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  • Animals  (3)
  • Base Sequence
  • Chemistry
  • Polymer and Materials Science
  • 2010-2014  (3)
  • 2010  (3)
  • 1
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    Systematic genetic analysis of muscle morphogenesis and function in Drosophila (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-12
    Description: Systematic genetic approaches have provided deep insight into the molecular and cellular mechanisms that operate in simple unicellular organisms. For multicellular organisms, however, the pleiotropy of gene function has largely restricted such approaches to the study of early embryogenesis. With the availability of genome-wide transgenic RNA interference (RNAi) libraries in Drosophila, it is now possible to perform a systematic genetic dissection of any cell or tissue type at any stage of the lifespan. Here we apply these methods to define the genetic basis for formation and function of the Drosophila muscle. We identify a role in muscle for 2,785 genes, many of which we assign to specific functions in the organization of muscles, myofibrils or sarcomeres. Many of these genes are phylogenetically conserved, including genes implicated in mammalian sarcomere organization and human muscle diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnorrer, Frank -- Schonbauer, Cornelia -- Langer, Christoph C H -- Dietzl, Georg -- Novatchkova, Maria -- Schernhuber, Katharina -- Fellner, Michaela -- Azaryan, Anna -- Radolf, Martin -- Stark, Alexander -- Keleman, Krystyna -- Dickson, Barry J -- England -- Nature. 2010 Mar 11;464(7286):287-91. doi: 10.1038/nature08799.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany. schnorrer@biochem.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Computational Biology ; Drosophila melanogaster/*embryology ; Genes, Insect/*genetics ; Genome-Wide Association Study ; Genomic Library ; Larva ; Male ; Muscles/embryology ; RNA Interference
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Impaired hippocampal-prefrontal synchrony in a genetic mouse model of schizophrenia (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-03
    Description: Abnormalities in functional connectivity between brain areas have been postulated as an important pathophysiological mechanism underlying schizophrenia. In particular, macroscopic measurements of brain activity in patients suggest that functional connectivity between the frontal and temporal lobes may be altered. However, it remains unclear whether such dysconnectivity relates to the aetiology of the illness, and how it is manifested in the activity of neural circuits. Because schizophrenia has a strong genetic component, animal models of genetic risk factors are likely to aid our understanding of the pathogenesis and pathophysiology of the disease. Here we study Df(16)A(+/-) mice, which model a microdeletion on human chromosome 22 (22q11.2) that constitutes one of the largest known genetic risk factors for schizophrenia. To examine functional connectivity in these mice, we measured the synchronization of neural activity between the hippocampus and the prefrontal cortex during the performance of a task requiring working memory, which is one of the cognitive functions disrupted in the disease. In wild-type mice, hippocampal-prefrontal synchrony increased during working memory performance, consistent with previous reports in rats. Df(16)A(+/-) mice, which are impaired in the acquisition of the task, showed drastically reduced synchrony, measured both by phase-locking of prefrontal cells to hippocampal theta oscillations and by coherence of prefrontal and hippocampal local field potentials. Furthermore, the magnitude of hippocampal-prefrontal coherence at the onset of training could be used to predict the time it took the Df(16)A(+/-) mice to learn the task and increased more slowly during task acquisition. These data suggest how the deficits in functional connectivity observed in patients with schizophrenia may be realized at the single-neuron level. Our findings further suggest that impaired long-range synchrony of neural activity is one consequence of the 22q11.2 deletion and may be a fundamental component of the pathophysiology underlying schizophrenia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864584/" 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/PMC2864584/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sigurdsson, Torfi -- Stark, Kimberly L -- Karayiorgou, Maria -- Gogos, Joseph A -- Gordon, Joshua A -- MH081968/MH/NIMH NIH HHS/ -- MH67068/MH/NIMH NIH HHS/ -- R01 MH081968/MH/NIMH NIH HHS/ -- R01 MH081968-02/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Apr 1;464(7289):763-7. doi: 10.1038/nature08855.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360742" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Alleles ; Animals ; Behavior, Animal/physiology ; Chromosomes, Human, Pair 22/genetics ; Chromosomes, Mammalian/*genetics ; *Disease Models, Animal ; Female ; Genetic Predisposition to Disease/genetics ; Hippocampus/*physiopathology ; Humans ; Male ; Memory/physiology ; Mice ; Mice, Inbred C57BL ; Models, Genetic ; Models, Neurological ; Prefrontal Cortex/*physiopathology ; Schizophrenia/*genetics/*physiopathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: The Tasmanian devil, a marsupial carnivore, is endangered because of the emergence of a transmissible cancer known as devil facial tumor disease (DFTD). This fatal cancer is clonally derived and is an allograft transmitted between devils by biting. We performed a large-scale genetic analysis of DFTD with microsatellite genotyping, a mitochondrial genome analysis, and deep sequencing of the DFTD transcriptome and microRNAs. These studies confirm that DFTD is a monophyletic clonally transmissible tumor and suggest that the disease is of Schwann cell origin. On the basis of these results, we have generated a diagnostic marker for DFTD and identify a suite of genes relevant to DFTD pathology and transmission. We provide a genomic data set for the Tasmanian devil that is applicable to cancer diagnosis, disease evolution, and conservation biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982769/" 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/PMC2982769/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murchison, Elizabeth P -- Tovar, Cesar -- Hsu, Arthur -- Bender, Hannah S -- Kheradpour, Pouya -- Rebbeck, Clare A -- Obendorf, David -- Conlan, Carly -- Bahlo, Melanie -- Blizzard, Catherine A -- Pyecroft, Stephen -- Kreiss, Alexandre -- Kellis, Manolis -- Stark, Alexander -- Harkins, Timothy T -- Marshall Graves, Jennifer A -- Woods, Gregory M -- Hannon, Gregory J -- Papenfuss, Anthony T -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-38/CA/NCI NIH HHS/ -- R01 GM062534/GM/NIGMS NIH HHS/ -- R01 GM062534-10/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):84-7. doi: 10.1126/science.1180616.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA. elizabeth.murchison@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/analysis ; Bites and Stings/veterinary ; Cell Differentiation ; Facial Neoplasms/diagnosis/genetics/pathology/*veterinary ; *Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm ; Genome, Mitochondrial ; Genotype ; *Marsupialia/genetics ; Membrane Proteins/genetics/metabolism ; MicroRNAs/genetics ; Microsatellite Repeats ; Myelin Basic Protein/genetics ; Nerve Sheath Neoplasms/diagnosis/genetics/pathology/*veterinary ; *Schwann Cells/physiology ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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