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  • 1
    Publikationsdatum: 2020-12-21
    Beschreibung: This paper introduces the three-dimensional Hamburg Model of the Neutral and Ionized Atmosphere (HAMMONIA), which treats atmospheric dynamics, radiation, and chemistry interactively for the height range from the earth’s surface to the thermosphere (approximately 250 km). It is based on the latest version of the ECHAM atmospheric general circulation model of the Max Planck Institute for Meteorology in Hamburg, Germany, which is extended to include important radiative and dynamical processes of the upper atmosphere and is coupled to a chemistry module containing 48 compounds. The model is applied to study the effects of natural and anthropogenic climate forcing on the atmosphere, represented, on the one hand, by the 11-yr solar cycle and, on the other hand, by a doubling of the present-day concentration of carbon dioxide. The numerical experiments are analyzed with the focus on the effects on temperature and chemical composition in the mesopause region. Results include a temperature response to the solar cycle by 2 to 10 K in the mesopause region with the largest values occurring slightly above the summer mesopause. Ozone in the secondary maximum increases by up to 20% for solar maximum conditions. Changes in winds are in general small. In the case of a doubling of carbon dioxide the simulation indicates a cooling of the atmosphere everywhere above the tropopause but by the smallest values around the mesopause. It is shown that the temperature response up to the mesopause is strongly influenced by changes in dynamics. During Northern Hemisphere summer, dynamical processes alone would lead to an almost global warming of up to 3 K in the uppermost mesosphere.
    Beschreibung: Published
    Beschreibung: 3903-3931
    Beschreibung: reserved
    Schlagwort(e): Sensitivity ; Chemistry ; 01. Atmosphere::01.01. Atmosphere::01.01.02. Climate
    Repository-Name: Istituto Nazionale di Geofisica e Vulcanologia (INGV)
    Materialart: article
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  • 2
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    Alexandria: National Institute of Oceanography and Fisheries
    Publikationsdatum: 2021-05-19
    Beschreibung: This journal is published by the NIOF, Egypt
    Beschreibung: Lake Manzalah; the largest delta Lake in Egypt represents a dynamic system that has been undergoing continuous and pronounced changes since long times. In the last year’s this Lake faced drastic problems that retarded its environmental and fisheries development; the most serious one is the discharge of waste water. It is attempted in the present study to investigate the chemical characters of Lake Manzalah water during 2001-2002. Water temperature ranged from an average of 12.35oC in January and 29.14oC in July. Dissolved Oxygen, pH and total dissolved solids were found in ranges optimum for the living of marine and freshwater fish species. The average concentrations of nutrients lied in the following ranges: 1.24 to 4.89 μmol PO4 -3 l-1 , 5.08 to 28.73 μmol SiO4 -2 l-1 and 1.81 to 17.7 μ_mol NO3-1 l-1 The concentrations of phosphorus and nitrogen compounds were found to be relatively higher at the southern regions of the Lake near to the outlets of the drains.
    Beschreibung: NIOF
    Beschreibung: Published
    Schlagwort(e): Hydrography ; Water ; Chemistry ; Chemical composition ; Water content ; Environment ; Chemical composition ; Environments ; Water content ; Fisheries
    Repository-Name: AquaDocs
    Materialart: Journal Contribution , Refereed , Article
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    Format: 46916 bytes
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    Format: application/pdf
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  • 3
    Publikationsdatum: 2023-01-19
    Beschreibung: Bromine monoxide (BrO) and sulphur dioxide (SO2) abundances as a function of the distance from the source were measured by ground-based scattered-light Multi AXis Differential Optical Absorption Spectroscopy (MAX-DOAS) in the volcanic plumes of Mt. Etna on Sicily, Italy in August-October 2004 and May 2005 and Villarica in Chile in November 2004. BrO and SO2 spatial distributions in a cross section of Mt. Etna’s plume were also determined by Imaging DOAS. We observed an increase in the BrO/SO2 ratio in the plume from below the detection limit near the vent to about 4.5 x 10-4 at 19 km (Mt. Etna) and to about 1.3 x 10-4 at 3 km (Villarica) distance, respectively. Additional attempts were undertaken to evaluate the compositions of individual vents on Mt. Etna. Furthermore, we detected the halogen species ClO and OClO. This is the first time that OClO could be detected in a volcanic plume. Using calculated thermodynamic equilibrium compositions as input data for a one–dimensional photochemical model, we could reproduce the observed BrO and SO2 vertical columns in the plume and their ratio as function of distance from the volcano as well as vertical BrO and SO2 profiles across the plume with current knowledge of multiphase halogen chemistry, but only when we assumed the existence of an ”effective source region”, where volcanic volatiles and ambient air are mixed at about 600°C (in the proportions of 60% and 40%, respectively)
    Beschreibung: Published
    Beschreibung: D06311
    Beschreibung: 3V. Proprietà chimico-fisiche dei magmi e dei prodotti vulcanici
    Beschreibung: JCR Journal
    Beschreibung: open
    Schlagwort(e): Chemistry ; Volcanic Plumes ; 04. Solid Earth::04.08. Volcanology::04.08.01. Gases ; 04. Solid Earth::04.08. Volcanology::04.08.06. Volcano monitoring ; 04. Solid Earth::04.08. Volcanology::04.08.07. Instruments and techniques
    Repository-Name: Istituto Nazionale di Geofisica e Vulcanologia (INGV)
    Materialart: article
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  • 4
    Publikationsdatum: 2006-02-25
    Beschreibung: The transcription factor NF-kappaB modulates apoptotic responses induced by genotoxic stress. We show that NF-kappaB essential modulator (NEMO), the regulatory subunit of IkappaB kinase (IKK) (which phosphorylates the NF-kappaB inhibitor IkappaB), associates with activated ataxia telangiectasia mutated (ATM) after the induction of DNA double-strand breaks. ATM phosphorylates serine-85 of NEMO to promote its ubiquitin-dependent nuclear export. ATM is also exported in a NEMO-dependent manner to the cytoplasm, where it associates with and causes the activation of IKK in a manner dependent on another IKK regulator, a protein rich in glutamate, leucine, lysine, and serine (ELKS). Thus, regulated nuclear shuttling of NEMO links two signaling kinases, ATM and IKK, to activate NF-kappaB by genotoxic signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Zhao-Hui -- Shi, Yuling -- Tibbetts, Randal S -- Miyamoto, Shigeki -- R01-CA77474/CA/NCI NIH HHS/ -- R01-CA81065/CA/NCI NIH HHS/ -- R01-GM067868/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1141-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin-Madison, 301 SMI, 1300 University Avenue, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497931" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Adaptor Proteins, Signal Transducing/genetics/metabolism ; Amino Acid Motifs ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/*metabolism ; Humans ; I-kappa B Kinase/*metabolism ; I-kappa B Proteins/genetics/metabolism ; NF-kappa B/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/metabolism ; *Signal Transduction ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 5
    Publikationsdatum: 2006-05-20
    Beschreibung: 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〉
    Schlagwort(e): 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
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 6
    Publikationsdatum: 2006-09-09
    Beschreibung: Chromosomal integration enables human immunodeficiency virus (HIV) to establish a permanent reservoir that can be therapeutically suppressed but not eradicated. Participation of cellular proteins in this obligate replication step is poorly understood. We used intensified RNA interference and dominant-negative protein approaches to show that the cellular transcriptional coactivator lens epithelium-derived growth factor (LEDGF)/p75 (p75) is an essential HIV integration cofactor. The mechanism requires both linkages of a molecular tether that p75 forms between integrase and chromatin. Fractionally minute levels of endogenous p75 are sufficient to enable integration, showing that cellular factors that engage HIV after entry may elude identification in less intensive knockdowns. Perturbing the p75-integrase interaction may have therapeutic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Llano, Manuel -- Saenz, Dyana T -- Meehan, Anne -- Wongthida, Phonphimon -- Peretz, Mary -- Walker, William H -- Teo, Wulin -- Poeschla, Eric M -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):461-4. Epub 2006 Sep 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Medicine Program, 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/16959972" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/chemistry/genetics/metabolism/*physiology ; CD4-Positive T-Lymphocytes/metabolism/*virology ; Cell Line ; Chromatin/*metabolism ; HIV Integrase/*metabolism ; HIV-1/*physiology ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/metabolism/*physiology ; *Virus Integration ; Virus Replication
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 7
    Publikationsdatum: 2006-07-22
    Beschreibung: 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〉
    Schlagwort(e): 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
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-29
    Beschreibung: Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that the same molecular mechanism responsible for HGPS is active in healthy cells. Cell nuclei from old individuals acquire defects similar to those of HGPS patient cells, including changes in histone modifications and increased DNA damage. Age-related nuclear defects are caused by sporadic use, in healthy individuals, of the same cryptic splice site in lamin A whose constitutive activation causes HGPS. Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1855250/" 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/PMC1855250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scaffidi, Paola -- Misteli, Tom -- Z01 BC010309-07/BC/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1059-63. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645051" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged, 80 and over ; Aging/*physiology ; Cell Line ; Cell Nucleus/pathology ; DNA Damage ; Exons ; Histones/metabolism ; Humans ; Lamin Type A/genetics/*physiology ; Progeria/genetics/pathology ; RNA Splicing/genetics ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/metabolism
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 9
    Publikationsdatum: 2006-08-26
    Beschreibung: The ataxia telangiectasia mutated (ATM) protein kinase is a critical component of a DNA-damage response network configured to maintain genomic integrity. The abundance of an essential downstream effecter of this pathway, the tumor suppressor protein p53, is tightly regulated by controlled degradation through COP1 and other E3 ubiquitin ligases, such as MDM2 and Pirh2; however, the signal transduction pathway that regulates the COP1-p53 axis following DNA damage remains enigmatic. We observed that in response to DNA damage, ATM phosphorylated COP1 on Ser(387) and stimulated a rapid autodegradation mechanism. Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53. Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornan, David -- Shimizu, Harumi -- Mah, Angie -- Dudhela, Tanay -- Eby, Michael -- O'rourke, Karen -- Seshagiri, Somasekar -- Dixit, Vishva M -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931761" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/genetics/*metabolism ; Escherichia coli/genetics/metabolism ; Etoposide/pharmacology ; Humans ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA, Small Interfering ; Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/metabolism ; Tumor Suppressor Proteins/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 10
    Publikationsdatum: 2006-10-21
    Beschreibung: The tumor suppressor programmed cell death protein 4 (PDCD4) inhibits the translation initiation factor eIF4A, an RNA helicase that catalyzes the unwinding of secondary structure at the 5' untranslated region (5'UTR) of messenger RNAs (mRNAs). In response to mitogens, PDCD4 was rapidly phosphorylated on Ser67 by the protein kinase S6K1 and subsequently degraded via the ubiquitin ligase SCF(betaTRCP). Expression in cultured cells of a stable PDCD4 mutant that is unable to bind betaTRCP inhibited translation of an mRNA with a structured 5'UTR, resulted in smaller cell size, and slowed down cell cycle progression. We propose that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis and consequently cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorrello, N Valerio -- Peschiaroli, Angelo -- Guardavaccaro, Daniele -- Colburn, Nancy H -- Sherman, Nicholas E -- Pagano, Michele -- R01-CA76584/CA/NCI NIH HHS/ -- R01-GM57587/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):467-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053147" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5' Untranslated Regions ; Amino Acid Motifs ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Size ; Eukaryotic Initiation Factor-4A/antagonists & inhibitors/metabolism ; Eukaryotic Initiation Factor-4F/metabolism ; Eukaryotic Initiation Factor-4G/metabolism ; Eukaryotic Initiation Factors/metabolism ; Humans ; Mitogens/pharmacology ; Phosphorylation ; *Protein Biosynthesis ; RNA, Small Interfering ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Ribosomal Protein S6 Kinases/metabolism ; SKP Cullin F-Box Protein Ligases/*metabolism ; Serine/metabolism ; Serum ; Signal Transduction ; beta-Transducin Repeat-Containing Proteins/genetics/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 11
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-22
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szathmary, Eors -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):306-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biology, Eotvos University Budapest, and Collegium Budapest (Institute for Advanced Study), 2 Szentharomsag utca, H-1014 Budapest, Hungary. szathmary@colbud.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857926" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Biological Evolution ; Chemical Phenomena ; Chemistry ; Computational Biology ; Cooperative Behavior ; Cultural Evolution ; Exobiology ; Humans ; Language ; Models, Biological ; Models, Theoretical ; Molecular Biology ; Origin of Life ; *Research ; Selection, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 12
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-11-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1235-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124302" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Chemistry ; *Cooking ; *Food ; France ; History, 20th Century ; History, 21st Century
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 13
    Publikationsdatum: 2006-08-12
    Beschreibung: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 14
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-02-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Mildred K -- McGee, Glenn -- Magnus, David -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):614-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford Center for Biomedical Ethics, Department of Pediatrics; Palo Alto, CA 94304, USA. micho@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456065" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Academies and Institutes/ethics/*standards ; Authorship ; Biomedical Research/*ethics/*standards ; Cell Line ; *Ethics, Research ; Female ; Humans ; Korea ; Oocyte Donation/adverse effects ; Research Personnel/*ethics/standards ; Research Support as Topic ; Scientific Misconduct ; Stem Cells ; United States
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 15
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-09
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1372.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959980" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; Cloning, Organism/legislation & jurisprudence ; Embryo Research/ethics/*legislation & jurisprudence ; Embryo, Mammalian/cytology ; Humans ; Massachusetts ; Research Embryo Creation/ethics/legislation & jurisprudence ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 16
    Publikationsdatum: 2007-01-06
    Beschreibung: We have designed a microfluidic device in which we can manipulate, lyse, label, separate, and quantify the protein contents of a single cell using single-molecule fluorescence counting. Generic labeling of proteins is achieved through fluorescent-antibody binding. The use of cylindrical optics enables high-efficiency (approximately 60%) counting of molecules in micrometer-sized channels. We used this microfluidic device to quantify beta2 adrenergic receptors expressed in insect cells (SF9). We also analyzed phycobiliprotein contents in individual cyanobacterial cells (Synechococcus sp. PCC 7942) and observed marked differences in the levels of specific complexes in cell populations that were grown under nitrogen-depleted conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Bo -- Wu, Hongkai -- Bhaya, Devaki -- Grossman, Arthur -- Granier, Sebastien -- Kobilka, Brian K -- Zare, Richard N -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, Stanford, CA 94305-5080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204646" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Monoclonal ; Bacterial Proteins/*analysis ; Bacteriolysis ; Carbocyanines ; Cell Line ; Culture Media ; Fluorescence ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Humans ; Lasers ; *Microfluidic Analytical Techniques/instrumentation ; Microfluidics ; Nitrogen/metabolism ; Optics and Photonics ; Phycobilisomes/metabolism ; Phycocyanin/*analysis ; Receptors, Adrenergic, beta-2/*analysis ; Synechococcus/*chemistry/growth & development/metabolism
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  • 17
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-11-04
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 18
    Publikationsdatum: 2007-08-19
    Beschreibung: Recent advances in far-field optical nanoscopy have enabled fluorescence imaging with a spatial resolution of 20 to 50 nanometers. Multicolor super-resolution imaging, however, remains a challenging task. Here, we introduce a family of photo-switchable fluorescent probes and demonstrate multicolor stochastic optical reconstruction microscopy (STORM). Each probe consists of a photo-switchable "reporter" fluorophore that can be cycled between fluorescent and dark states, and an "activator" that facilitates photo-activation of the reporter. Combinatorial pairing of reporters and activators allows the creation of probes with many distinct colors. Iterative, color-specific activation of sparse subsets of these probes allows their localization with nanometer accuracy, enabling the construction of a super-resolution STORM image. Using this approach, we demonstrate multicolor imaging of DNA model samples and mammalian cells with 20- to 30-nanometer resolution. This technique will facilitate direct visualization of molecular interactions at the nanometer scale.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633025/" 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/PMC2633025/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bates, Mark -- Huang, Bo -- Dempsey, Graham T -- Zhuang, Xiaowei -- GM 068518/GM/NIGMS NIH HHS/ -- R01 GM068518/GM/NIGMS NIH HHS/ -- R01 GM068518-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1749-53. Epub 2007 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702910" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cercopithecus aethiops ; Clathrin-Coated Vesicles ; DNA/*analysis ; *DNA Probes ; *Fluorescent Dyes ; Microscopy, Fluorescence/methods ; Microtubules ; Nanotechnology
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  • 19
    Publikationsdatum: 2007-01-06
    Beschreibung: Cell migration requires the transmission of motion generated in the actin cytoskeleton to the extracellular environment through a complex assembly of proteins in focal adhesions. We developed correlational fluorescent speckle microscopy to measure the coupling of focal-adhesion proteins to actin filaments. Different classes of focal-adhesion structural and regulatory molecules exhibited varying degrees of correlated motions with actin filaments, indicating hierarchical transmission of actin motion through focal adhesions. Interactions between vinculin, talin, and actin filaments appear to constitute a slippage interface between the cytoskeleton and integrins, generating a molecular clutch that is regulated during the morphodynamic transitions of cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Ke -- Ji, Lin -- Applegate, Kathryn T -- Danuser, Gaudenz -- Waterman-Storer, Clare M -- GM67230/GM/NIGMS NIH HHS/ -- U54GM64346/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):111-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The 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/17204653" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actin Cytoskeleton/*metabolism ; Actinin/metabolism ; Actins/*metabolism ; Animals ; Cell Line ; Cell Movement ; Extracellular Matrix/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Focal Adhesions/*metabolism ; Integrin alphaVbeta3/metabolism ; Microfilament Proteins/*metabolism ; Microscopy, Fluorescence ; Monte Carlo Method ; Paxillin/metabolism ; Potoroidae ; Recombinant Fusion Proteins/metabolism ; Talin/metabolism ; Vinculin/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 20
    Publikationsdatum: 2007-02-10
    Beschreibung: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 21
    Publikationsdatum: 2007-09-29
    Beschreibung: The SAX-3/roundabout (Robo) receptor has SLT-1/Slit-dependent and -independent functions in guiding cell and axon migrations. We identified enhancer of ventral-axon guidance defects of unc-40 mutants (EVA-1) as a Caenorhabditis elegans transmembrane receptor for SLT-1. EVA-1 has two predicted galactose-binding ectodomains, acts cell-autonomously for SLT-1/Slit-dependent axon migration functions of SAX-3/Robo, binds to SLT-1 and SAX-3, colocalizes with SAX-3 on cells, and provides cell specificity to the activation of SAX-3 signaling by SLT-1. Double mutants of eva-1 or slt-1 with sax-3 mutations suggest that SAX-3 can (when slt-1 or eva-1 function is reduced) inhibit a parallel-acting guidance mechanism, which involves UNC-40/deleted in colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisawa, Kazuko -- Wrana, Jeffrey L -- Culotti, Joseph G -- NS41397/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1934-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute of Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901337" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/*chemistry/genetics/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Movement ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*metabolism ; Nervous System/growth & development/metabolism ; Neurons/physiology ; Protein Structure, Tertiary ; Receptors, Immunologic/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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  • 22
    Publikationsdatum: 2007-05-26
    Beschreibung: Mutations affecting the BRCT domains of the breast cancer-associated tumor suppressor BRCA1 disrupt the recruitment of this protein to DNA double-strand breaks (DSBs). The molecular structures at DSBs recognized by BRCA1 are presently unknown. We report the interaction of the BRCA1 BRCT domain with RAP80, a ubiquitin-binding protein. RAP80 targets a complex containing the BRCA1-BARD1 (BRCA1-associated ring domain protein 1) E3 ligase and the deubiquitinating enzyme (DUB) BRCC36 to MDC1-gammaH2AX-dependent lysine(6)- and lysine(63)-linked ubiquitin polymers at DSBs. These events are required for cell cycle checkpoint and repair responses to ionizing radiation, implicating ubiquitin chain recognition and turnover in the BRCA1-mediated repair of DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706583/" 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/PMC2706583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sobhian, Bijan -- Shao, Genze -- Lilli, Dana R -- Culhane, Aedin C -- Moreau, Lisa A -- Xia, Bing -- Livingston, David M -- Greenberg, Roger A -- K08 CA106597/CA/NCI NIH HHS/ -- K08 CA106597-01A2/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1198-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Genetics and Department of Medicine, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525341" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; BRCA1 Protein/*metabolism ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair/physiology ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Nucleic Acid Conformation ; Protein Structure, Tertiary ; Tumor Suppressor Proteins/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligases/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 23
    Publikationsdatum: 2007-10-27
    Beschreibung: The melanocortin 1 receptor (MC1R) regulates pigmentation in humans and other vertebrates. Variants of MC1R with reduced function are associated with pale skin color and red hair in humans of primarily European origin. We amplified and sequenced a fragment of the MC1R gene (mc1r) from two Neanderthal remains. Both specimens have a mutation that was not found in approximately 3700 modern humans analyzed. Functional analyses show that this variant reduces MC1R activity to a level that alters hair and/or skin pigmentation in humans. The impaired activity of this variant suggests that Neanderthals varied in pigmentation levels, potentially on the scale observed in modern humans. Our data suggest that inactive MC1R variants evolved independently in both modern humans and Neanderthals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lalueza-Fox, Carles -- Rompler, Holger -- Caramelli, David -- Staubert, Claudia -- Catalano, Giulio -- Hughes, David -- Rohland, Nadin -- Pilli, Elena -- Longo, Laura -- Condemi, Silvana -- de la Rasilla, Marco -- Fortea, Javier -- Rosas, Antonio -- Stoneking, Mark -- Schoneberg, Torsten -- Bertranpetit, Jaume -- Hofreiter, Michael -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1453-5. Epub 2007 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Animal, Universitat de Barcelona, Spain. clalueza@ub.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962522" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Substitution ; Animals ; Biological Evolution ; Cell Line ; DNA/genetics ; *Fossils ; Hair Color/*genetics ; Hominidae/*genetics ; Humans ; Molecular Sequence Data ; *Mutation ; Polymerase Chain Reaction ; Receptor, Melanocortin, Type 1/chemistry/*genetics/metabolism ; Sequence Analysis, DNA ; Skin Pigmentation/*genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 24
    Publikationsdatum: 2007-10-13
    Beschreibung: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 25
    Publikationsdatum: 2007-02-17
    Beschreibung: Migrating cells extend protrusions, probing the surrounding matrix in search of permissive sites to form adhesions. We found that actin fibers polymerizing along the leading edge directed local protrusions and drove synchronous sideways movement of beta1 integrin adhesion receptors. These movements lead to the clustering and positioning of conformationally activated, but unligated, beta1 integrins along the leading edge of fibroblast lamellae and growth cone filopodia. Thus, rapid actin-based movement of primed integrins along the leading edge suggests a "sticky fingers" mechanism to probe for new adhesion sites and to direct migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galbraith, Catherine G -- Yamada, Kenneth M -- Galbraith, James A -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):992-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Dental and Craniofacial Research, 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/17303755" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/*physiology ; Animals ; Antigens, CD29/*physiology ; Cell Adhesion/*physiology ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Movement/*physiology ; Extracellular Matrix/metabolism ; Fibroblasts/physiology ; Fibronectins/metabolism ; Green Fluorescent Proteins/metabolism ; Mice ; Microfilament Proteins/metabolism ; NIH 3T3 Cells ; Phosphoproteins/metabolism ; Protein Binding ; Pseudopodia/metabolism
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  • 26
    Publikationsdatum: 2007-07-14
    Beschreibung: Many human cancers involve up-regulation of the phosphoinositide 3-kinase PI3Kalpha, with oncogenic mutations identified in both the p110alpha catalytic and the p85alpha regulatory subunits. We used crystallographic and biochemical approaches to gain insight into activating mutations in two noncatalytic p110alpha domains-the adaptor-binding and the helical domains. A structure of the adaptor-binding domain of p110alpha in a complex with the p85alpha inter-Src homology 2 (inter-SH2) domain shows that oncogenic mutations in the adaptor-binding domain are not at the inter-SH2 interface but in a polar surface patch that is a plausible docking site for other domains in the holo p110/p85 complex. We also examined helical domain mutations and found that the Glu545 to Lys545 (E545K) oncogenic mutant disrupts an inhibitory charge-charge interaction with the p85 N-terminal SH2 domain. These studies extend our understanding of the architecture of PI3Ks and provide insight into how two classes of mutations that cause a gain in function can lead to cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miled, Nabil -- Yan, Ying -- Hon, Wai-Ching -- Perisic, Olga -- Zvelebil, Marketa -- Inbar, Yuval -- Schneidman-Duhovny, Dina -- Wolfson, Haim J -- Backer, Jonathan M -- Williams, Roger L -- GM55692/GM/NIGMS NIH HHS/ -- MC_U105184308/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):239-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626883" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Amino Acid Sequence ; Animals ; *Catalytic Domain ; Cattle ; Cell Line ; Cell Transformation, Neoplastic ; Crystallography, X-Ray ; Dimerization ; Humans ; Models, Molecular ; Molecular Sequence Data ; *Mutation ; Neoplasms/*genetics ; Phosphatidylinositol 3-Kinases/antagonists & ; inhibitors/chemistry/*genetics/*metabolism ; Protein Structure, Secondary ; Protein Structure, Tertiary ; src Homology Domains
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  • 27
    Publikationsdatum: 2007-03-31
    Beschreibung: Telomerase is a ribonucleoprotein enzyme complex that adds 5'-TTAGGG-3' repeats onto the ends of human chromosomes, providing a telomere maintenance mechanism for approximately 90% of human cancers. We have purified human telomerase approximately 10(8)-fold, with the final elution dependent on the enzyme's ability to catalyze nucleotide addition onto a DNA oligonucleotide of telomeric sequence, thereby providing specificity for catalytically active telomerase. Mass spectrometric sequencing of the protein components and molecular size determination indicated an enzyme composition of two molecules each of telomerase reverse transcriptase, telomerase RNA, and dyskerin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Scott B -- Graham, Mark E -- Lovrecz, George O -- Bache, Nicolai -- Robinson, Phillip J -- Reddel, Roger R -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1850-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Unit, Children's Medical Research Institute, 214 Hawkesbury Road, Westmead NSW 2145, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395830" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Cell Cycle Proteins/*chemistry/isolation & purification ; Cell Line ; Cell Line, Tumor ; Centrifugation, Density Gradient ; Humans ; Molecular Sequence Data ; Molecular Weight ; Multienzyme Complexes/chemistry ; Nuclear Proteins/*chemistry/isolation & purification ; RNA/*chemistry/isolation & purification ; Tandem Mass Spectrometry ; Telomerase/*chemistry/isolation & purification/metabolism
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  • 28
    Publikationsdatum: 2006-12-16
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 29
    Publikationsdatum: 2007-10-20
    Beschreibung: To investigate the unregulated Ras activation associated with cancer, we developed and validated a mathematical model of Ras signaling. The model-based predictions and associated experiments help explain why only one of two classes of activating Ras point mutations with in vitro transformation potential is commonly found in cancers. Model-based analysis of these mutants uncovered a systems-level process that contributes to total Ras activation in cells. This predicted behavior was supported by experimental observations. We also used the model to identify a strategy in which a drug could cause stronger inhibition on the cancerous Ras network than on the wild-type network. This system-level analysis of the oncogenic Ras network provides new insights and potential therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stites, Edward C -- Trampont, Paul C -- Ma, Zhong -- Ravichandran, Kodi S -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):463-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beirne B. Carter Center for Immunology Research and the Department of Microbiology, University of Virginia, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947584" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antineoplastic Agents/metabolism/pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; *Computer Simulation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; GTP Phosphohydrolases/metabolism ; GTPase-Activating Proteins/antagonists & inhibitors/metabolism ; Genes, ras ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Mathematics ; *Metabolic Networks and Pathways ; *Models, Biological ; Neoplasms/*metabolism ; Phosphorylation ; Point Mutation ; *Signal Transduction ; ras Proteins/antagonists & inhibitors/genetics/*metabolism
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  • 30
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2007-03-10
    Beschreibung: Cellular memory is maintained at homeotic genes by cis-regulatory elements whose mechanism of action is unknown. We have examined chromatin at Drosophila homeotic gene clusters by measuring, at high resolution, levels of histone replacement and nucleosome occupancy. Homeotic gene clusters display conspicuous peaks of histone replacement at boundaries of cis-regulatory domains superimposed over broad regions of low replacement. Peaks of histone replacement closely correspond to nuclease-hypersensitive sites, binding sites for Polycomb and trithorax group proteins, and sites of nucleosome depletion. Our results suggest the existence of a continuous process that disrupts nucleosomes and maintains accessibility of cis-regulatory elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mito, Yoshiko -- Henikoff, Jorja G -- Henikoff, Steven -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Sciences Division, 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/17347439" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Binding Sites ; Cell Line ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Genes, Homeobox ; Genes, Insect ; HSP70 Heat-Shock Proteins/genetics ; Histones/*metabolism ; Multigene Family ; Nuclear Proteins/metabolism ; Nucleosomes/*metabolism ; Oligonucleotide Array Sequence Analysis ; Polycomb Repressive Complex 1 ; Polycomb Repressive Complex 2 ; Protein Binding ; *Regulatory Sequences, Nucleic Acid ; Repressor Proteins/metabolism ; Response Elements ; Transcription Factors/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 31
    Publikationsdatum: 2007-08-11
    Beschreibung: Tricyclic antidepressants exert their pharmacological effect-inhibiting the reuptake of serotonin, norepinephrine, and dopamine-by directly blocking neurotransmitter transporters (SERT, NET, and DAT, respectively) in the presynaptic membrane. The drug-binding site and the mechanism of this inhibition are poorly understood. We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine. Desipramine binds at the inner end of the extracellular cavity of the transporter and is held in place by a hairpin loop and by a salt bridge. This binding site is separated from the leucine-binding site by the extracellular gate of the transporter. By directly locking the gate, desipramine prevents conformational changes and blocks substrate transport. Mutagenesis experiments on human SERT and DAT indicate that both the desipramine-binding site and its inhibition mechanism are probably conserved in the human neurotransmitter transporters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711652/" 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/PMC3711652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Zheng -- Zhen, Juan -- Karpowich, Nathan K -- Goetz, Regina M -- Law, Christopher J -- Reith, Maarten E A -- Wang, Da-Neng -- DA013261/DA/NIDA NIH HHS/ -- DA019676/DA/NIDA NIH HHS/ -- GM075026/GM/NIGMS NIH HHS/ -- GM075936/GM/NIGMS NIH HHS/ -- R01 DA013261/DA/NIDA NIH HHS/ -- R01 DA019676/DA/NIDA NIH HHS/ -- R01 DK053973/DK/NIDDK NIH HHS/ -- R21 DK060841/DK/NIDDK NIH HHS/ -- R21 GM075936/GM/NIGMS NIH HHS/ -- U54 GM075026/GM/NIGMS NIH HHS/ -- U54 GM095315/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1390-3. Epub 2007 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine and Department of Cell Biology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690258" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Antidepressive Agents, Tricyclic/chemistry/*metabolism ; Bacterial Proteins/chemistry/*metabolism ; Binding Sites ; Caenorhabditis elegans Proteins/chemistry/metabolism ; Cell Line ; Conserved Sequence ; Crystallography, X-Ray ; Desipramine/chemistry/*metabolism ; Dopamine/chemistry/metabolism ; Dopamine Uptake Inhibitors/chemistry/metabolism ; Drosophila Proteins/chemistry/metabolism ; Humans ; Leucine/chemistry/metabolism ; Models, Molecular ; Molecular Sequence Data ; Neurotransmitter Uptake Inhibitors/chemistry/*metabolism ; Norepinephrine/chemistry/metabolism ; Norepinephrine Plasma Membrane Transport Proteins/antagonists & ; inhibitors/chemistry/metabolism ; Plasma Membrane Neurotransmitter Transport Proteins/chemistry/*metabolism ; Protein Binding ; Protein Conformation ; Sequence Homology, Amino Acid ; Serotonin/chemistry/metabolism ; Serotonin Uptake Inhibitors/chemistry/metabolism
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  • 32
    Publikationsdatum: 2007-09-01
    Beschreibung: Methylation of histone H3 lysine 27 (H3K27) is a posttranslational modification that is highly correlated with genomic silencing. Here we show that human UTX, a member of the Jumonji C family of proteins, is a di- and trimethyl H3K27 demethylase. UTX occupies the promoters of HOX gene clusters and regulates their transcriptional output by modulating the recruitment of polycomb repressive complex 1 and the monoubiquitination of histone H2A. Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during retinoic acid signaling events, the recruitment of the UTX complex to HOX genes results in H3K27 demethylation and a concomitant methylation of H3K4. Our results suggest a concerted mechanism for transcriptional activation in which cycles of H3K4 methylation by MLL2/3 are linked with the demethylation of H3K27 through UTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Min Gyu -- Villa, Raffaella -- Trojer, Patrick -- Norman, Jessica -- Yan, Kai-Ping -- Reinberg, Danny -- Di Croce, Luciano -- Shiekhattar, Ramin -- R01CA090758/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):447-50. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761849" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Differentiation ; Cell Line ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells ; *Genes, Homeobox ; Histone Demethylases ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Methylation ; Multigene Family ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics/*metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Repressor Proteins/*metabolism ; Signal Transduction ; Transcription, Genetic ; Transcriptional Activation ; Tretinoin/metabolism/pharmacology ; Ubiquitin/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 33
    Publikationsdatum: 2007-01-27
    Beschreibung: Vitamin A has diverse biological functions. It is transported in the blood as a complex with retinol binding protein (RBP), but the molecular mechanism by which vitamin A is absorbed by cells from the vitamin A-RBP complex is not clearly understood. We identified in bovine retinal pigment epithelium cells STRA6, a multitransmembrane domain protein, as a specific membrane receptor for RBP. STRA6 binds to RBP with high affinity and has robust vitamin A uptake activity from the vitamin A-RBP complex. It is widely expressed in embryonic development and in adult organ systems. The RBP receptor represents a major physiological mediator of cellular vitamin A uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaguchi, Riki -- Yu, Jiamei -- Honda, Jane -- Hu, Jane -- Whitelegge, Julian -- Ping, Peipei -- Wiita, Patrick -- Bok, Dean -- Sun, Hui -- 5T32EY07026/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):820-5. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, David Geffen School of Medicine at UCLA, 650 Charles E. Young Drive South, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255476" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Blood-Retinal Barrier ; COS Cells ; Cattle ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Embryonic Development ; Endocytosis ; Humans ; Molecular Sequence Data ; Mutation, Missense ; Pigment Epithelium of Eye/*metabolism ; Placenta/metabolism ; Receptors, Cell Surface/*metabolism ; Retinal Vessels/metabolism ; Retinol-Binding Proteins/*metabolism ; Spleen/metabolism ; Transfection ; Vitamin A/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 34
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2007-03-24
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1646.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379778" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Biomedical Research/*economics ; *Budgets ; Cell Line ; Embryo Research/*economics ; *Embryonic Stem Cells ; Financing, Government ; Humans ; National Institutes of Health (U.S.)/*economics ; Politics ; *Research Support as Topic ; United States
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 35
    Publikationsdatum: 2007-11-17
    Beschreibung: Monoallelic expression with random choice between the maternal and paternal alleles defines an unusual class of genes comprising X-inactivated genes and a few autosomal gene families. Using a genome-wide approach, we assessed allele-specific transcription of about 4000 human genes in clonal cell lines and found that more than 300 were subject to random monoallelic expression. For a majority of monoallelic genes, we also observed some clonal lines displaying biallelic expression. Clonal cell lines reflect an independent choice to express the maternal, the paternal, or both alleles for each of these genes. This can lead to differences in expressed protein sequence and to differences in levels of gene expression. Unexpectedly widespread monoallelic expression suggests a mechanism that generates diversity in individual cells and their clonal descendants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gimelbrant, Alexander -- Hutchinson, John N -- Thompson, Benjamin R -- Chess, Andrew -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1136-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Genetic Research and Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006746" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Alleles ; Animals ; Apoptosis Regulatory Proteins/genetics ; Calcium-Calmodulin-Dependent Protein Kinases/genetics ; Cell Line ; Clone Cells ; DNA-Binding Proteins/genetics ; Death-Associated Protein Kinases ; Dosage Compensation, Genetic ; Female ; *Gene Expression ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genotype ; Humans ; In Situ Hybridization, Fluorescence ; Polymerase Chain Reaction ; Trans-Activators/genetics
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  • 36
    Publikationsdatum: 2007-11-10
    Beschreibung: Production of type I interferon (IFN-I) is a critical host defense triggered by pattern-recognition receptors (PRRs) of the innate immune system. Deubiquitinating enzyme A (DUBA), an ovarian tumor domain-containing deubiquitinating enzyme, was discovered in a small interfering RNA-based screen as a regulator of IFN-I production. Reduction of DUBA augmented the PRR-induced IFN-I response, whereas ectopic expression of DUBA had the converse effect. DUBA bound tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein essential for the IFN-I response. TRAF3 is an E3 ubiquitin ligase that preferentially assembled lysine-63-linked polyubiquitin chains. DUBA selectively cleaved the lysine-63-linked polyubiquitin chains on TRAF3, resulting in its dissociation from the downstream signaling complex containing TANK-binding kinase 1. A discrete ubiquitin interaction motif within DUBA was required for efficient deubiquitination of TRAF3 and optimal suppression of IFN-I. Our data identify DUBA as a negative regulator of innate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Phung, Qui -- Chan, Salina -- Chaudhari, Ruchir -- Quan, Casey -- O'Rourke, Karen M -- Eby, Michael -- Pietras, Eric -- Cheng, Genhong -- Bazan, J Fernando -- Zhang, Zemin -- Arnott, David -- Dixit, Vishva M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1628-32. Epub 2007 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991829" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Line ; Endopeptidases/*metabolism ; Humans ; Interferon Type I/*biosynthesis/genetics ; Interferon-alpha/genetics ; Molecular Sequence Data ; NF-kappa B/metabolism ; Protein Structure, Tertiary ; RNA, Small Interfering ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 3/metabolism ; Ubiquitin/metabolism ; Ubiquitination
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  • 37
    Publikationsdatum: 2007-08-25
    Beschreibung: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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  • 38
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2007-01-06
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapienza, Carmen -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):46-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fels Institute for Cancer Research and Department of Pathology, Temple University Medical School, 3307 North Broad Street, Philadelphia, PA 19140, USA. sapienza@temple.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204629" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Axonemal Dyneins ; Body Patterning ; Cell Line ; Cells, Cultured ; Chromatids/*physiology ; *Chromosome Segregation ; DNA Replication ; Dyneins/*genetics/*physiology ; Ectoderm/*cytology ; Embryonic Stem Cells/*cytology ; Endoderm/*cytology ; Interphase ; Mice ; Mitosis ; Recombination, Genetic ; Spindle Apparatus/physiology/ultrastructure
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 39
    Publikationsdatum: 2007-09-01
    Beschreibung: MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" 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/PMC2782470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongpil -- Inoue, Keiichi -- Ishii, Jennifer -- Vanti, William B -- Voronov, Sergey V -- Murchison, Elizabeth -- Hannon, Gregory -- Abeliovich, Asa -- R01 NS064433/NS/NINDS NIH HHS/ -- R01 NS064433-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Neurology, Center for Neurobiology and Behavior, and Taub Institute, Columbia University, College of Physicians and Surgeons 15-403, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761882" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Dopamine/*metabolism ; Embryonic Stem Cells ; *Feedback, Physiological ; Female ; Gene Expression Regulation ; Homeodomain Proteins/*metabolism ; Humans ; Locomotion ; Male ; Mesencephalon/cytology/*metabolism ; Mice ; MicroRNAs/*metabolism ; Middle Aged ; Models, Biological ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Rats ; Ribonuclease III/genetics/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 40
    Publikationsdatum: 2006-12-16
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 41
    Publikationsdatum: 2007-08-04
    Beschreibung: Toll-like receptors (TLRs) trigger the production of inflammatory cytokines and shape adaptive and innate immunity to pathogens. We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulator of TLR signaling. By blocking ubiquitination of p50, a member of the nuclear factor (NF)-kappaB family, Bcl-3 stabilizes a p50 complex that inhibits gene transcription. As a consequence, Bcl-3-deficient mice and cells were found to be hypersensitive to TLR activation and unable to control responses to lipopolysaccharides. Thus, p50 ubiquitination blockade by Bcl-3 limits the strength of TLR responses and maintains innate immune homeostasis. These findings indicate that the p50 ubiquitination pathway can be selectively targeted to control deleterious inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmody, Ruaidhri J -- Ruan, Qingguo -- Palmer, Scott -- Hilliard, Brendan -- Chen, Youhai H -- AI069289/AI/NIAID NIH HHS/ -- AI50059/AI/NIAID NIH HHS/ -- DK070691/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):675-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673665" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cells, Cultured ; DNA/metabolism ; Female ; Half-Life ; Immune Tolerance ; Immunity, Innate ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages, Peritoneal/*immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; *Signal Transduction ; Toll-Like Receptors/*metabolism ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/genetics/metabolism ; Ubiquitin/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 42
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2007-02-27
    Beschreibung: Differential DNA methylation is important for the epigenetic regulation of gene expression. Allele-specific methylation of the inactive X chromosome has been demonstrated at promoter CpG islands, but the overall pattern of methylation on the active X(Xa) and inactive X (Xi) chromosomes is unknown. We performed allele-specific analysis of more than 1000 informative loci along the human X chromosome. The Xa displays more than two times as much allele-specific methylation as Xi. This methylation is concentrated at gene bodies, affecting multiple neighboring CpGs. Before X inactivation, all of these Xa gene body-methylated sites are biallelically methylated. Thus, a bipartite methylation-demethylation program results in Xa-specific hypomethylation at gene promoters and hypermethylation at gene bodies. These results suggest a relationship between global methylation and expression potentiality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hellman, Asaf -- Chess, Andrew -- New York, N.Y. -- Science. 2007 Feb 23;315(5815):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Genetic Research and Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA. hellman@chgr.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322062" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Cell Line ; Chromosomes, Human, X/*genetics/metabolism ; CpG Islands ; *DNA Methylation ; Embryonic Stem Cells ; Epigenesis, Genetic ; Female ; Gene Expression Regulation ; Gene Silencing ; Heterozygote ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; X Chromosome Inactivation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 43
    Publikationsdatum: 2006-12-23
    Beschreibung: Synonymous single-nucleotide polymorphisms (SNPs) do not produce altered coding sequences, and therefore they are not expected to change the function of the protein in which they occur. We report that a synonymous SNP in the Multidrug Resistance 1 (MDR1) gene, part of a haplotype previously linked to altered function of the MDR1 gene product P-glycoprotein (P-gp), nonetheless results in P-gp with altered drug and inhibitor interactions. Similar mRNA and protein levels, but altered conformations, were found for wild-type and polymorphic P-gp. We hypothesize that the presence of a rare codon, marked by the synonymous polymorphism, affects the timing of cotranslational folding and insertion of P-gp into the membrane, thereby altering the structure of substrate and inhibitor interaction sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimchi-Sarfaty, Chava -- Oh, Jung Mi -- Kim, In-Wha -- Sauna, Zuben E -- Calcagno, Anna Maria -- Ambudkar, Suresh V -- Gottesman, Michael M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):525-8. Epub 2006 Dec 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. kimchi@cber.fda.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185560" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Codon ; Cyclosporine/pharmacology ; *Genes, MDR ; Haplotypes ; HeLa Cells ; Humans ; Mutagenesis, Site-Directed ; P-Glycoprotein/antagonists & inhibitors/*chemistry/genetics/*metabolism ; *Polymorphism, Single Nucleotide ; Protein Biosynthesis ; Protein Conformation ; *Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rhodamine 123/metabolism/pharmacology ; Sirolimus/pharmacology ; Substrate Specificity ; Transfection ; Verapamil/metabolism/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 44
    Publikationsdatum: 2007-12-01
    Beschreibung: AU-rich elements (AREs) and microRNA target sites are conserved sequences in messenger RNA (mRNA) 3' untranslated regions (3'UTRs) that control gene expression posttranscriptionally. Upon cell cycle arrest, the ARE in tumor necrosis factor-alpha (TNFalpha) mRNA is transformed into a translation activation signal, recruiting Argonaute (AGO) and fragile X mental retardation-related protein 1 (FXR1), factors associated with micro-ribonucleoproteins (microRNPs). We show that human microRNA miR369-3 directs association of these proteins with the AREs to activate translation. Furthermore, we document that two well-studied microRNAs-Let-7 and the synthetic microRNA miRcxcr4-likewise induce translation up-regulation of target mRNAs on cell cycle arrest, yet they repress translation in proliferating cells. Thus, activation is a common function of microRNPs on cell cycle arrest. We propose that translation regulation by microRNPs oscillates between repression and activation during the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasudevan, Shobha -- Tong, Yingchun -- Steitz, Joan A -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1931-4. Epub 2007 Nov 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048652" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *3' Untranslated Regions ; Argonaute Proteins ; Base Pairing ; Cell Cycle ; Cell Line ; Cell Proliferation ; Computational Biology ; Eukaryotic Initiation Factor-2/genetics/metabolism ; *Gene Expression Regulation ; HMGA2 Protein/genetics ; HeLa Cells ; Humans ; Interphase ; MicroRNAs/*metabolism ; *Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/metabolism ; Ribonucleoproteins/metabolism ; Transfection ; Tumor Necrosis Factor-alpha/biosynthesis/*genetics ; *Up-Regulation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 45
    Publikationsdatum: 2006-04-29
    Beschreibung: Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells to identify proteins that inhibit store-operated Ca2+ influx. A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulators of Drosophila CRAC currents. We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by gene FLJ14466. Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vig, M -- Peinelt, C -- Beck, A -- Koomoa, D L -- Rabah, D -- Koblan-Huberson, M -- Kraft, S -- Turner, H -- Fleig, A -- Penner, R -- Kinet, J-P -- 5-R37-GM053950/GM/NIGMS NIH HHS/ -- R01-AI050200/AI/NIAID NIH HHS/ -- R01-GM065360/GM/NIGMS NIH HHS/ -- R01-NS040927/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1220-3. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. mvig@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645049" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/*metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Ion Transport ; Jurkat Cells ; Membrane Proteins/genetics/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 46
    Publikationsdatum: 2006-08-12
    Beschreibung: We introduce a method for optically imaging intracellular proteins at nanometer spatial resolution. Numerous sparse subsets of photoactivatable fluorescent protein molecules were activated, localized (to approximately 2 to 25 nanometers), and then bleached. The aggregate position information from all subsets was then assembled into a superresolution image. We used this method--termed photoactivated localization microscopy--to image specific target proteins in thin sections of lysosomes and mitochondria; in fixed whole cells, we imaged vinculin at focal adhesions, actin within a lamellipodium, and the distribution of the retroviral protein Gag at the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Betzig, Eric -- Patterson, George H -- Sougrat, Rachid -- Lindwasser, O Wolf -- Olenych, Scott -- Bonifacino, Juan S -- Davidson, Michael W -- Lippincott-Schwartz, Jennifer -- Hess, Harald F -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1642-5. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, VA 20147, USA. betzige@janelia.hhmi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902090" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/analysis ; Algorithms ; Animals ; COS Cells ; Cell Line ; Cell Membrane/*chemistry ; Cercopithecus aethiops ; Fluorescence ; Focal Adhesions/chemistry ; Gene Products, gag/analysis ; Hiv-1 ; Light ; Luminescent Proteins/*analysis ; Lysosomes/chemistry ; Microscopy/*methods ; Mitochondria/chemistry ; *Nanotechnology ; Organelles/*chemistry ; Photobleaching ; Proteins/*analysis ; Pseudopodia/chemistry ; Recombinant Fusion Proteins/*analysis ; Vinculin/analysis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 47
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-15
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):155-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840666" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastocyst ; Cattle ; Cell Line ; *Cloning, Organism ; Embryo, Mammalian/cytology ; Humans ; Mice ; *Nuclear Transfer Techniques ; *Oocytes ; *Stem Cells ; *Transplantation, Heterologous
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 48
    Publikationsdatum: 2006-10-28
    Beschreibung: The spindle assembly checkpoint guards the fidelity of chromosome segregation. It requires the close cooperation of cell cycle regulatory proteins and cytoskeletal elements to sense spindle integrity. The role of the centrosome, the organizing center of the microtubule cytoskeleton, in the spindle checkpoint is unclear. We found that the molecular requirements for a functional spindle checkpoint included components of the large gamma-tubulin ring complex (gamma-TuRC). However, their localization at the centrosome and centrosome integrity were not essential for this function. Thus, the spindle checkpoint can be activated at the level of microtubule nucleation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Hannah -- Fogeron, Marie-Laure -- Lehmann, Verena -- Lehrach, Hans -- Lange, Bodo M H -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):654-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Vertebrate Genomics, Max-Planck Institute for Molecular Genetics, Ihnestrasse 73, D-14195 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068266" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Cycle Proteins/metabolism ; Cell Line ; Centrosome/physiology ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster ; Homeodomain Proteins/genetics/metabolism ; Humans ; Kinetochores/metabolism ; Microtubule-Associated Proteins/genetics/*metabolism ; Microtubules/ultrastructure ; *Mitosis ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases ; RNA Interference ; Spindle Apparatus/*metabolism/ultrastructure ; Tubulin/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 49
    Publikationsdatum: 2006-09-30
    Beschreibung: To pursue a systematic approach to the discovery of functional connections among diseases, genetic perturbation, and drug action, we have created the first installment of a reference collection of gene-expression profiles from cultured human cells treated with bioactive small molecules, together with pattern-matching software to mine these data. We demonstrate that this "Connectivity Map" resource can be used to find connections among small molecules sharing a mechanism of action, chemicals and physiological processes, and diseases and drugs. These results indicate the feasibility of the approach and suggest the value of a large-scale community Connectivity Map project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamb, Justin -- Crawford, Emily D -- Peck, David -- Modell, Joshua W -- Blat, Irene C -- Wrobel, Matthew J -- Lerner, Jim -- Brunet, Jean-Philippe -- Subramanian, Aravind -- Ross, Kenneth N -- Reich, Michael -- Hieronymus, Haley -- Wei, Guo -- Armstrong, Scott A -- Haggarty, Stephen J -- Clemons, Paul A -- Wei, Ru -- Carr, Steven A -- Lander, Eric S -- Golub, Todd R -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1929-35.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. justin@broad.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008526" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alzheimer Disease/drug therapy/genetics ; Cell Line ; Cell Line, Tumor ; *Databases, Factual ; Dexamethasone/pharmacology/therapeutic use ; Drug Evaluation, Preclinical/*methods ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/pharmacology ; Estrogens/pharmacology ; Gene Expression/*drug effects ; *Gene Expression Profiling ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; Histone Deacetylase Inhibitors ; Humans ; Limonins/pharmacology ; Obesity/genetics/physiopathology ; Oligonucleotide Array Sequence Analysis ; Phenothiazines/pharmacology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/physiopathology ; Sirolimus/pharmacology/therapeutic use ; Software
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  • 50
    Publikationsdatum: 2006-03-25
    Beschreibung: Innate immunity against bacterial and fungal pathogens is mediated by Toll and immune deficiency (Imd) pathways, but little is known about the antiviral response in Drosophila. Here, we demonstrate that an RNA interference pathway protects adult flies from infection by two evolutionarily diverse viruses. Our work also describes a molecular framework for the viral immunity, in which viral double-stranded RNA produced during infection acts as the pathogen trigger whereas Drosophila Dicer-2 and Argonaute-2 act as host sensor and effector, respectively. These findings establish a Drosophila model for studying the innate immunity against viruses in animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1509097/" 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/PMC1509097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiao-Hong -- Aliyari, Roghiyh -- Li, Wan-Xiang -- Li, Hong-Wei -- Kim, Kevin -- Carthew, Richard -- Atkinson, Peter -- Ding, Shou-Wei -- AI052447/AI/NIAID NIH HHS/ -- R01 AI052447/AI/NIAID NIH HHS/ -- R01 GM068743/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program for Microbiology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556799" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Argonaute Proteins ; Cell Line ; Drosophila Proteins/genetics/metabolism/physiology ; Drosophila melanogaster/embryology/genetics/*immunology/*virology ; Embryo, Nonmammalian/immunology/virology ; Escherichia coli/physiology ; *Immunity, Innate ; Insect Viruses/genetics/*physiology ; Micrococcus luteus/physiology ; Mutation ; Nodaviridae/*physiology ; RNA Helicases/genetics/metabolism ; *RNA Interference ; RNA Viruses/genetics/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/metabolism ; RNA, Viral/genetics/metabolism ; RNA-Binding Proteins/genetics/physiology ; RNA-Induced Silencing Complex/genetics/physiology ; Ribonuclease III ; Signal Transduction ; Toll-Like Receptors/physiology ; Transfection ; Virus Replication
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 51
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-08-26
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1031.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931729" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastomeres/*cytology ; Cell Culture Techniques ; Cell Division ; Cell Line ; *Embryo Research ; Embryo, Mammalian/cytology ; Humans ; Mice ; *Stem Cells/cytology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 52
    Publikationsdatum: 2006-04-22
    Beschreibung: G protein betagamma subunits have potential as a target for therapeutic treatment of a number of diseases. We performed virtual docking of a small-molecule library to a site on Gbetagamma subunits that mediates protein interactions. We hypothesized that differential targeting of this surface could allow for selective modulation of Gbetagamma subunit functions. Several compounds bound to Gbetagamma subunits with affinities from 0.1 to 60 muM and selectively modulated functional Gbetagamma-protein-protein interactions in vitro, chemotactic peptide signaling pathways in HL-60 leukocytes, and opioid receptor-dependent analgesia in vivo. These data demonstrate an approach for modulation of G protein-coupled receptor signaling that may represent an important therapeutic strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonacci, Tabetha M -- Mathews, Jennifer L -- Yuan, Chujun -- Lehmann, David M -- Malik, Sundeep -- Wu, Dianqing -- Font, Jose L -- Bidlack, Jean M -- Smrcka, Alan V -- GM60286/GM/NIGMS NIH HHS/ -- HL-T3207949/HL/NHLBI NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- K05-DA00360/DA/NIDA NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM054597-09/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- T32DA07232/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627746" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Analgesics/pharmacology ; Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Computer Simulation ; Cyclohexanes/chemistry/*metabolism/*pharmacology ; Drug Evaluation, Preclinical/*methods ; Enzyme-Linked Immunosorbent Assay ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Protein alpha Subunits/metabolism ; GTP-Binding Protein beta Subunits/chemistry/*metabolism ; GTP-Binding Protein gamma Subunits/chemistry/*metabolism ; HL-60 Cells ; Humans ; Isoenzymes/metabolism ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Structure ; Morphine/pharmacology ; N-Formylmethionine Leucyl-Phenylalanine/metabolism ; Peptide Library ; Peptides/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase C beta ; Protein Binding ; Protein Interaction Mapping ; *Signal Transduction ; Software ; Structure-Activity Relationship ; Type C Phospholipases/metabolism ; Xanthenes/chemistry/*metabolism/*pharmacology ; beta-Adrenergic Receptor Kinases/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 53
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):516-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645063" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Blastocyst ; Cell Line ; *Cloning, Organism ; Embryo Research/economics ; Embryo, Mammalian/cytology ; Female ; Humans ; Nuclear Transfer Techniques ; Oocyte Donation ; Research Support as Topic ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 54
    Publikationsdatum: 2006-07-01
    Beschreibung: Axonal guidance and vascular patterning share several guidance cues, including proteins in the netrin family. We demonstrate that netrins stimulate proliferation, migration, and tube formation of human endothelial cells in vitro and that this stimulation is independent of known netrin receptors. Suppression of netrin1a messenger RNA in zebrafish inhibits vascular sprouting, implying a proangiogenic role for netrins during vertebrate development. We also show that netrins accelerate neovascularization in an in vivo model of ischemia and that they reverse neuropathy and vasculopathy in a diabetic murine model. We propose that the attractive vascular and neural guidance functions of netrins offer a unique therapeutic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577078/" 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/PMC2577078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Brent D -- Ii, Masaaki -- Park, Kye Won -- Suli, Arminda -- Sorensen, Lise K -- Larrieu-Lahargue, Frederic -- Urness, Lisa D -- Suh, Wonhee -- Asai, Jun -- Kock, Gerhardus A H -- Thorne, Tina -- Silver, Marcy -- Thomas, Kirk R -- Chien, Chi-Bin -- Losordo, Douglas W -- Li, Dean Y -- R01 HL068873/HL/NHLBI NIH HHS/ -- R01 HL077671/HL/NHLBI NIH HHS/ -- R01 HL077671-03/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):640-4. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809490" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Angiogenesis Inducing Agents ; Animals ; Cell Line ; Cell Movement ; Chemotaxis ; DNA, Complementary ; Diabetic Angiopathies/therapy ; Diabetic Neuropathies/therapy ; Embryo, Nonmammalian ; Endothelial Cells/*physiology ; Endothelium, Vascular/cytology ; Genetic Therapy ; Humans ; Ischemia/drug therapy ; Mice ; Muscle, Skeletal/blood supply ; *Neovascularization, Physiologic ; Nerve Growth Factors/genetics/pharmacology/*physiology ; Neural Conduction ; Receptors, Cell Surface/physiology ; Tumor Suppressor Proteins/genetics/pharmacology/*physiology ; Vascular Endothelial Growth Factor A/therapeutic use ; Zebrafish
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 55
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krajick, Kevin -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1230-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513956" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Zoo ; Biodiversity ; *Bufonidae/physiology ; Cell Line ; *Conservation of Natural Resources ; Developed Countries ; *Ecosystem ; Environment ; Population Dynamics ; Rivers ; Tanzania ; Water Movements
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 56
    Publikationsdatum: 2006-09-23
    Beschreibung: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 57
    Publikationsdatum: 2006-04-29
    Beschreibung: Wnt proteins function as morphogens that can form long-range concentration gradients to pattern developing tissues. Here, we show that the retromer, a multiprotein complex involved in intracellular protein trafficking, is required for long-range signaling of the Caenorhabditis elegans Wnt ortholog EGL-20. The retromer functions in EGL-20-producing cells to allow the formation of an EGL-20 gradient along the anteroposterior axis. This function is evolutionarily conserved, because Wnt target gene expression is also impaired in the absence of the retromer complex in vertebrates. These results demonstrate that the ability of Wnt to regulate long-range patterning events is dependent on a critical and conserved function of the retromer complex within Wnt-producing cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coudreuse, Damien Y M -- Roel, Giulietta -- Betist, Marco C -- Destree, Olivier -- Korswagen, Hendrik C -- New York, N.Y. -- Science. 2006 May 12;312(5775):921-4. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory and Center for Biomedical Genetics, Uppsalalaan 8, 3584 CT, Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645052" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Body Patterning ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/analysis/genetics/*physiology ; Cell Line ; Gene Expression ; Glycoproteins/analysis/genetics/*physiology ; Humans ; Multiprotein Complexes/*physiology ; Mutation ; Neurons/cytology/physiology ; RNA Interference ; *Signal Transduction ; Transgenes ; Vesicular Transport Proteins/genetics/physiology ; Wnt Proteins/*physiology ; Xenopus
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 58
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-12-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185568" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; *Embryonic Stem Cells ; Humans ; Periodicals as Topic ; Publishing/standards ; *Scientific Misconduct
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 59
    Publikationsdatum: 2006-08-05
    Beschreibung: Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sudha B -- Davis, Alexander S -- Taylor, Gregory A -- Deretic, Vojo -- AI42999/AI/NIAID NIH HHS/ -- AI45148/AI/NIAID NIH HHS/ -- AI57831/AI/NIAID NIH HHS/ -- R01 AI057831/AI/NIAID NIH HHS/ -- T32 AI007538/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1438-41. Epub 2006 Aug 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888103" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Autophagy ; Cell Line ; Cytosol/metabolism ; GTP-Binding Proteins/genetics/*physiology ; HeLa Cells ; Humans ; Interferon-gamma/immunology ; Lysosomes/metabolism/microbiology/ultrastructure ; Macrophages/*immunology/*microbiology ; Mice ; Microbial Viability ; Microtubule-Associated Proteins/metabolism ; Mycobacterium bovis/*immunology/physiology ; Phagosomes/metabolism/microbiology/*ultrastructure ; RNA, Small Interfering ; Transfection ; Vacuoles/metabolism/ultrastructure
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 60
    Publikationsdatum: 2006-05-27
    Beschreibung: Yersinia species use a variety of type III effector proteins to target eukaryotic signaling systems. The effector YopJ inhibits mitogen-activated protein kinase (MAPK) and the nuclear factor kappaB (NFkappaB) signaling pathways used in innate immune response by preventing activation of the family of MAPK kinases (MAPKK). We show that YopJ acted as an acetyltransferase, using acetyl-coenzyme A (CoA) to modify the critical serine and threonine residues in the activation loop of MAPKK6 and thereby blocking phosphorylation. The acetylation on MAPKK6 directly competed with phosphorylation, preventing activation of the modified protein. This covalent modification may be used as a general regulatory mechanism in biological signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukherjee, Sohini -- Keitany, Gladys -- Li, Yan -- Wang, Yong -- Ball, Haydn L -- Goldsmith, Elizabeth J -- Orth, Kim -- R01-AI056404/AI/NIAID NIH HHS/ -- R21-DK072134/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1211-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728640" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetyl Coenzyme A/metabolism ; Acetylation ; Acetyltransferases/metabolism ; Bacterial Proteins/*metabolism ; Catalytic Domain ; Cell Line ; Cell-Free System ; Electrophoresis, Polyacrylamide Gel ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase 6/chemistry/*metabolism ; MAP Kinase Signaling System ; NF-kappa B/metabolism ; Phosphorylation ; Recombinant Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Yersinia/*metabolism/pathogenicity
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 61
    Publikationsdatum: 2006-05-27
    Beschreibung: Genetic mutations that disrupt osteoblast function can result in skeletal dysmorphogenesis or, more rarely, in increased postnatal bone formation. Here we show that Schnurri-3 (Shn3), a mammalian homolog of the Drosophila zinc finger adapter protein Shn, is an essential regulator of adult bone formation. Mice lacking Shn3 display adult-onset osteosclerosis with increased bone mass due to augmented osteoblast activity. Shn3 was found to control protein levels of Runx2, the principal transcriptional regulator of osteoblast differentiation, by promoting its degradation through recruitment of the E3 ubiquitin ligase WWP1 to Runx2. By this means, Runx2-mediated extracellular matrix mineralization was antagonized, revealing an essential role for Shn3 as a central regulator of postnatal bone mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Dallas C -- Wein, Marc N -- Oukka, Mohamed -- Hofstaetter, Jochen G -- Glimcher, Melvin J -- Glimcher, Laurie H -- AI29673/AI/NIAID NIH HHS/ -- AR46983/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1223-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728642" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Binding Sites ; *Bone Density ; Bone and Bones/*anatomy & histology/chemistry/physiology ; Cell Line ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit/genetics/metabolism ; DNA-Binding Proteins/analysis/genetics/*metabolism ; Gene Expression Regulation ; Immunoprecipitation ; Mice ; Osteoblasts/chemistry/physiology ; Osteoclasts/physiology ; Osteogenesis ; Protein Binding ; Protein Structure, Tertiary ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Transcriptional Activation ; Transfection ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Zinc Fingers
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 62
    Publikationsdatum: 2006-06-24
    Beschreibung: During fasting, increased concentrations of circulating catecholamines promote the mobilization of lipid stores from adipose tissue in part by phosphorylating and inactivating acetyl-coenzyme A carboxylase (ACC), the rate-limiting enzyme in fatty acid synthesis. Here, we describe a parallel pathway, in which the pseudokinase Tribbles 3 (TRB3), whose abundance is increased during fasting, stimulates lipolysis by triggering the degradation of ACC in adipose tissue. TRB3 promoted ACC ubiquitination through an association with the E3 ubiquitin ligase constitutive photomorphogenic protein 1 (COP1). Indeed, adipocytes deficient in TRB3 accumulated larger amounts of ACC protein than did wild-type cells. Because transgenic mice expressing TRB3 in adipose tissue are protected from diet-induced obesity due to enhanced fatty acid oxidation, these results demonstrate how phosphorylation and ubiquitination pathways converge on a key regulator of lipid metabolism to maintain energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qi, Ling -- Heredia, Jose E -- Altarejos, Judith Y -- Screaton, Robert -- Goebel, Naomi -- Niessen, Sherry -- Macleod, Ian X -- Liew, Chong Wee -- Kulkarni, Rohit N -- Bain, James -- Newgard, Christopher -- Nelson, Michael -- Evans, Ronald M -- Yates, John -- Montminy, Marc -- DK064142/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories and Gene Expression Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794074" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3-L1 Cells ; Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/cytology/*metabolism ; Adipose Tissue, Brown/cytology/metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Cell Line ; Dietary Fats/administration & dosage ; Energy Metabolism ; Fasting ; Fatty Acids/metabolism ; Gene Expression ; Humans ; *Lipid Metabolism ; Lipolysis ; Mice ; Mice, Transgenic ; Nuclear Proteins/*metabolism ; Obesity/prevention & control ; Oxidation-Reduction ; Phosphorylation ; Thinness ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism ; Weight Gain
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 63
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-04
    Beschreibung: The restoration of catalytic activity to mutant enzymes by small molecules is well established for in vitro systems. Here, we show that the protein tyrosine kinase Src arginine-388--〉alanine (R388A) mutant can be rescued in live cells with the use of the small molecule imidazole. Cellular rescue of a viral Src homolog was rapid and reversible and conferred predicted oncogenic properties. Using chemical rescue in combination with mass spectrometry, we confirmed six known Src kinase substrates and identified several new protein targets. Chemical rescue data suggest that cellular Src is active under basal conditions. Rescue of R388A cellular Src provided insights into the mitogen-activated protein kinase pathway. This chemical rescue approach will likely have many applications in cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Yingfeng -- Molina, Henrik -- Pandey, Akhilesh -- Zhang, Jin -- Cole, Philip A -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1293-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, 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/16513984" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Fluorescence Resonance Energy Transfer ; Gene Expression Profiling ; Gene Expression Regulation ; Growth Substances/metabolism/pharmacology ; Humans ; Imidazoles/*metabolism/pharmacology ; Kinetics ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Phosphorylation ; Phosphotyrosine/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins pp60(c-src)/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Transfection ; src Homology Domains
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 64
    Publikationsdatum: 2006-10-14
    Beschreibung: Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pichlmair, Andreas -- Schulz, Oliver -- Tan, Choon Ping -- Naslund, Tanja I -- Liljestrom, Peter -- Weber, Friedemann -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):997-1001. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038589" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cells, Cultured ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/genetics/*metabolism ; Dendritic Cells/virology ; Encephalomyocarditis virus/genetics/immunology/metabolism ; Genome, Viral ; Humans ; *Immunity, Innate ; Influenza A virus/*genetics/*immunology/metabolism/physiology ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Mice ; Mice, Inbred C57BL ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/metabolism ; RNA, Viral/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Vesicular stomatitis Indiana virus/genetics/immunology/metabolism ; Viral Nonstructural Proteins/genetics/metabolism ; Virus Replication
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 65
    Publikationsdatum: 2006-01-18
    Beschreibung: In contrast to current models, fluorescence resonance energy transfer measurements using a single-cell imaging assay with fluorescent forms of PER and TIM showed that these proteins bind rapidly and persist in the cytoplasm while gradually accumulating in discrete foci. After approximately 6 hours, complexes abruptly dissociated, as PER and TIM independently moved to the nucleus in a narrow time frame. The per(L) mutation delayed nuclear accumulation in vivo and in our cultured cell system, but without affecting rates of PER/TIM assembly or dissociation. This finding points to a previously unrecognized form of temporal regulation that underlies the periodicity of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Pablo -- Saez, Lino -- Young, Michael W -- GM54339/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 13;311(5758):226-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410523" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Cytoplasm/metabolism ; Drosophila Proteins/*metabolism ; Drosophila melanogaster ; Fluorescence Resonance Energy Transfer ; Models, Biological ; Nuclear Proteins/*metabolism ; Period Circadian Proteins ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Time Factors
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 66
    Publikationsdatum: 2006-04-01
    Beschreibung: Kaposi's sarcoma-associated herpesvirus (KSHV, human herpesvirus 8) is the causative agent of Kaposi's sarcoma and other lymphoproliferative syndromes often associated with HIV/AIDS. Functional complementary DNA selection for a receptor mediating KSHV cell fusion identified xCT, the 12-transmembrane light chain of the human cystine/glutamate exchange transporter system x-c. Expression of recombinant xCT rendered otherwise not susceptible target cells permissive for both KSHV cell fusion and virion entry. Antibodies against xCT blocked KSHV fusion and entry with naturally permissive target cells. KSHV target cell permissiveness correlated closely with endogenous expression of xCT messenger RNA and protein in diverse human and nonhuman cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaleeba, Johnan A R -- Berger, Edward A -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), 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/16574866" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Transport System y+/genetics/immunology/*metabolism ; Animals ; Cell Fusion ; Cell Line ; Cell Line, Tumor ; DNA, Complementary ; Herpesvirus 8, Human/*metabolism ; Humans ; Immune Sera ; Mice ; RNA, Messenger/analysis/genetics ; Receptors, Virus/genetics/immunology/*metabolism ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 67
    Publikationsdatum: 2006-10-21
    Beschreibung: Diverse bacterial and viral pathogens induce actin polymerization in the cytoplasm of host cells to facilitate infection. Here, we describe a pathogenic mechanism for promoting dynamic actin assembly in the nucleus to enable viral replication. The baculovirus Autographa californica multiple nucleopolyhedrovirus induced nuclear actin polymerization by translocating the host actin-nucleating Arp2/3 complex into the nucleus, where it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein. Nuclear actin assembly by p78/83 and Arp2/3 complex was essential for viral progeny production. Recompartmentalizing dynamic host actin may represent a conserved mode of pathogenesis and reflect viral manipulation of normal functions of nuclear actin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goley, Erin D -- Ohkawa, Taro -- Mancuso, Joel -- Woodruff, Jeffrey B -- D'Alessio, Joseph A -- Cande, W Zacheus -- Volkman, Loy E -- Welch, Matthew D -- AI054693/AI/NIAID NIH HHS/ -- GM59609/GM/NIGMS NIH HHS/ -- R01 GM059609/GM/NIGMS NIH HHS/ -- R01 GM059609-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053146" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actin-Related Protein 2-3 Complex/*metabolism ; Actins/*metabolism ; Animals ; Biopolymers/metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Fluorescence Recovery After Photobleaching ; Moths ; Mutation ; Nucleocapsid/metabolism/ultrastructure ; Nucleopolyhedrovirus/genetics/*physiology ; Transfection ; Viral Proteins/chemistry/genetics/isolation & purification/*metabolism ; Virion/ultrastructure ; Virus Replication ; Wiskott-Aldrich Syndrome Protein/chemistry
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 68
    Publikationsdatum: 2006-01-21
    Beschreibung: The stable propagation of genetic material during cell division depends on the congression of chromosomes to the spindle equator before the cell initiates anaphase. It is generally assumed that congression requires that chromosomes are connected to the opposite poles of the bipolar spindle ("bioriented"). In mammalian cells, we found that chromosomes can congress before becoming bioriented. By combining the use of reversible chemical inhibitors, live-cell light microscopy, and correlative electron microscopy, we found that monooriented chromosomes could glide toward the spindle equator alongside kinetochore fibers attached to other already bioriented chromosomes. This congression mechanism depended on the kinetochore-associated, plus end-directed microtubule motor CENP-E (kinesin-7).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768465/" 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/PMC4768465/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapoor, Tarun M -- Lampson, Michael A -- Hergert, Polla -- Cameron, Lisa -- Cimini, Daniela -- Salmon, E D -- McEwen, Bruce F -- Khodjakov, Alexey -- GM06627/GM/NIGMS NIH HHS/ -- GM24364/GM/NIGMS NIH HHS/ -- GM59363/GM/NIGMS NIH HHS/ -- GM65933/GM/NIGMS NIH HHS/ -- R01 GM024364/GM/NIGMS NIH HHS/ -- R01 GM059363/GM/NIGMS NIH HHS/ -- R37 GM024364/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 20;311(5759):388-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemistry and Cell Biology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424343" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aurora Kinases ; Cell Line ; Chromosomal Proteins, Non-Histone/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; HeLa Cells ; Humans ; Indoles/pharmacology ; Kinesin/antagonists & inhibitors ; Kinetochores/*physiology/ultrastructure ; Metaphase ; Microscopy, Confocal ; Microscopy, Electron ; Microscopy, Interference ; Microscopy, Video ; Microtubules/*physiology/ultrastructure ; *Mitosis ; Molecular Motor Proteins/physiology ; Movement ; Potoroidae ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Pyrimidines/pharmacology ; RNA Interference ; RNA, Small Interfering ; Spindle Apparatus/*physiology/ultrastructure ; Sulfonamides/pharmacology ; Thiones/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 69
    Publikationsdatum: 2006-10-14
    Beschreibung: The treelike structures of many organs, including the mammary gland, are generated by branching morphogenesis, a reiterative process of branch initiation and invasion from a preexisting epithelium. Using a micropatterning approach to control the initial three-dimensional structure of mouse mammary epithelial tubules in culture, combined with an algorithm to quantify the extent of branching, we found that the geometry of tubules dictates the position of branches. We predicted numerically and confirm experimentally that branches initiate at sites with a local minimum in the concentration of autocrine inhibitory morphogens, such as transforming growth factor-beta. These results reveal that tissue geometry can control organ morphogenesis by defining the local cellular microenvironment, a finding that has relevance to control of invasion and metastasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933179/" 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/PMC2933179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Celeste M -- Vanduijn, Martijn M -- Inman, Jamie L -- Fletcher, Daniel A -- Bissell, Mina J -- CA57621/CA/NCI NIH HHS/ -- CA64786/CA/NCI NIH HHS/ -- GM72736/GM/NIGMS NIH HHS/ -- R01 CA057621/CA/NCI NIH HHS/ -- R01 CA057621-10/CA/NCI NIH HHS/ -- R01 CA064786/CA/NCI NIH HHS/ -- R01 CA064786-10/CA/NCI NIH HHS/ -- R01 GM072736/GM/NIGMS NIH HHS/ -- R01 GM072736-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038622" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Animals ; Cell Line ; Diffusion ; Epidermal Growth Factor/pharmacology ; Epithelial Cells/*cytology/metabolism ; Epithelium/growth & development ; Female ; Hepatocyte Growth Factor/pharmacology ; Mammary Glands, Animal/cytology/*growth & development ; Mice ; *Morphogenesis ; Organ Culture Techniques ; Organoids/cytology/*growth & development ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Receptors, Transforming Growth Factor beta/metabolism ; Tissue Engineering ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1
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    Standort Signatur Erwartet Verfügbarkeit
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  • 70
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-22
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Stem Cell Forum Ethics Working Party -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):366-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627723" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Bioethical Issues ; Cell Line ; Cloning, Organism/ethics/legislation & jurisprudence ; Embryo Research/*ethics/legislation & jurisprudence ; Guidelines as Topic ; Humans ; *Internationality ; Research Embryo Creation/ethics/legislation & jurisprudence ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 71
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-11
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ron, David -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):52-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. ron@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825557" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cytosol/metabolism ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/genetics/metabolism ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/chemistry/genetics/*metabolism ; Evolution, Molecular ; Gene Expression Regulation ; Membrane Proteins/chemistry/genetics/*metabolism ; Models, Biological ; Protein Biosynthesis ; *Protein Folding ; Protein Sorting Signals/physiology ; Protein Structure, Tertiary ; *RNA Stability ; RNA, Messenger/genetics/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 72
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-01-21
    Beschreibung: Mammalian X inactivation turns off one female X chromosome to enact dosage compensation between XX and XY individuals. X inactivation is known to be regulated in cis by Xite, Tsix, and Xist, but in principle the two Xs must also be regulated in trans to ensure mutually exclusive silencing. Here, we demonstrate that interchromosomal pairing mediates this communication. Pairing occurs transiently at the onset of X inactivation and is specific to the X-inactivation center. Deleting Xite and Tsix perturbs pairing and counting/choice, whereas their autosomal insertion induces de novo X-autosome pairing. Ectopic X-autosome interactions inhibit endogenous X-X pairing and block the initiation of X-chromosome inactivation. Thus, Tsix and Xite function both in cis and in trans. We propose that Tsix and Xite regulate counting and mutually exclusive choice through X-X pairing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Na -- Tsai, Chia-Lun -- Lee, Jeannie T -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1149-52. Epub 2006 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424298" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Line ; *Chromosome Pairing ; Female ; In Situ Hybridization, Fluorescence ; Male ; Mice ; Mice, Transgenic ; Models, Genetic ; Mutation ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Regulatory Elements, Transcriptional ; Stem Cells ; Transgenes ; X Chromosome/genetics/*physiology ; *X Chromosome Inactivation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 73
    Publikationsdatum: 2006-10-07
    Beschreibung: TFII-I is a transcription factor and a target of phosphorylation by Bruton's tyrosine kinase. In humans, deletions spanning the TFII-I locus are associated with a cognitive defect, the Williams-Beuren cognitive profile. We report an unanticipated role of TFII-I outside the nucleus as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation of TRPC3 (transient receptor potential C3) channels. Inhibition of ACE by TFII-I requires phosphotyrosine residues that engage the SH2 (Src-homology 2) domains of phospholipase C-g (PLC-g) and an interrupted, pleckstrin homology (PH)-like domain that binds the split PH domain of PLC-g. Our observations suggest a model in which TFII-I suppresses ACE by competing with TRPC3 for binding to PLC-g.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caraveo, Gabriela -- van Rossum, Damian B -- Patterson, Randen L -- Snyder, Solomon H -- Desiderio, Stephen -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Institute for Cell Engineering, 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/17023658" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Bradykinin/pharmacology ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Humans ; Models, Biological ; Molecular Sequence Data ; PC12 Cells ; Phospholipase C gamma/chemistry/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Rats ; TRPC Cation Channels/*metabolism ; Transcription Factors, TFII/chemistry/*metabolism ; Uridine Triphosphate/pharmacology ; src Homology Domains
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 74
    Publikationsdatum: 2006-03-18
    Beschreibung: The parietal-eye photoreceptor is unique because it has two antagonistic light signaling pathways in the same cell-a hyperpolarizing pathway maximally sensitive to blue light and a depolarizing pathway maximally sensitive to green light. Here, we report the molecular components of these two pathways. We found two opsins in the same cell: the blue-sensitive pinopsin and a previously unidentified green-sensitive opsin, which we name parietopsin. Signaling components included gustducin-alpha and Galphao, but not rod or cone transducin-alpha. Single-cell recordings demonstrated that Go mediates the depolarizing response. Gustducin-alpha resembles transducin-alpha functionally and likely mediates the hyperpolarizing response. The parietopsin-Go signaling pair provides clues about how rod and cone phototransduction might have evolved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Chih-Ying -- Luo, Dong-Gen -- Terakita, Akihisa -- Shichida, Yoshinori -- Liao, Hsi-Wen -- Kazmi, Manija A -- Sakmar, Thomas P -- Yau, King-Wai -- EY06837/EY/NEI NIH HHS/ -- R01 DC006904/DC/NIDCD NIH HHS/ -- R01 DC006904-01/DC/NIDCD NIH HHS/ -- R01 DC006904-02/DC/NIDCD NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R01 EY006837-16A1/EY/NEI NIH HHS/ -- R01 EY006837-17/EY/NEI NIH HHS/ -- R01 EY006837-18/EY/NEI NIH HHS/ -- R01 EY006837-19/EY/NEI NIH HHS/ -- R01 EY014596/EY/NEI NIH HHS/ -- R01 EY014596-01/EY/NEI NIH HHS/ -- R01 EY014596-02/EY/NEI NIH HHS/ -- R01 EY014596-03/EY/NEI NIH HHS/ -- R01 EY014596-04/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- R37 EY006837-15S1/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1617-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. chih-ying.su@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543463" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3',5'-Cyclic-GMP Phosphodiesterases/metabolism ; Amino Acid Sequence ; Animals ; *Biological Evolution ; Cell Line ; Cyclic GMP/metabolism ; GTP-Binding Protein alpha Subunits/genetics/physiology ; Humans ; Lizards/genetics/*physiology ; Molecular Sequence Data ; *Ocular Physiological Phenomena ; Patch-Clamp Techniques ; Photoreceptor Cells, Vertebrate/chemistry/*physiology ; Rod Opsins/analysis/genetics/*physiology ; Transducin/genetics/physiology ; *Vision, Ocular
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 75
    Publikationsdatum: 2006-02-18
    Beschreibung: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism
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  • 76
    Publikationsdatum: 2006-05-13
    Beschreibung: The DKC1 gene encodes a pseudouridine synthase that modifies ribosomal RNA (rRNA). DKC1 is mutated in people with X-linked dyskeratosis congenita (X-DC), a disease characterized by bone marrow failure, skin abnormalities, and increased susceptibility to cancer. How alterations in ribosome modification might lead to cancer and other features of the disease remains unknown. Using an unbiased proteomics strategy, we discovered a specific defect in IRES (internal ribosome entry site)-dependent translation in Dkc1(m) mice and in cells from X-DC patients. This defect results in impaired translation of messenger RNAs containing IRES elements, including those encoding the tumor suppressor p27(Kip1) and the antiapoptotic factors Bcl-xL and XIAP (X-linked Inhibitor of Apoptosis Protein). Moreover, Dkc1(m) ribosomes were unable to direct translation from IRES elements present in viral messenger RNAs. These findings reveal a potential mechanism by which defective ribosome activity leads to disease and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, Andrew -- Peng, Guang -- Brandenburger, Yves -- Zollo, Ornella -- Xu, Wei -- Rego, Eduardo -- Ruggero, Davide -- New York, N.Y. -- Science. 2006 May 12;312(5775):902-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690864" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *5' Untranslated Regions ; Animals ; Cell Cycle Proteins/chemistry/*genetics/physiology ; Cell Line ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p27/biosynthesis/genetics ; Dyskeratosis Congenita/*genetics ; Humans ; Insect Viruses/genetics ; Lymphocytes/metabolism ; Male ; Mice ; Nuclear Proteins/chemistry/*genetics/physiology ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Polyribosomes/metabolism ; *Protein Biosynthesis ; Proteomics ; Pseudouridine/metabolism ; RNA Viruses/genetics ; RNA, Messenger/*genetics/metabolism ; RNA, Ribosomal/metabolism ; Transfection ; X-Linked Inhibitor of Apoptosis Protein/biosynthesis/genetics ; bcl-X Protein/biosynthesis/genetics
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  • 77
    Publikationsdatum: 2006-09-23
    Beschreibung: To resolve the controversy about messengers regulating KCNQ ion channels during phospholipase C-mediated suppression of current, we designed translocatable enzymes that quickly alter the phosphoinositide composition of the plasma membrane after application of a chemical cue. The KCNQ current falls rapidly to zero when phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2 or PI(4,5)P2] is depleted without changing Ca2+, diacylglycerol, or inositol 1,4,5-trisphosphate. Current rises by 30% when PI(4,5)P2 is overproduced and does not change when phosphatidylinositol 3,4,5-trisphosphate is raised. Hence, the depletion of PI(4,5)P2 suffices to suppress current fully, and other second messengers are not needed. Our approach is ideally suited to study biological signaling networks involving membrane phosphoinositides.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579521/" 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/PMC3579521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Byung-Chang -- Inoue, Takanari -- Meyer, Tobias -- Hille, Bertil -- AR17803/AR/NIAMS NIH HHS/ -- GM63702/GM/NIGMS NIH HHS/ -- MH64801/MH/NIMH NIH HHS/ -- NS08174/NS/NINDS NIH HHS/ -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM030179-24A1/GM/NIGMS NIH HHS/ -- R01 GM030179-25/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- R01 MH064801/MH/NIMH NIH HHS/ -- R01 NS008174/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1454-7. Epub 2006 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990515" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Diglycerides/metabolism ; Dimerization ; Humans ; *Ion Channel Gating ; KCNQ Potassium Channels/*metabolism ; KCNQ2 Potassium Channel/metabolism ; KCNQ3 Potassium Channel/metabolism ; Mice ; NIH 3T3 Cells ; Oxotremorine/analogs & derivatives/pharmacology ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Sirolimus/analogs & derivatives/pharmacology
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  • 78
    Publikationsdatum: 2006-09-09
    Beschreibung: Yeast is a widely used recombinant protein expression system. We expanded its utility by engineering the yeast Pichia pastoris to secrete human glycoproteins with fully complex terminally sialylated N-glycans. After the knockout of four genes to eliminate yeast-specific glycosylation, we introduced 14 heterologous genes, allowing us to replicate the sequential steps of human glycosylation. The reported cell lines produce complex glycoproteins with greater than 90% terminal sialylation. Finally, to demonstrate the utility of these yeast strains, functional recombinant erythropoietin was produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, Stephen R -- Davidson, Robert C -- Sethuraman, Natarajan -- Nett, Juergen H -- Jiang, Youwei -- Rios, Sandra -- Bobrowicz, Piotr -- Stadheim, Terrance A -- Li, Huijuan -- Choi, Byung-Kwon -- Hopkins, Daniel -- Wischnewski, Harry -- Roser, Jessica -- Mitchell, Teresa -- Strawbridge, Rendall R -- Hoopes, Jack -- Wildt, Stefan -- Gerngross, Tillman U -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1441-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GlycoFi Inc., 21 Lafayette Street, Suite 200, Lebanon, NH 03766, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16960007" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cloning, Molecular ; Cytidine Monophosphate N-Acetylneuraminic Acid/metabolism ; Erythropoietin/chemistry/genetics/*metabolism ; Genetic Vectors ; Glycosylation ; Humans ; Pichia/*genetics/metabolism ; *Protein Engineering ; Rats ; Recombinant Proteins/biosynthesis/chemistry ; Sialic Acids/metabolism ; Sialoglycoproteins/*biosynthesis/chemistry/genetics ; Transformation, Genetic
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  • 79
    Publikationsdatum: 2006-03-18
    Beschreibung: How the widely used botulinum neurotoxin A (BoNT/A) recognizes and enters neurons is poorly understood. We found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C). Fragments of SV2 that harbor the toxin interaction domain inhibited BoNT/A from binding to neurons. BoNT/A binding to SV2A and SV2B knockout hippocampal neurons was abolished and was restored by expressing SV2A, SV2B, or SV2C. Reduction of SV2 expression in PC12 and Neuro-2a cells also inhibited entry of BoNT/A, which could be restored by expressing SV2 isoforms. Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, Min -- Yeh, Felix -- Tepp, William H -- Dean, Camin -- Johnson, Eric A -- Janz, Roger -- Chapman, Edwin R -- R01 EY016452/EY/NEI NIH HHS/ -- R01 EY016452-03/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):592-6. Epub 2006 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543415" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Botulinum Toxins, Type A/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endocytosis ; Hippocampus/cytology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neuromuscular Junction/metabolism ; Neurons/*metabolism ; PC12 Cells ; Protein Binding ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; R-SNARE Proteins/metabolism ; Rats ; Synaptic Vesicles/*metabolism ; Synaptotagmins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 80
    Publikationsdatum: 2006-09-23
    Beschreibung: The posttranslational modification sumoylation can have multiple effects on its substrate proteins. We studied a patient with isolated cleft lip and palate and a balanced chromosomal translocation that disrupts the SUMO1 (small ubiquitin-related modifier) gene, resulting in haploinsufficiency. In mouse, we found that Sumo1 is expressed in the developing lip and palate and that a Sumo1 hypomorphic allele manifests an incompletely penetrant orofacial clefting phenotype. Products of several genes implicated in clefting are sumoylated, and the Sumo1 hypomorphic allele interacts genetically with a loss-of-function allele for one of these loci. Thus, sumoylation defines a network of genes important for palatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alkuraya, Fowzan S -- Saadi, Irfan -- Lund, Jennifer J -- Turbe-Doan, Annick -- Morton, Cynthia C -- Maas, Richard L -- DE015246/DE/NIDCR NIH HHS/ -- DE11697/DE/NIDCR NIH HHS/ -- GM061365/GM/NIGMS NIH HHS/ -- HD043430/HD/NICHD NIH HHS/ -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1751.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, NRB-458, 77 Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990542" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Animals ; Cell Line ; Child, Preschool ; Cleft Lip/*genetics ; Cleft Palate/*genetics ; Embryo, Mammalian/cytology/metabolism ; Gene Dosage ; Gene Expression Regulation, Developmental ; Humans ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Karyotyping ; Mice ; Mice, Inbred C57BL ; Morphogenesis ; Nuclear Proteins/genetics/metabolism ; Palate/embryology/metabolism ; Protein Tyrosine Phosphatases/genetics/metabolism ; SUMO-1 Protein/*genetics/physiology ; Small Ubiquitin-Related Modifier Proteins/*genetics/physiology ; Stem Cells/metabolism ; Translocation, Genetic
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  • 81
    Publikationsdatum: 2006-12-16
    Beschreibung: Although type 2 immune responses contribute to allergy and asthma, these responses are essential for clearing intestinal helminth infestations by mechanisms that include increased epithelial shedding. We show that T helper 2 cells (T(H)2), but not other T cell subsets, express amphiregulin, a member of the epidermal growth factor (EGF) family. EGF receptor ligands directly induce epithelial cell proliferation, and lack of amphiregulin delayed expulsion of the nematode Trichuris muris. This newly recognized link between T(H)2 cells and epithelial proliferation should help in planning therapeutic interventions for helminth infections and other diseases that involve both cell proliferation and allergy, such as asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaiss, Dietmar M -- Yang, Li -- Shah, Pranav R -- Kobie, James J -- Urban, Joseph F -- Mosmann, Tim R -- AI48604/AI/NIAID NIH HHS/ -- DFG/ZA280/PHS HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1746.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Smith Center for Vaccine Biology and Immunology and Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170297" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amphiregulin ; Animals ; Bone Marrow Cells/immunology/metabolism ; Cecum/pathology ; Cell Line ; Cell Proliferation ; Cytokines/biosynthesis/immunology ; EGF Family of Proteins ; Gene Expression Regulation ; Glycoproteins/biosynthesis/genetics/*physiology ; Immunity, Innate ; Intercellular Signaling Peptides and Proteins/biosynthesis/genetics/*physiology ; Intestinal Mucosa/pathology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Polymerase Chain Reaction ; Th2 Cells/*immunology/metabolism ; Trichuriasis/*immunology/parasitology/pathology ; Trichuris/immunology/physiology
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  • 82
    Publikationsdatum: 2006-06-24
    Beschreibung: The formation of the neuromuscular synapse requires muscle-specific receptor kinase (MuSK) to orchestrate postsynaptic differentiation, including the clustering of receptors for the neurotransmitter acetylcholine. Upon innervation, neural agrin activates MuSK to establish the postsynaptic apparatus, although agrin-independent formation of neuromuscular synapses can also occur experimentally in the absence of neurotransmission. Dok-7, a MuSK-interacting cytoplasmic protein, is essential for MuSK activation in cultured myotubes; in particular, the Dok-7 phosphotyrosine-binding domain and its target in MuSK are indispensable. Mice lacking Dok-7 formed neither acetylcholine receptor clusters nor neuromuscular synapses. Thus, Dok-7 is essential for neuromuscular synaptogenesis through its interaction with MuSK.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Kumiko -- Inoue, Akane -- Okada, Momoko -- Murata, Yoji -- Kakuta, Shigeru -- Jigami, Takafumi -- Kubo, Sachiko -- Shiraishi, Hirokazu -- Eguchi, Katsumi -- Motomura, Masakatsu -- Akiyama, Tetsu -- Iwakura, Yoichiro -- Higuchi, Osamu -- Yamanashi, Yuji -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794080" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Agrin/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Differentiation ; Cell Line ; Down-Regulation ; Enzyme Activation ; Humans ; In Situ Hybridization ; Mice ; Molecular Sequence Data ; Motor Endplate/embryology/metabolism ; Muscle Denervation ; Muscle Fibers, Skeletal/cytology/metabolism ; Muscle Proteins/chemistry/genetics/*metabolism ; Muscle, Skeletal/embryology/*innervation/metabolism ; Mutation ; Neuromuscular Junction/*physiology ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Receptor Aggregation ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Cholinergic/genetics/*metabolism ; Synapses/*physiology ; Synaptic Transmission
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  • 83
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-25
    Beschreibung: Voltage-gated proton channels have been widely observed but have not been identified at a molecular level. Here we report that a four-transmembrane protein similar to the voltage-sensor domain of voltage-gated ion channels is a voltage-gated proton channel. Cells overexpressing this protein showed depolarization-induced outward currents accompanied by tail currents. Current reversal occured at equilibrium potentials for protons. The currents exhibited pH-dependent gating and zinc ion sensitivity, two features which are characteristic of voltage-gated proton channels. Responses of voltage dependence to sequence changes suggest that mouse voltage-sensor domain-only protein is itself a channel, rather than a regulator of another channel protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Mari -- Takagi, Masahiro -- Okamura, Yasushi -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):589-92. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Developmental Neurophysiology, Okazaki Institute for Integrative Bioscience, Higashiyama 5-1, Myodaiji-cho, Okazaki, Aichi 444-8787, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556803" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Ciona intestinalis ; Electric Conductivity ; Humans ; Hydrogen-Ion Concentration ; *Ion Channel Gating ; Ion Channels/*chemistry/genetics/*physiology ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Mutation ; Patch-Clamp Techniques ; Protein Structure, Tertiary ; *Protons ; Transfection
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  • 84
    Publikationsdatum: 2006-10-07
    Beschreibung: Because HIV-1 does not infect most nonhuman primates, animal modeling of human HIV infection and AIDS has primarily consisted of experimentally infecting macaques with related simian immunodeficiency viruses (SIVMAC). However, the usefulness of such models is limited by the substantial divergence between SIVMAC and HIV-1. We derived an HIV-1-based virus that includes only small portions of SIVMAC yet replicates robustly in both transformed and primary rhesus macaque T cells. Derivation of simian-tropic HIV-1 (stHIV-1) has important implications for understanding primate lentivirus zoonosis and should allow the development of improved animal models for studies of AIDS and the evaluation of vaccines and treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatziioannou, Theodora -- Princiotta, Michael -- Piatak, Michael Jr -- Yuan, Fang -- Zhang, Fengwen -- Lifson, Jeffrey D -- Bieniasz, Paul D -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center and Rockefeller University, 455 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023652" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Capsid Proteins/genetics ; Cell Line ; Cloning, Molecular ; Cytopathogenic Effect, Viral ; Disease Models, Animal ; Genes, vif ; HIV Infections ; HIV-1/*genetics/*physiology ; Humans ; Lymphocytes/virology ; Macaca mulatta ; Recombination, Genetic ; Simian Immunodeficiency Virus/*genetics ; T-Lymphocytes/*virology ; Virus Replication
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  • 85
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-02-07
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, T John -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):606-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16459361" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; *Editorial Policies ; Embryo, Mammalian/cytology ; Humans ; Peer Review, Research ; Periodicals as Topic ; *Publishing ; *Scientific Misconduct ; Stem Cells
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  • 86
    Publikationsdatum: 2006-08-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mathews, Debra J H -- Donovan, Peter -- Harris, John -- Lovell-Badge, Robin -- Savulescu, Julian -- Faden, Ruth -- MC_U117562207/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):921-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Phoebe R. Berman Bioethics Institute, Johns Hopkins University, Baltimore, MD 21205, USA. dmathews@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917046" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; Embryo Research/*ethics/*legislation & jurisprudence ; Embryo, Mammalian/cytology ; Humans ; International Cooperation/legislation & jurisprudence ; Periodicals as Topic/ethics/standards ; *Public Policy ; Publishing/ethics/standards ; Research Subjects ; *Stem Cells
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  • 87
    Publikationsdatum: 2006-07-11
    Beschreibung: Natural populations of beach mice exhibit a characteristic color pattern, relative to their mainland conspecifics, driven by natural selection for crypsis. We identified a derived, charge-changing amino acid mutation in the melanocortin-1 receptor (Mc1r) in beach mice, which decreases receptor function. In genetic crosses, allelic variation at Mc1r explains 9.8% to 36.4% of the variation in seven pigmentation traits determining color pattern. The derived Mc1r allele is present in Florida's Gulf Coast beach mice but not in Atlantic coast mice with similar light coloration, suggesting that different molecular mechanisms are responsible for convergent phenotypic evolution. Here, we link a single mutation in the coding region of a pigmentation gene to adaptive quantitative variation in the wild.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoekstra, Hopi E -- Hirschmann, Rachel J -- Bundey, Richard A -- Insel, Paul A -- Crossland, Janet P -- P40-RR14279/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA. hoekstra@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825572" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptation, Biological ; Alleles ; Amino Acid Substitution ; Animals ; Cell Line ; Crosses, Genetic ; Cyclic AMP/metabolism ; Female ; Florida ; Gene Frequency ; Genotype ; Hair ; Hair Color/*genetics ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Peromyscus/*genetics ; Phenotype ; Pigmentation/*genetics ; Polymorphism, Single Nucleotide ; Principal Component Analysis ; Receptor, Melanocortin, Type 1/chemistry/*genetics/metabolism ; Sequence Analysis, DNA
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  • 88
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):512.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645058" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Chemistry ; China ; *Fatty Acids ; France ; History, 21st Century ; *Theft
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 89
    Publikationsdatum: 2006-08-19
    Beschreibung: Dynamic modulation of ion channels by phosphorylation underlies neuronal plasticity. The Kv2.1 potassium channel is highly phosphorylated in resting mammalian neurons. Activity-dependent Kv2.1 dephosphorylation by calcineurin induces graded hyperpolarizing shifts in voltage-dependent activation, causing suppression of neuronal excitability. Mass spectrometry-SILAC (stable isotope labeling with amino acids in cell culture) identified 16 Kv2.1 phosphorylation sites, of which 7 were dephosphorylated by calcineurin. Mutation of individual calcineurin-regulated sites to alanine produced incremental shifts mimicking dephosphorylation, whereas mutation to aspartate yielded equivalent resistance to calcineurin. Mutations at multiple sites were additive, showing that variable phosphorylation of Kv2.1 at a large number of sites allows graded activity-dependent regulation of channel gating and neuronal firing properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Kang-Sik -- Mohapatra, Durga P -- Misonou, Hiroaki -- Trimmer, James S -- NS42225/NS/NINDS NIH HHS/ -- R01 NS042225/NS/NINDS NIH HHS/ -- R01 NS042225-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):976-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917065" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alanine/genetics/metabolism ; Alkaline Phosphatase/metabolism ; Animals ; Aspartic Acid/genetics/metabolism ; Brain/metabolism ; Calcineurin/metabolism ; Calcium/metabolism ; Cell Line ; Chromatography, Liquid ; Humans ; *Ion Channel Gating ; Ionomycin/pharmacology ; Mass Spectrometry ; Mutation ; Neurons/physiology ; Patch-Clamp Techniques ; Phosphorylation ; Phosphoserine/metabolism ; Phosphothreonine/metabolism ; Point Mutation ; Rats ; Recombinant Proteins/metabolism ; Serine/genetics ; Shab Potassium Channels/*metabolism ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 90
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):420-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873614" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Academies and Institutes/economics ; Cell Line ; Embryo Research/*economics/legislation & jurisprudence ; Embryo, Mammalian/cytology ; *Foundations ; Fund Raising ; Humans ; *Research Support as Topic ; *State Government ; *Stem Cells ; United States
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 91
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-11
    Beschreibung: The unfolded protein response (UPR) allows the endoplasmic reticulum (ER) to recover from the accumulation of misfolded proteins, in part by increasing its folding capacity. Inositol-requiring enzyme-1 (IRE1) promotes this remodeling by detecting misfolded ER proteins and activating a transcription factor, X-box-binding protein 1, through endonucleolytic cleavage of its messenger RNA (mRNA). Here, we report that IRE1 independently mediates the rapid degradation of a specific subset of mRNAs, based both on their localization to the ER membrane and on the amino acid sequence they encode. This response is well suited to complement other UPR mechanisms because it could selectively halt production of proteins that challenge the ER and clear the translocation and folding machinery for the subsequent remodeling process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hollien, Julie -- Weissman, Jonathan S -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California San Francisco, Howard Hughes Medical Institute, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825573" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/metabolism ; Dithiothreitol/pharmacology ; Down-Regulation ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/genetics/metabolism ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/genetics/*metabolism ; Exoribonucleases/genetics/metabolism ; Gene Expression Regulation ; Genes, Insect ; Membrane Proteins/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Oligonucleotide Array Sequence Analysis ; Protein Biosynthesis ; *Protein Folding ; Protein Sorting Signals ; *RNA Stability ; RNA, Messenger/genetics/*metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 92
    Publikationsdatum: 2006-01-21
    Beschreibung: RhoA signaling plays a critical role in many cellular processes, including cell migration. Here we show that the vaccinia F11L protein interacts directly with RhoA, inhibiting its signaling by blocking the interaction with its downstream effectors Rho-associated kinase (ROCK) and mDia. RNA interference-mediated depletion of F11L during infection resulted in an absence of vaccinia-induced cell motility and inhibition of viral morphogenesis. Disruption of the RhoA binding site in F11L, which resembles that of ROCK, led to an identical phenotype. Thus, inhibition of RhoA signaling is required for both vaccinia morphogenesis and virus-induced cell motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valderrama, Ferran -- Cordeiro, Joao V -- Schleich, Sibylle -- Frischknecht, Friedrich -- Way, Michael -- New York, N.Y. -- Science. 2006 Jan 20;311(5759):377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Motility Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, WC2A 3PX London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424340" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amides/pharmacology ; Animals ; Cell Line ; *Cell Movement ; Cytoskeletal Proteins ; Enzyme Inhibitors/pharmacology ; Genes, Viral ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins ; Morphogenesis ; Phosphoproteins/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Pyridines/pharmacology ; RNA Interference ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection ; Vaccinia virus/genetics/growth & development/*physiology ; Viral Proteins/chemistry/genetics/*metabolism ; Virus Assembly ; rho-Associated Kinases ; rhoA GTP-Binding Protein/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 93
    Publikationsdatum: 2006-10-14
    Beschreibung: The structural basis for the distinction of viral RNA from abundant self RNA in the cytoplasm of virally infected cells is largely unknown. We demonstrated that the 5'-triphosphate end of RNA generated by viral polymerases is responsible for retinoic acid-inducible protein I (RIG-I)-mediated detection of RNA molecules. Detection of 5'-triphosphate RNA is abrogated by capping of the 5'-triphosphate end or by nucleoside modification of RNA, both occurring during posttranscriptional RNA processing in eukaryotes. Genomic RNA prepared from a negative-strand RNA virus and RNA prepared from virus-infected cells (but not from noninfected cells) triggered a potent interferon-alpha response in a phosphatase-sensitive manner. 5'-triphosphate RNA directly binds to RIG-I. Thus, uncapped 5'-triphosphate RNA (now termed 3pRNA) present in viruses known to be recognized by RIG-I, but absent in viruses known to be detected by MDA-5 such as the picornaviruses, serves as the molecular signature for the detection of viral infection by RIG-I.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hornung, Veit -- Ellegast, Jana -- Kim, Sarah -- Brzozka, Krzysztof -- Jung, Andreas -- Kato, Hiroki -- Poeck, Hendrik -- Akira, Shizuo -- Conzelmann, Karl-Klaus -- Schlee, Martin -- Endres, Stefan -- Hartmann, Gunther -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):994-7. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Clinical Pharmacology, Department of Internal Medicine, University of Munich, 80336 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038590" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cells, Cultured ; Cytosol/metabolism/virology ; DEAD-box RNA Helicases/*metabolism ; DNA-Directed RNA Polymerases/metabolism ; Humans ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Ligands ; Mice ; Monocytes/metabolism ; Oligoribonucleotides/metabolism ; Phosphates/metabolism ; Phosphorylation ; RNA/chemistry/*metabolism ; RNA Caps/metabolism ; RNA, Double-Stranded/chemistry/metabolism ; RNA, Viral/chemistry/*metabolism ; Rabies virus/genetics/immunology/physiology ; Transcription, Genetic ; Transfection ; Viral Proteins/metabolism ; Virus Replication
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 94
    Publikationsdatum: 2006-02-18
    Beschreibung: Postsynaptic differentiation of dendrites is an essential step in synapse formation. We report here a requirement for the transcription factor myocyte enhancer factor 2A (MEF2A) in the morphogenesis of postsynaptic granule neuron dendritic claws in the cerebellar cortex. A transcriptional repressor form of MEF2A that is sumoylated at lysine-403 promoted dendritic claw differentiation. Activity-dependent calcium signaling induced a calcineurin-mediated dephosphorylation of MEF2A at serine-408 and, thereby, promoted a switch from sumoylation to acetylation at lysine-403, which led to inhibition of dendritic claw differentiation. Our findings define a mechanism underlying postsynaptic differentiation that may modulate activity-dependent synapse development and plasticity in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shalizi, Aryaman -- Gaudilliere, Brice -- Yuan, Zengqiang -- Stegmuller, Judith -- Shirogane, Takahiro -- Ge, Qingyuan -- Tan, Yi -- Schulman, Brenda -- Harper, J Wade -- Bonni, Azad -- AG11085/AG/NIA NIH HHS/ -- NS41021/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1012-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Louis Pasteur Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484498" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Animals ; Calcineurin/metabolism ; Calcium/*metabolism ; Calcium Signaling ; Cell Differentiation ; Cell Line ; Cerebellar Cortex/cytology/*physiology ; Dendrites/physiology/*ultrastructure ; Electroporation ; Humans ; In Vitro Techniques ; MEF2 Transcription Factors ; Morphogenesis ; Myogenic Regulatory Factors/genetics/*metabolism ; Neurons/*cytology/physiology ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/metabolism ; Small Ubiquitin-Related Modifier Proteins/*metabolism ; Synapses/*physiology ; Transcription, Genetic ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 95
    Publikationsdatum: 2006-08-19
    Beschreibung: Congenital myasthenic syndromes (CMSs) are a group of inherited disorders of neuromuscular transmission characterized by fatigable muscle weakness. One major subgroup of patients shows a characteristic "limb girdle" pattern of muscle weakness, in which the muscles have small, simplified neuromuscular junctions but normal acetylcholine receptor and acetylcholinesterase function. We showed that recessive inheritance of mutations in Dok-7, which result in a defective structure of the neuromuscular junction, is a cause of CMS with proximal muscle weakness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beeson, David -- Higuchi, Osamu -- Palace, Jackie -- Cossins, Judy -- Spearman, Hayley -- Maxwell, Susan -- Newsom-Davis, John -- Burke, Georgina -- Fawcett, Peter -- Motomura, Masakatsu -- Muller, Juliane S -- Lochmuller, Hanns -- Slater, Clarke -- Vincent, Angela -- Yamanashi, Yuji -- G117/490/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1975-8. Epub 2006 Aug 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK. dbeeson@hammer.imm.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917026" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; Cells, Cultured ; Female ; *Frameshift Mutation ; Genes, Recessive ; Humans ; Male ; Muscle Fibers, Skeletal/metabolism ; Muscle Proteins/*genetics/physiology ; Muscle Weakness/physiopathology ; Mutation ; Myasthenic Syndromes, Congenital/*genetics/pathology/physiopathology ; Neuromuscular Junction/*pathology/*physiopathology ; Pedigree ; Polymerase Chain Reaction ; Receptor Protein-Tyrosine Kinases/physiology ; Receptors, Cholinergic/metabolism/physiology ; Sequence Analysis, DNA ; Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 96
    Publikationsdatum: 2007-11-24
    Beschreibung: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 97
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2007-04-21
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaren, Anne -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):339.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446356" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Embryo Research ; Embryonic Stem Cells/*cytology/physiology ; Female ; Humans ; Male ; Mice ; Nuclear Transfer Techniques ; *Oocyte Donation/ethics ; Ovum/*cytology/physiology ; Spermatozoa/cytology/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 98
    Publikationsdatum: 2007-11-10
    Beschreibung: The mammalian target of rapamycin, mTOR, is a central regulator of cell growth. Its activity is regulated by Rheb, a Ras-like small guanosine triphosphatase (GTPase), in response to growth factor stimulation and nutrient availability. We show that Rheb regulates mTOR through FKBP38, a member of the FK506-binding protein (FKBP) family that is structurally related to FKBP12. FKBP38 binds to mTOR and inhibits its activity in a manner similar to that of the FKBP12-rapamycin complex. Rheb interacts directly with FKBP38 and prevents its association with mTOR in a guanosine 5'-triphosphate (GTP)-dependent manner. Our findings suggest that FKBP38 is an endogenous inhibitor of mTOR, whose inhibitory activity is antagonized by Rheb in response to growth factor stimulation and nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bai, Xiaochun -- Ma, Dongzhu -- Liu, Anling -- Shen, Xiaoyun -- Wang, Qiming J -- Liu, Yongjian -- Jiang, Yu -- GM068832/GM/NIGMS NIH HHS/ -- R01 CA129821/CA/NCI NIH HHS/ -- R01 GM068832/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):977-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pittsburgh School of Medicine, E1357 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991864" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acids/metabolism ; Cell Line ; Culture Media ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Neuropeptides/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins ; Recombinant Proteins/metabolism ; Serum ; Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 99
    Publikationsdatum: 2007-06-26
    Beschreibung: Although classical genetic and biochemical approaches have identified hundreds of proteins that function in the dynamic remodeling of cell shape in response to upstream signals, there is currently little systems-level understanding of the organization and composition of signaling networks that regulate cell morphology. We have developed quantitative morphological profiling methods to systematically investigate the role of individual genes in the regulation of cell morphology in a fast, robust, and cost-efficient manner. We analyzed a compendium of quantitative morphological signatures and described the existence of local signaling networks that act to regulate cell protrusion, adhesion, and tension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakal, Chris -- Aach, John -- Church, George -- Perrimon, Norbert -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1753-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588932" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cell Movement/genetics/physiology ; Cell Shape/*genetics/physiology ; Drosophila ; Green Fluorescent Proteins ; Metabolic Networks and Pathways/*genetics ; Phenotype ; RNA Interference ; Signal Transduction/*genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 100
    Publikationsdatum: 2007-01-16
    Beschreibung: alphabeta and gammadelta T cells originate from a common, multipotential precursor population in the thymus, but the molecular mechanisms regulating this lineage-fate decision are unknown. We have identified Sox13 as a gammadelta-specific gene in the immune system. Using Sox13 transgenic mice, we showed that this transcription factor promotes gammadelta T cell development while opposing alphabeta T cell differentiation. Conversely, mice deficient in Sox13 expression exhibited impaired development of gammadelta T cells but not alphabeta T cells. One mechanism of SOX13 function is the inhibition of signaling by the developmentally important Wnt/T cell factor (TCF) pathway. Our data thus reveal a dominant pathway regulating the developmental fate of these two lineages of T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melichar, Heather J -- Narayan, Kavitha -- Der, Sandy D -- Hiraoka, Yoshiki -- Gardiol, Noemie -- Jeannet, Gregoire -- Held, Werner -- Chambers, Cynthia A -- Kang, Joonsoo -- R01CA100382/92614/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Graduate Program in Immunology and Virology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218525" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD4/genetics ; Autoantigens/genetics/*metabolism ; Cell Line ; Cell Lineage ; Cell Proliferation ; Embryonic Development ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; High Mobility Group Proteins/genetics/*metabolism ; Humans ; *Lymphopoiesis ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; Receptors, Antigen, T-Cell, gamma-delta/*analysis/genetics ; Signal Transduction ; T Cell Transcription Factor 1/physiology ; T-Lymphocyte Subsets/*cytology/immunology/metabolism ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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