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  • Mice  (47)
  • American Association for the Advancement of Science (AAAS)  (47)
  • 2005-2009  (47)
  • 2000-2004
  • 1975-1979
  • 2008  (47)
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  • 2005-2009  (47)
  • 2000-2004
  • 1975-1979
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  • 1
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" 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/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; Transfection
    Print ISSN: 0036-8075
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  • 2
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" 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/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2008-04-12
    Description: The toxicity of ionizing radiation is associated with massive apoptosis in radiosensitive organs. Here, we investigate whether a drug that activates a signaling mechanism used by tumor cells to suppress apoptosis can protect healthy cells from the harmful effects of radiation. We studied CBLB502, a polypeptide drug derived from Salmonella flagellin that binds to Toll-like receptor 5 (TLR5) and activates nuclear factor-kappaB signaling. A single injection of CBLB502 before lethal total-body irradiation protected mice from both gastrointestinal and hematopoietic acute radiation syndromes and resulted in improved survival. CBLB502 injected after irradiation also enhanced survival, but at lower radiation doses. It is noteworthy that the drug did not decrease tumor radiosensitivity in mouse models. CBLB502 also showed radioprotective activity in lethally irradiated rhesus monkeys. Thus, TLR5 agonists could potentially improve the therapeutic index of cancer radiotherapy and serve as biological protectants in radiation emergencies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" 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/PMC4322935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burdelya, Lyudmila G -- Krivokrysenko, Vadim I -- Tallant, Thomas C -- Strom, Evguenia -- Gleiberman, Anatoly S -- Gupta, Damodar -- Kurnasov, Oleg V -- Fort, Farrel L -- Osterman, Andrei L -- Didonato, Joseph A -- Feinstein, Elena -- Gudkov, Andrei V -- AI066497/AI/NIAID NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- CA84406/CA/NCI NIH HHS/ -- R01 CA084406/CA/NCI NIH HHS/ -- R01 CA084406-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):226-30. doi: 10.1126/science.1154986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403709" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/drug effects/radiation effects ; Chemotherapy, Adjuvant ; Flagellin/chemistry/pharmacology ; Gamma Rays ; Hematopoietic System/drug effects/radiation effects ; Intestine, Small/cytology/drug effects/radiation effects ; Macaca mulatta ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Neoplasms, Experimental/drug therapy/radiotherapy ; Peptides/administration & dosage/chemistry/*pharmacology/toxicity ; Radiation Dosage ; Radiation Injuries, Experimental/*prevention & control ; Radiation Tolerance/*drug effects ; Radiation-Protective Agents/administration & ; dosage/chemistry/*pharmacology/toxicity ; Salmonella enterica ; Signal Transduction ; Toll-Like Receptor 5/*agonists/metabolism ; Whole-Body Irradiation
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  • 4
    Publication Date: 2008-06-07
    Description: Fluorescence light microscopy allows multicolor visualization of cellular components with high specificity, but its utility has until recently been constrained by the intrinsic limit of spatial resolution. We applied three-dimensional structured illumination microscopy (3D-SIM) to circumvent this limit and to study the mammalian nucleus. By simultaneously imaging chromatin, nuclear lamina, and the nuclear pore complex (NPC), we observed several features that escape detection by conventional microscopy. We could resolve single NPCs that colocalized with channels in the lamin network and peripheral heterochromatin. We could differentially localize distinct NPC components and detect double-layered invaginations of the nuclear envelope in prophase as previously seen only by electron microscopy. Multicolor 3D-SIM opens new and facile possibilities to analyze subcellular structures beyond the diffraction limit of the emitted light.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916659/" 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/PMC2916659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schermelleh, Lothar -- Carlton, Peter M -- Haase, Sebastian -- Shao, Lin -- Winoto, Lukman -- Kner, Peter -- Burke, Brian -- Cardoso, M Cristina -- Agard, David A -- Gustafsson, Mats G L -- Leonhardt, Heinrich -- Sedat, John W -- GM-2501-25/GM/NIGMS NIH HHS/ -- R01 GM025101/GM/NIGMS NIH HHS/ -- R01 GM025101-25/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 6;320(5881):1332-6. doi: 10.1126/science.1156947.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrated Protein Science, Department of Biology, Ludwig Maximilians University Munich, 82152 Planegg-Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18535242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/*ultrastructure ; Chromatin/*ultrastructure ; Fluorescent Dyes ; Heterochromatin/ultrastructure ; Imaging, Three-Dimensional/instrumentation/*methods ; Indoles ; Interphase ; Lamins/ultrastructure ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence/instrumentation/*methods ; Myoblasts ; Nuclear Envelope/*ultrastructure ; Nuclear Lamina/ultrastructure ; Nuclear Pore/ultrastructure ; Optics and Photonics
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  • 5
    Publication Date: 2008-09-13
    Description: Homologous sets of transcription factors direct conserved tissue-specific gene expression, yet transcription factor-binding events diverge rapidly between closely related species. We used hepatocytes from an aneuploid mouse strain carrying human chromosome 21 to determine, on a chromosomal scale, whether interspecies differences in transcriptional regulation are primarily directed by human genetic sequence or mouse nuclear environment. Virtually all transcription factor-binding locations, landmarks of transcription initiation, and the resulting gene expression observed in human hepatocytes were recapitulated across the entire human chromosome 21 in the mouse hepatocyte nucleus. Thus, in homologous tissues, genetic sequence is largely responsible for directing transcriptional programs; interspecies differences in epigenetic machinery, cellular environment, and transcription factors themselves play secondary roles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717767/" 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/PMC3717767/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Michael D -- Barbosa-Morais, Nuno L -- Schmidt, Dominic -- Conboy, Caitlin M -- Vanes, Lesley -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- Tavare, Simon -- Odom, Duncan T -- 080174/Wellcome Trust/United Kingdom -- 15603/Cancer Research UK/United Kingdom -- 202218/European Research Council/International -- A15603/Cancer Research UK/United Kingdom -- G0601056/Medical Research Council/United Kingdom -- MC_U117527252/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):434-8. doi: 10.1126/science.1160930. Epub 2008 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/metabolism ; Chromatin Assembly and Disassembly ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 21/*genetics/metabolism ; Disease Models, Animal ; Down Syndrome/genetics ; *Gene Expression Regulation ; Hepatocyte Nuclear Factors/*metabolism ; Hepatocytes/*metabolism ; Histones/metabolism ; Humans ; Methylation ; Mice ; Oligonucleotide Array Sequence Analysis ; *Regulatory Sequences, Nucleic Acid ; Species Specificity ; Transcription Initiation Site ; *Transcription, Genetic
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  • 6
    Publication Date: 2008-01-19
    Description: The earliest step in creating the cerebral cortex is the specification of neuroepithelium to a cortical fate. Using mouse genetic mosaics and timed inactivations, we demonstrated that Lhx2 acts as a classic selector gene and essential intrinsic determinant of cortical identity. Lhx2 selector activity is restricted to an early critical period when stem cells comprise the cortical neuroepithelium, where it acts cell-autonomously to specify cortical identity and suppress alternative fates in a spatially dependent manner. Laterally, Lhx2 null cells adopt antihem identity, whereas medially they become cortical hem cells, which can induce and organize ectopic hippocampal fields. In addition to providing functional evidence for Lhx2 selector activity, these findings show that the cortical hem is a hippocampal organizer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2494603/" 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/PMC2494603/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mangale, Vishakha S -- Hirokawa, Karla E -- Satyaki, Prasad R V -- Gokulchandran, Nandini -- Chikbire, Satyadeep -- Subramanian, Lakshmi -- Shetty, Ashwin S -- Martynoga, Ben -- Paul, Jolly -- Mai, Mark V -- Li, Yuqing -- Flanagan, Lisa A -- Tole, Shubha -- Monuki, Edwin S -- 056684/Z/99/Z/Wellcome Trust/United Kingdom -- AG23583/AG/NIA NIH HHS/ -- MH02029/MH/NIMH NIH HHS/ -- NS053511/NS/NINDS NIH HHS/ -- NS07444/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):304-9. doi: 10.1126/science.1151695.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai 400005, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aggregation ; Cerebral Cortex/cytology/*embryology/metabolism ; Chimera ; Dentate Gyrus/cytology/embryology/metabolism ; Embryonic Induction ; Embryonic Stem Cells/metabolism ; Epithelium/embryology/metabolism ; Gene Expression Regulation, Developmental ; Hippocampus/cytology/*embryology ; Homeodomain Proteins/*genetics/*metabolism ; LIM-Homeodomain Proteins ; Mice ; Mice, Knockout ; Mutation ; Neuroepithelial Cells/cytology/metabolism ; Organizers, Embryonic/embryology/*physiology ; Prosencephalon/embryology/metabolism ; Pyramidal Cells/cytology/embryology ; Recombination, Genetic ; Telencephalon/cytology/embryology ; Transcription Factors/*genetics/*metabolism
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  • 7
    Publication Date: 2008-01-19
    Description: Dynein and kinesin motor proteins transport cellular cargoes toward opposite ends of microtubule tracks. In neurons, microtubules are abundantly decorated with microtubule-associated proteins (MAPs) such as tau. Motor proteins thus encounter MAPs frequently along their path. To determine the effects of tau on dynein and kinesin motility, we conducted single-molecule studies of motor proteins moving along tau-decorated microtubules. Dynein tended to reverse direction, whereas kinesin tended to detach at patches of bound tau. Kinesin was inhibited at about a tenth of the tau concentration that inhibited dynein, and the microtubule-binding domain of tau was sufficient to inhibit motor activity. The differential modulation of dynein and kinesin motility suggests that MAPs can spatially regulate the balance of microtubule-dependent axonal transport.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866193/" 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/PMC2866193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dixit, Ram -- Ross, Jennifer L -- Goldman, Yale E -- Holzbaur, Erika L F -- GM-48661/GM/NIGMS NIH HHS/ -- P01 AR051174/AR/NIAMS NIH HHS/ -- P01 AR051174-050002/AR/NIAMS NIH HHS/ -- P01-AR-051174/AR/NIAMS NIH HHS/ -- R01 GM048661/GM/NIGMS NIH HHS/ -- R01 GM048661-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 22;319(5866):1086-9. doi: 10.1126/science.1152993. Epub 2008 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pennsylvania Muscle Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202255" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism ; Animals ; Axonal Transport ; Dyneins/chemistry/*metabolism ; Kinesin/chemistry/*metabolism ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Microtubules/*metabolism ; Models, Neurological ; Neurons/metabolism/physiology ; Protein Binding ; Protein Isoforms/metabolism ; Recombinant Fusion Proteins/metabolism ; tau Proteins/chemistry/*metabolism
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  • 8
    Publication Date: 2008-11-15
    Description: Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753175/" 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/PMC2753175/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Eun Young -- Chavakis, Emmanouil -- Czabanka, Marcus A -- Langer, Harald F -- Fraemohs, Line -- Economopoulou, Matina -- Kundu, Ramendra K -- Orlandi, Alessia -- Zheng, Ying Yi -- Prieto, Darue A -- Ballantyne, Christie M -- Constant, Stephanie L -- Aird, William C -- Papayannopoulou, Thalia -- Gahmberg, Carl G -- Udey, Mark C -- Vajkoczy, Peter -- Quertermous, Thomas -- Dimmeler, Stefanie -- Weber, Christian -- Chavakis, Triantafyllos -- AI067254/AI/NIAID NIH HHS/ -- R01 HL082927/HL/NHLBI NIH HHS/ -- Z01 BC010790-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 14;322(5904):1101-4. doi: 10.1126/science.1165218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19008446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Carrier Proteins/*physiology ; *Cell Adhesion ; Endothelial Cells/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; Leukocyte Rolling ; Ligands ; Lipopolysaccharides/immunology ; Lung/blood supply/immunology ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Monocytes/*physiology ; *Neutrophil Infiltration ; Neutrophils/*physiology ; Peritonitis/immunology ; Pneumonia/*immunology ; Recombinant Fusion Proteins/metabolism
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  • 9
    Publication Date: 2008-01-05
    Description: In vivo experience can occlude subsequent induction of long-term potentiation and enhance long-term depression of synaptic responses. Although a reduced capacity for synaptic strengthening may function to prevent excessive excitation, such an effect paradoxically implies that continued experience or training should not improve and may even degrade neural representations. In mice, we examined the effect of ongoing whisker stimulation on synaptic strengthening at layer 4-2/3 synapses in the barrel cortex. Although N-methyl-d-aspartate receptors were required to initiate strengthening, they subsequently suppressed further potentiation at these synapses in vitro and in vivo. Despite this transition, synaptic strengthening continued with additional sensory activity but instead required the activation of metabotropic glutamate receptors, suggesting a mechanism by which continued experience can result in increasing synaptic strength over time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clem, Roger L -- Celikel, Tansu -- Barth, Alison L -- DA017188-01/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 4;319(5859):101-4. doi: 10.1126/science.1143808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18174444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association Learning ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Mice ; Mice, Transgenic ; Neocortex/*physiology ; *Neuronal Plasticity ; Neurons/physiology ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/chemistry ; Signal Transduction ; Somatosensory Cortex/*physiology ; Synapses/*physiology ; Vibrissae/*innervation/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2008-05-20
    Description: Development of axonal tracts requires interactions between growth cones and the environment. Tracts such as the anterior commissure and internal capsule are defective in mice with null mutation of Celsr3. We generated a conditional Celsr3 allele, allowing regional inactivation. Inactivation in telencephalon, ventral forebrain, or cortex demonstrated essential roles for Celsr3 in neurons that project axons to the anterior commissure and subcerebral targets, as well as in cells that guide axons through the internal capsule. When Celsr3 was inactivated in cortex, subcerebral projections failed to grow, yet corticothalamic axons developed normally, indicating that besides guidepost cells, additional Celsr3-independent cues can assist their progression. These observations provide in vivo evidence that Celsr3-mediated interactions between axons and guidepost cells govern axonal tract formation in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746700/" 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/PMC2746700/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Libing -- Bar, Isabelle -- Achouri, Younes -- Campbell, Kenneth -- De Backer, Olivier -- Hebert, Jean M -- Jones, Kevin -- Kessaris, Nicoletta -- de Rouvroit, Catherine Lambert -- O'Leary, Dennis -- Richardson, William D -- Goffinet, Andre M -- Tissir, Fadel -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- G9708005/Medical Research Council/United Kingdom -- R01 MH086147/MH/NIMH NIH HHS/ -- R01 MH086147-05/MH/NIMH NIH HHS/ -- R37 NS031558/NS/NINDS NIH HHS/ -- R37 NS031558-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):946-9. doi: 10.1126/science.1155244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neurobiology, Universite Catholique de Louvain, 1200 Bruxelles, Belgique.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cadherins/*genetics/*physiology ; Cerebral Cortex/cytology/embryology ; Female ; Gene Silencing ; Internal Capsule/cytology/embryology/physiology ; Male ; Mice ; Neural Pathways/*embryology/physiology ; Neurons/*physiology ; Prosencephalon/cytology/*embryology/physiology ; Receptors, Cell Surface/*genetics/*physiology ; Septal Nuclei/embryology/physiology ; Thalamus/cytology/embryology ; Tissue Culture Techniques
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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