is induced by CLOCK, the heterodimerization partner of BMAL1. Ectopic expression of a SUMO-deficient BMAL1 demonstrates that SUMOylation plays an important role in BMAL1 circadian expression and clock rhythmicity. This reveals an additional level of regulation within the core mechanism of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardone, Luca -- Hirayama, Jun -- Giordano, Francesca -- Tamaru, Teruya -- Palvimo, Jorma J -- Sassone-Corsi, Paolo -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1390-4. Epub 2005 Aug 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, 1 rue Laurent Fries, 67404 Illkirch, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109848" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; CLOCK Proteins ; COS Cells ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; Dimerization ; Ethylmaleimide/pharmacology ; Gene Expression Regulation ; Liver/metabolism ; Lysine/metabolism ; Mice ; Mutation ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/*metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/chemistry/genetics/*metabolism
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    Regulation of mammalian tooth cusp patterning by ectodin (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: Mammalian tooth crowns have precise functional requirements but cannot be substantially remodeled after eruption. In developing teeth, epithelial signaling centers, the enamel knots, form at future cusp positions and are the first signs of cusp patterns that distinguish species. We report that ectodin, a secreted bone morphogenetic protein (BMP) inhibitor, is expressed as a "negative" image of mouse enamel knots. Furthermore, we show that ectodin-deficient mice have enlarged enamel knots, highly altered cusp patterns, and extra teeth. Unlike in normal teeth, excess BMP accelerates patterning in ectodin-deficient teeth. We propose that ectodin is critical for robust spatial delineation of enamel knots and cusps.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kassai, Yoshiaki -- Munne, Pauliina -- Hotta, Yuhei -- Penttila, Enni -- Kavanagh, Kathryn -- Ohbayashi, Norihiko -- Takada, Shinji -- Thesleff, Irma -- Jernvall, Jukka -- Itoh, Nobuyuki -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2067-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic ; Proteins/biosynthesis/genetics/metabolism/pharmacology/*physiology ; Cell Cycle Proteins/biosynthesis/genetics/physiology ; Chimera ; Cyclin-Dependent Kinase Inhibitor p21 ; Dental Enamel/embryology ; Gene Expression Regulation, Developmental ; Hedgehog Proteins ; Heterozygote ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Molar/embryology/metabolism ; Mutation ; *Odontogenesis ; Organ Culture Techniques ; Tooth Crown/*embryology ; Trans-Activators/biosynthesis/genetics
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    Stimulus specificity of gene expression programs determined by temporal control of IKK activity (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
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    Nicotinic acid limitation regulates silencing of Candida adhesins during UTI (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-03-19
    Description: The adherence of Candida glabrata to host cells is mediated, at least in part, by the EPA genes, a family of adhesins encoded at subtelomeric loci, where they are subject to transcriptional silencing. We show that normally silent EPA genes are expressed during murine urinary tract infection (UTI) and that the inducing signal is the limitation of nicotinic acid (NA), a precursor of nicotinamide adenine dinucleotide (NAD+). C. glabrata is an NA auxotroph, and NA-induced EPA expression is likely the result of a reduction in NAD+ availability for the NAD+-dependent histone deacetylase Sir2p. The adaptation of C. glabrata to the host, therefore, involves a loss of metabolic capacity and exploitation of the resulting auxotrophy to signal a particular host environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Domergue, Renee -- Castano, Irene -- De Las Penas, Alejandro -- Zupancic, Margaret -- Lockatell, Virginia -- Hebel, J Richard -- Johnson, David -- Cormack, Brendan P -- 2PO1DK49720/DK/NIDDK NIH HHS/ -- R01AI46223/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 May 6;308(5723):866-70. Epub 2005 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, 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/15774723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida glabrata/*genetics/growth & development/*pathogenicity/physiology ; Candidiasis/*microbiology ; Cell Adhesion ; Culture Media ; Female ; Gene Expression Regulation, Fungal ; *Gene Silencing ; Genes, Fungal ; Histone Deacetylases/genetics/metabolism ; Lectins/*genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; NAD/metabolism ; Niacin/administration & dosage/*metabolism/pharmacology/urine ; Niacinamide/pharmacology/urine ; Sirtuins/genetics/metabolism ; Transcription, Genetic ; Urinary Bladder/microbiology ; Urinary Tract Infections/*microbiology ; Urine/microbiology ; Urothelium/microbiology ; Virulence
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    Bacterial injectisomes: needle length does matter (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: Many pathogenic bacteria use a type III secretion nanomachine (an injectisome) to deliver virulence proteins into the cytosol of their eukaryotic host cells. Most injectisomes possess a stiff needlelike structure of a genetically defined length. We found that a minimal needle length was required for efficient functioning of the Yersinia enterocolitica injectisome. This minimal needle length correlated with the length of the major adhesin at the bacterial surface. The needle may be required for triggering type III secretion, and its length may have evolved to match specific structures at the bacterial and host cell surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mota, Luis Jaime -- Journet, Laure -- Sorg, Isabel -- Agrain, Celine -- Cornelis, Guy R -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum, Universitat Basel, 4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731447" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/chemistry/*metabolism ; Animals ; Bacterial Outer Membrane Proteins/metabolism ; Bacterial Proteins/chemistry/genetics/metabolism ; Cell Line ; Macrophages/metabolism/microbiology ; Mice ; Plasmids ; Protein-Serine-Threonine Kinases/metabolism ; Virulence ; Virulence Factors/metabolism ; Yersinia enterocolitica/genetics/*metabolism/*pathogenicity
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  • 89
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    Uncharged tRNA and sensing of amino acid deficiency in mammalian piriform cortex (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: Recognizing a deficiency of indispensable amino acids (IAAs) for protein synthesis is vital for dietary selection in metazoans, including humans. Cells in the brain's anterior piriform cortex (APC) are sensitive to IAA deficiency, signaling diet rejection and foraging for complementary IAA sources, but the mechanism is unknown. Here we report that the mechanism for recognizing IAA-deficient foods follows the conserved general control (GC) system, wherein uncharged transfer RNA induces phosphorylation of eukaryotic initiation factor 2 (eIF2) via the GC nonderepressing 2 (GCN2) kinase. Thus, a basic mechanism of nutritional stress management functions in mammalian brain to guide food selection for survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hao, Shuzhen -- Sharp, James W -- Ross-Inta, Catherine M -- McDaniel, Brent J -- Anthony, Tracy G -- Wek, Ronald C -- Cavener, Douglas R -- McGrath, Barbara C -- Rudell, John B -- Koehnle, Thomas J -- Gietzen, Dorothy W -- GM49164/GM/NIGMS NIH HHS/ -- NS043231/NS/NINDS NIH HHS/ -- NS33347/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1776-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Veterinary Medicine, Department of Anatomy, Physiology and Cell Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774759" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Amino Acids, Essential/*administration & dosage/analysis/*deficiency ; Animals ; Diet ; Eating ; Eukaryotic Initiation Factor-2/*metabolism ; *Food ; Food Preferences ; Leucine/administration & dosage/*analogs & derivatives/pharmacology ; Mice ; Mice, Inbred C57BL ; Olfactory Pathways/*metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases ; RNA, Transfer/*metabolism ; Rats ; Stereoisomerism ; Threonine/administration & dosage ; eIF-2 Kinase/metabolism
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    Endosomal proteolysis of the Ebola virus glycoprotein is necessary for infection (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: Ebola virus (EboV) causes rapidly fatal hemorrhagic fever in humans and there is currently no effective treatment. We found that the infection of African green monkey kidney (Vero) cells by vesicular stomatitis viruses bearing the EboV glycoprotein (GP) requires the activity of endosomal cysteine proteases. Using selective protease inhibitors and protease-deficient cell lines, we identified an essential role for cathepsin B (CatB) and an accessory role for cathepsin L (CatL) in EboV GP-dependent entry. Biochemical studies demonstrate that CatB and CatL mediate entry by carrying out proteolysis of the EboV GP subunit GP1 and support a multistep mechanism that explains the relative contributions of these enzymes to infection. CatB and CatB/CatL inhibitors diminish the multiplication of infectious EboV-Zaire in cultured cells and may merit investigation as anti-EboV drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandran, Kartik -- Sullivan, Nancy J -- Felbor, Ute -- Whelan, Sean P -- Cunningham, James M -- R01 AI059371/AI/NIAID NIH HHS/ -- R01 AI059371-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1643-5. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831716" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cathepsin B/antagonists & inhibitors/*metabolism ; Cathepsin L ; Cathepsins/antagonists & inhibitors/*metabolism ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Ebolavirus/metabolism/*physiology ; Endosomes/*metabolism ; Hydrogen-Ion Concentration ; Mice ; Vero Cells ; Vesicular stomatitis Indiana virus/genetics/physiology ; Viral Envelope Proteins/*metabolism ; Virion/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: Blood calcium concentration is maintained within a narrow range despite large variations in dietary input and body demand. The Transient Receptor Potential ion channel TRPV5 has been implicated in this process. We report here that TRPV5 is stimulated by the mammalian hormone klotho. Klotho, a beta-glucuronidase, hydrolyzes extracellular sugar residues on TRPV5, entrapping the channel in the plasma membrane. This maintains durable calcium channel activity and membrane calcium permeability in kidney. Thus, klotho activates a cell surface channel by hydrolysis of its extracellular N-linked oligosaccharides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Q -- Hoefs, S -- van der Kemp, A W -- Topala, C N -- Bindels, R J -- Hoenderop, J G -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Glucuronidase/antagonists & inhibitors/metabolism ; Glycosylation ; Humans ; Hydrolysis ; Kidney/cytology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Patch-Clamp Techniques ; Protein Transport ; Rabbits ; Sodium/metabolism ; TRPV Cation Channels/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    A strategy for probing the function of noncoding RNAs finds a repressor of NFAT (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-06
    Description: Noncoding RNA molecules (ncRNAs) have been implicated in numerous biological processes including transcriptional regulation and the modulation of protein function. Yet, in spite of the apparent abundance of ncRNA, little is known about the biological role of the projected thousands of ncRNA genes present in the human genome. To facilitate functional analysis of these RNAs, we have created an arrayed library of short hairpin RNAs (shRNAs) directed against 512 evolutionarily conserved putative ncRNAs and, via cell-based assays, we have begun to determine their roles in cellular pathways. Using this system, we have identified an ncRNA repressor of the nuclear factor of activated T cells (NFAT), which interacts with multiple proteins including members of the importin-beta superfamily and likely functions as a specific regulator of NFAT nuclear trafficking.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willingham, A T -- Orth, A P -- Batalov, S -- Peters, E C -- Wen, B G -- Aza-Blanc, P -- Hogenesch, J B -- Schultz, P G -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, 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/16141075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA-Binding Proteins/*antagonists & inhibitors ; Humans ; Mice ; NFATC Transcription Factors ; Nuclear Proteins/*antagonists & inhibitors ; *RNA Interference ; RNA, Long Noncoding ; RNA, Untranslated/antagonists & inhibitors/genetics/*physiology ; Transcription Factors/*antagonists & inhibitors ; beta Karyopherins/metabolism
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  • 93
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    Spongiform diseases. Waiting for the final experiment (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1758.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cricetinae ; Humans ; Mice ; PrPC Proteins/*chemistry ; PrPSc Proteins/*chemistry/*pathogenicity ; Prion Diseases/*etiology ; Protein Folding
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  • 94
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    Increase in activity during calorie restriction requires Sirt1 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-13
    Description: Sir2 (silent information regulator 2) is a nicotinamide adenine dinucleotide-dependent deacetylase required for longevity due to calorie restriction in yeast and Drosophila. In mammals, calorie restriction induces a complex pattern of physiological and behavioral changes. Here we report that the mammalian Sir2 ortholog, Sirt1, is required for the induction of a phenotype by calorie restriction in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Danica -- Steele, Andrew D -- Lindquist, Susan -- Guarente, Leonard -- AG11119/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1641.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Caloric Restriction ; Eating ; Mice ; Mice, Knockout ; *Motor Activity ; Movement ; Sirtuin 1 ; Sirtuins/genetics/*physiology
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  • 95
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    CX3CR1-mediated dendritic cell access to the intestinal lumen and bacterial clearance (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Dendritic cells (DCs) and macrophages are critical to innate and adaptive immunity to the intestinal bacterial microbiota. Here, we identify a myeloid-derived mucosal DC in mice, which populates the entire lamina propria of the small intestine. Lamina propria DCs were found to depend on the chemokine receptor CX3CR1 to form transepithelial dendrites, which enable the cells to directly sample luminal antigens. CX3CR1 was also found to control the clearance of entero-invasive pathogens by DCs. Thus, CX3CR1-dependent processes, which control host interactions of specialized DCs with commensal and pathogenic bacteria, may regulate immunological tolerance and inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niess, Jan Hendrik -- Brand, Stephan -- Gu, Xiubin -- Landsman, Limor -- Jung, Steffen -- McCormick, Beth A -- Vyas, Jatin M -- Boes, Marianne -- Ploegh, Hidde L -- Fox, James G -- Littman, Dan R -- Reinecker, Hans-Christian -- AI33856/AI/NIAID NIH HHS/ -- DK33506/DK/NIDDK NIH HHS/ -- DK54427/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):254-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokine CX3CL1 ; Chemokines, CX3C/metabolism ; Dendritic Cells/cytology/*immunology/microbiology ; Escherichia coli/*immunology/isolation & purification ; Gene Deletion ; Green Fluorescent Proteins/metabolism ; Ileum/cytology/immunology ; *Immunity, Mucosal ; Intestinal Mucosa/*immunology/microbiology ; Intestine, Small/immunology/microbiology ; Lymphoid Tissue/cytology/immunology ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Peyer's Patches/immunology/microbiology ; Phagocytosis ; Receptors, Chemokine/genetics/metabolism/*physiology ; Salmonella Infections, Animal/*immunology/microbiology ; Salmonella typhimurium/*immunology/isolation & purification
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  • 96
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    Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: Microglial cells represent the immune system of the mammalian brain and therefore are critically involved in various injuries and diseases. Little is known about their role in the healthy brain and their immediate reaction to brain damage. By using in vivo two-photon imaging in neocortex, we found that microglial cells are highly active in their presumed resting state, continually surveying their microenvironment with extremely motile processes and protrusions. Furthermore, blood-brain barrier disruption provoked immediate and focal activation of microglia, switching their behavior from patroling to shielding of the injured site. Microglia thus are busy and vigilant housekeepers in the adult brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimmerjahn, Axel -- Kirchhoff, Frank -- Helmchen, Fritjof -- New York, N.Y. -- Science. 2005 May 27;308(5726):1314-8. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max Planck Institut fur Medizinische Forschung, Jahnstrasse 29, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology/ultrastructure ; Bicuculline/pharmacology ; Blood-Brain Barrier ; Brain Injuries/physiopathology ; Capillaries/injuries ; Cell Movement ; Cell Surface Extensions/*physiology/ultrastructure ; GABA Antagonists/pharmacology ; Green Fluorescent Proteins ; Lasers ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy, Fluorescence ; Neocortex/*cytology/*physiology ; Pseudopodia/physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology
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  • 97
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    Reciprocal interference between specific CJD and scrapie agents in neural cell cultures (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: Infection of mice with an attenuated Creutzfeldt-Jakob disease agent (SY-CJD) interferes with superinfection by a more virulent human-derived CJD agent (FU-CJD) and does not require pathological prion protein (PrPres). Using a rapid coculture system, we found that a neural cell line free of immune system cells similarly supported substantial CJD agent interference without PrPres. In addition, SY-CJD prevented superinfection by sheep-derived Chandler (Ch) and 22L scrapie agents. However, only 22L and not Ch prevented FU-CJD infection, even though both scrapie strains provoked abundant PrPres. This relationship between particular strains of sheep- and human-derived agents is likely to affect their prevalence and epidemic spread.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishida, Noriuki -- Katamine, Shigeru -- Manuelidis, Laura -- NS12674/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):493-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale Medical School, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Coculture Techniques ; *Creutzfeldt-Jakob Syndrome ; Humans ; Mice ; Neurons/metabolism/*physiology ; PrPSc Proteins/metabolism/*pathogenicity ; Prions/metabolism/*pathogenicity/*physiology ; Scrapie ; Sheep ; Species Specificity ; Virulence
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  • 98
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    Small CTD phosphatases function in silencing neuronal gene expression (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: Neuronal gene transcription is repressed in non-neuronal cells by the repressor element 1 (RE-1)-silencing transcription factor/neuron-restrictive silencer factor (REST/NRSF) complex. To understand how this silencing is achieved, we examined a family of class-C RNA polymerase II (RNAPII) carboxyl-terminal domain (CTD) phosphatases [small CTD phosphatases (SCPs) 1 to 3], whose expression is restricted to non-neuronal tissues. We show that REST/NRSF recruits SCPs to neuronal genes that contain RE-1 elements, leading to neuronal gene silencing in non-neuronal cells. Phosphatase-inactive forms of SCP interfere with REST/NRSF function and promote neuronal differentiation of P19 stem cells. Likewise, small interfering RNA directed to the single Drosophila SCP unmasks neuronal gene expression in S2 cells. Thus, SCP activity is an evolutionarily conserved transcriptional regulator that acts globally to silence neuronal genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeo, Michele -- Lee, Soo-Kyung -- Lee, Bora -- Ruiz, Esmeralda C -- Pfaff, Samuel L -- Gill, Gordon N -- DK13149/DK/NIDDK NIH HHS/ -- NS37116/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):596-600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Differentiation ; Cell Line ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Drosophila/genetics/metabolism ; Drosophila Proteins/genetics/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; *Gene Silencing ; Humans ; In Situ Hybridization ; Mice ; Nerve Tissue Proteins/metabolism ; Neurons/cytology/*physiology ; Nuclear Proteins ; Phosphoprotein Phosphatases/genetics/*metabolism ; Phosphorylation ; RNA Interference ; Regulatory Sequences, Nucleic Acid ; Repressor Proteins/*metabolism ; TCF Transcription Factors ; Transcription Factor 7-Like 1 Protein ; Transcription Factors/*metabolism ; Tretinoin/pharmacology
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  • 99
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    NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-29
    Description: Hypothalamic neurons that express neuropeptide Y (NPY) and agouti-related protein (AgRP) are thought to be critical regulators of feeding behavior and body weight. To determine whether NPY/AgRP neurons are essential in mice, we targeted the human diphtheria toxin receptor to the Agrp locus, which allows temporally controlled ablation of NPY/AgRP neurons to occur after an injection of diphtheria toxin. Neonatal ablation of NPY/AgRP neurons had minimal effects on feeding, whereas their ablation in adults caused rapid starvation. These results suggest that network-based compensatory mechanisms can develop after the ablation of NPY/AgRP neurons in neonates but do not readily occur when these neurons become essential in adults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luquet, Serge -- Perez, Francisco A -- Hnasko, Thomas S -- Palmiter, Richard D -- K01 DA026504/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):683-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254186" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Agouti-Related Protein ; Animals ; Animals, Newborn ; Arcuate Nucleus of Hypothalamus/cytology ; Body Weight/physiology ; Diphtheria Toxin ; Feeding Behavior/*physiology ; Heparin-binding EGF-like Growth Factor ; Humans ; Intercellular Signaling Peptides and Proteins ; Mice ; Neurons/metabolism/*physiology ; Neuropeptide Y/*metabolism ; Proteins/*metabolism ; Receptors, Cell Surface/genetics
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  • 100
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    TLR11 activation of dendritic cells by a protozoan profilin-like protein (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-30
    Description: Mammalian Toll-like receptors (TLRs) play an important role in the innate recognition of pathogens by dendritic cells (DCs). Although TLRs are clearly involved in the detection of bacteria and viruses, relatively little is known about their function in the innate response to eukaryotic microorganisms. Here we identify a profilin-like molecule from the protozoan parasite Toxoplasma gondii that generates a potent interleukin-12 (IL-12) response in murine DCs that is dependent on myeloid differentiation factor 88. T. gondii profilin activates DCs through TLR11 and is the first chemically defined ligand for this TLR. Moreover, TLR11 is required in vivo for parasite-induced IL-12 production and optimal resistance to infection, thereby establishing a role for the receptor in host recognition of protozoan pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yarovinsky, Felix -- Zhang, Dekai -- Andersen, John F -- Bannenberg, Gerard L -- Serhan, Charles N -- Hayden, Matthew S -- Hieny, Sara -- Sutterwala, Fayyaz S -- Flavell, Richard A -- Ghosh, Sankar -- Sher, Alan -- 1R01AI045806-01A1/AI/NIAID NIH HHS/ -- AI05093/AI/NIAID NIH HHS/ -- R01-AI59440/AI/NIAID NIH HHS/ -- R01-GM38765/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1626-9. Epub 2005 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Section, Laboratory of Parasitic Diseases; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. fyarovinsky@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860593" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Antigens, Differentiation/genetics/metabolism ; Contractile Proteins/chemistry/*immunology/isolation & purification/metabolism ; Dendritic Cells/*immunology ; Genes, Protozoan ; Immunity, Innate ; Interleukin-12/biosynthesis/blood ; Ligands ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/chemistry/*immunology/isolation & purification/metabolism ; Molecular Sequence Data ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Profilins ; Protozoan Proteins/chemistry/*immunology/isolation & purification/metabolism ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/genetics/metabolism ; Recombinant Proteins/immunology ; Signal Transduction ; Toll-Like Receptors ; Toxoplasma/genetics/*immunology ; Toxoplasmosis, Animal/*immunology ; Transfection
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