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  • Female  (1,432)
  • Nature Publishing Group (NPG)  (1,432)
  • Oxford University Press
  • 1
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    A reserve stem cell population in small intestine renders Lgr5-positive cells dispensable (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-20
    Description: The small intestine epithelium renews every 2 to 5 days, making it one of the most regenerative mammalian tissues. Genetic inducible fate mapping studies have identified two principal epithelial stem cell pools in this tissue. One pool consists of columnar Lgr5-expressing cells that cycle rapidly and are present predominantly at the crypt base. The other pool consists of Bmi1-expressing cells that largely reside above the crypt base. However, the relative functions of these two pools and their interrelationship are not understood. Here we specifically ablated Lgr5-expressing cells in mice using a human diphtheria toxin receptor (DTR) gene knocked into the Lgr5 locus. We found that complete loss of the Lgr5-expressing cells did not perturb homeostasis of the epithelium, indicating that other cell types can compensate for the elimination of this population. After ablation of Lgr5-expressing cells, progeny production by Bmi1-expressing cells increased, indicating that Bmi1-expressing stem cells compensate for the loss of Lgr5-expressing cells. Indeed, lineage tracing showed that Bmi1-expressing cells gave rise to Lgr5-expressing cells, pointing to a hierarchy of stem cells in the intestinal epithelium. Our results demonstrate that Lgr5-expressing cells are dispensable for normal intestinal homeostasis, and that in the absence of these cells, Bmi1-expressing cells can serve as an alternative stem cell pool. These data provide the first experimental evidence for the interrelationship between these populations. The Bmi1-expressing stem cells may represent both a reserve stem cell pool in case of injury to the small intestine epithelium and a source for replenishment of the Lgr5-expressing cells under non-pathological conditions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4251967/" 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/PMC4251967/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Hua -- Biehs, Brian -- Warming, Soren -- Leong, Kevin G -- Rangell, Linda -- Klein, Ophir D -- de Sauvage, Frederic J -- 1-DP2-OD007191/OD/NIH HHS/ -- DP2 OD007191/OD/NIH HHS/ -- R01 DE021420/DE/NIDCR NIH HHS/ -- R01-DE021420/DE/NIDCR NIH HHS/ -- England -- Nature. 2011 Sep 18;478(7368):255-9. doi: 10.1038/nature10408.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21927002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Epithelial Cells/cytology/metabolism ; Female ; Heparin-binding EGF-like Growth Factor ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/genetics/metabolism ; Intestine, Small/*cytology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*metabolism ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins/*metabolism ; Receptors, G-Protein-Coupled/deficiency/genetics/*metabolism ; Regeneration ; Repressor Proteins/*metabolism ; Stem Cells/*cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-08-26
    Description: Genetic manipulations of insect populations for pest control have been advocated for some time, but there are few cases where manipulated individuals have been released in the field and no cases where they have successfully invaded target populations. Population transformation using the intracellular bacterium Wolbachia is particularly attractive because this maternally-inherited agent provides a powerful mechanism to invade natural populations through cytoplasmic incompatibility. When Wolbachia are introduced into mosquitoes, they interfere with pathogen transmission and influence key life history traits such as lifespan. Here we describe how the wMel Wolbachia infection, introduced into the dengue vector Aedes aegypti from Drosophila melanogaster, successfully invaded two natural A. aegypti populations in Australia, reaching near-fixation in a few months following releases of wMel-infected A. aegypti adults. Models with plausible parameter values indicate that Wolbachia-infected mosquitoes suffered relatively small fitness costs, leading to an unstable equilibrium frequency 〈30% that must be exceeded for invasion. These findings demonstrate that Wolbachia-based strategies can be deployed as a practical approach to dengue suppression with potential for area-wide implementation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, A A -- Montgomery, B L -- Popovici, J -- Iturbe-Ormaetxe, I -- Johnson, P H -- Muzzi, F -- Greenfield, M -- Durkan, M -- Leong, Y S -- Dong, Y -- Cook, H -- Axford, J -- Callahan, A G -- Kenny, N -- Omodei, C -- McGraw, E A -- Ryan, P A -- Ritchie, S A -- Turelli, M -- O'Neill, S L -- England -- Nature. 2011 Aug 24;476(7361):454-7. doi: 10.1038/nature10356.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bio21 Institute, Department of Genetics, The University of Melbourne, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21866160" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*microbiology/physiology/*virology ; Animals ; Dengue/microbiology/*prevention & control/*transmission/virology ; Dengue Virus/isolation & purification/*physiology ; Drosophila melanogaster/microbiology ; Female ; Humans ; Insect Vectors/microbiology/physiology/virology ; Male ; Pest Control, Biological/*methods ; Queensland ; Time Factors ; Wolbachia/isolation & purification/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Habenular alpha5 nicotinic receptor subunit signalling controls nicotine intake (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-01
    Description: Genetic variation in CHRNA5, the gene encoding the alpha5 nicotinic acetylcholine receptor subunit, increases vulnerability to tobacco addiction and lung cancer, but the underlying mechanisms are unknown. Here we report markedly increased nicotine intake in mice with a null mutation in Chrna5. This effect was 'rescued' in knockout mice by re-expressing alpha5 subunits in the medial habenula (MHb), and recapitulated in rats through alpha5 subunit knockdown in MHb. Remarkably, alpha5 subunit knockdown in MHb did not alter the rewarding effects of nicotine but abolished the inhibitory effects of higher nicotine doses on brain reward systems. The MHb extends projections almost exclusively to the interpeduncular nucleus (IPN). We found diminished IPN activation in response to nicotine in alpha5 knockout mice. Further, disruption of IPN signalling increased nicotine intake in rats. Our findings indicate that nicotine activates the habenulo-interpeduncular pathway through alpha5-containing nAChRs, triggering an inhibitory motivational signal that acts to limit nicotine intake.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079537/" 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/PMC3079537/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fowler, Christie D -- Lu, Qun -- Johnson, Paul M -- Marks, Michael J -- Kenny, Paul J -- DA020686/DA/NIDA NIH HHS/ -- DA026693/DA/NIDA NIH HHS/ -- F32 DA026693/DA/NIDA NIH HHS/ -- P30 DA015663/DA/NIDA NIH HHS/ -- P30 DA015663-10/DA/NIDA NIH HHS/ -- P30DA015663/DA/NIDA NIH HHS/ -- R01 DA020686/DA/NIDA NIH HHS/ -- R01 DA020686-05/DA/NIDA NIH HHS/ -- England -- Nature. 2011 Mar 31;471(7340):597-601. doi: 10.1038/nature09797. Epub 2011 Jan 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute-Scripps Florida, Jupiter, Florida 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21278726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Habenula/drug effects/*metabolism/physiology ; Male ; Mice ; Mice, Knockout ; Nicotine/*metabolism/pharmacokinetics/pharmacology ; Rats ; Receptors, Nicotinic/deficiency/genetics/*metabolism ; Reward ; *Signal Transduction/drug effects ; Tobacco Use Disorder/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Inference of human population history from individual whole-genome sequences (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-07-15
    Description: The history of human population size is important for understanding human evolution. Various studies have found evidence for a founder event (bottleneck) in East Asian and European populations, associated with the human dispersal out-of-Africa event around 60 thousand years (kyr) ago. However, these studies have had to assume simplified demographic models with few parameters, and they do not provide a precise date for the start and stop times of the bottleneck. Here, with fewer assumptions on population size changes, we present a more detailed history of human population sizes between approximately ten thousand and a million years ago, using the pairwise sequentially Markovian coalescent model applied to the complete diploid genome sequences of a Chinese male (YH), a Korean male (SJK), three European individuals (J. C. Venter, NA12891 and NA12878 (ref. 9)) and two Yoruba males (NA18507 (ref. 10) and NA19239). We infer that European and Chinese populations had very similar population-size histories before 10-20 kyr ago. Both populations experienced a severe bottleneck 10-60 kyr ago, whereas African populations experienced a milder bottleneck from which they recovered earlier. All three populations have an elevated effective population size between 60 and 250 kyr ago, possibly due to population substructure. We also infer that the differentiation of genetically modern humans may have started as early as 100-120 kyr ago, but considerable genetic exchanges may still have occurred until 20-40 kyr ago.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154645/" 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/PMC3154645/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Heng -- Durbin, Richard -- 077192/Wellcome Trust/United Kingdom -- WT077192/Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jul 13;475(7357):493-6. doi: 10.1038/nature10231.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21753753" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; Female ; *Genetics, Population ; *Genomics ; Humans ; Male ; *Models, Genetic ; Population Density ; Population Dynamics ; Sequence Analysis, DNA
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  • 5
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    Mutations causing syndromic autism define an axis of synaptic pathophysiology (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-25
    Description: Tuberous sclerosis complex and fragile X syndrome are genetic diseases characterized by intellectual disability and autism. Because both syndromes are caused by mutations in genes that regulate protein synthesis in neurons, it has been hypothesized that excessive protein synthesis is one core pathophysiological mechanism of intellectual disability and autism. Using electrophysiological and biochemical assays of neuronal protein synthesis in the hippocampus of Tsc2(+/-) and Fmr1(-/y) mice, here we show that synaptic dysfunction caused by these mutations actually falls at opposite ends of a physiological spectrum. Synaptic, biochemical and cognitive defects in these mutants are corrected by treatments that modulate metabotropic glutamate receptor 5 in opposite directions, and deficits in the mutants disappear when the mice are bred to carry both mutations. Thus, normal synaptic plasticity and cognition occur within an optimal range of metabotropic glutamate-receptor-mediated protein synthesis, and deviations in either direction can lead to shared behavioural impairments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228874/" 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/PMC3228874/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Auerbach, Benjamin D -- Osterweil, Emily K -- Bear, Mark F -- 2R01HD046943/HD/NICHD NIH HHS/ -- R01 HD046943/HD/NICHD NIH HHS/ -- R01 HD046943-07/HD/NICHD NIH HHS/ -- T32 MH-082718/MH/NIMH NIH HHS/ -- T32 MH074249/MH/NIMH NIH HHS/ -- T32 MH074249-02/MH/NIMH NIH HHS/ -- T32-MH-074249/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Nov 23;480(7375):63-8. doi: 10.1038/nature10658.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22113615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*genetics/*physiopathology ; Disease Models, Animal ; Electrical Synapses/*pathology ; Female ; Fragile X Mental Retardation Protein/genetics ; Gene Expression Regulation ; Hippocampus/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; *Mutation ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/metabolism ; Syndrome ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/genetics
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  • 6
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    Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis (2011)
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    Publication Date: 2011-03-04
    Description: Caspase-8 has two opposing biological functions--it promotes cell death by triggering the extrinsic pathway of apoptosis, but also has a survival activity, as it is required for embryonic development, T-lymphocyte activation, and resistance to necrosis induced by tumour necrosis factor-alpha (TNF-alpha) and related family ligands. Here we show that development of caspase-8-deficient mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3). Adult animals lacking both caspase-8 and RIPK3 display a progressive lymphoaccumulative disease resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively), and resist the lethal effects of CD95 ligation in vivo. We have found that caspase-8 prevents RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active complex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is required for the protective function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077893/" 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/PMC3077893/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberst, Andrew -- Dillon, Christopher P -- Weinlich, Ricardo -- McCormick, Laura L -- Fitzgerald, Patrick -- Pop, Cristina -- Hakem, Razq -- Salvesen, Guy S -- Green, Douglas R -- P01 CA069381/CA/NCI NIH HHS/ -- P01 CA069381-14/CA/NCI NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):363-7. doi: 10.1038/nature09852. Epub 2011 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dept. of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/deficiency/metabolism ; Apoptosis ; *Biocatalysis ; CASP8 and FADD-Like Apoptosis Regulating Protein/*metabolism ; Caspase 8/genetics/*metabolism ; Caspase Inhibitors ; Cell Line ; Female ; Male ; Mice ; Multiprotein Complexes/chemistry/metabolism ; *Necrosis ; Phenotype ; Receptor-Interacting Protein Serine-Threonine Kinases/*antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Serpins/pharmacology ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/biosynthesis/pharmacology ; Viral Proteins/pharmacology
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  • 7
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    Animal behaviour: the nexus of sex and violence (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saper, Clifford B -- England -- Nature. 2011 Feb 10;470(7333):179-81. doi: 10.1038/470179a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307926" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/drug effects/*physiology ; Animals ; Cats ; Electric Stimulation ; Female ; Gene Expression Regulation/genetics ; Genes, fos/genetics ; Humans ; Male ; Mice ; Neural Inhibition/drug effects/genetics/physiology ; Neural Pathways/drug effects/physiology ; Neurons/drug effects/physiology ; Rats ; Sex Characteristics ; Sexual Behavior, Animal/drug effects/physiology ; Time Factors ; Ventromedial Hypothalamic Nucleus/anatomy & histology/*cytology/drug ; effects/*physiology ; Violence
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    Scholars' awards go mainly to men (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lincoln, Anne E -- Pincus, Stephanie H -- Leboy, Phoebe S -- England -- Nature. 2011 Jan 27;469(7331):472. doi: 10.1038/469472a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21270876" target="_blank"〉PubMed〈/a〉
    Keywords: *Awards and Prizes ; Bias (Epidemiology) ; Female ; Humans ; Male ; Science/*statistics & numerical data ; Sex Factors
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  • 9
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    Motor antagonism exposed by spatial segregation and timing of neurogenesis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-21
    Description: Walking is a key motor behaviour of limbed animals, executed by contraction of functionally antagonistic muscle groups during swing and stance phases. Nevertheless, neuronal circuits regulating the activation of antagonistic extensor-flexor muscles remain poorly understood. Here we use monosynaptically restricted trans-synaptic viruses to elucidate premotor anatomical substrates for extensor-flexor control in mice. We observe a medio-lateral spatial segregation between extensor and flexor premotor interneurons in the dorsal spinal cord. These premotor interneuron populations are derived from common progenitor domains, but segregate by timing of neurogenesis. We find that proprioceptive sensory feedback from the periphery is targeted to medial extensor premotor populations and is required for extensor-specific connectivity profiles during development. Our findings provide evidence for a discriminating anatomical basis of antagonistic circuits at the level of premotor interneurons, and point to synaptic input and developmental ontogeny as key factors in the establishment of circuits regulating motor behavioural dichotomy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tripodi, Marco -- Stepien, Anna E -- Arber, Silvia -- England -- Nature. 2011 Oct 19;479(7371):61-6. doi: 10.1038/nature10538.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum, Department of Cell Biology, University of Basel, 4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22012263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Extremities/innervation/physiology ; Female ; Interneurons/cytology/metabolism ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Motor Neurons/*cytology/*physiology ; Muscle, Skeletal/cytology/innervation/physiology ; Nerve Net/cytology/physiology ; Neuroanatomical Tract-Tracing Techniques ; Neurogenesis/*physiology ; Proprioception/physiology ; Spinal Cord/cytology/physiology ; Synapses/metabolism ; Time Factors ; Walking/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    BRCA1 tumour suppression occurs via heterochromatin-mediated silencing (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-09
    Description: Mutations in the tumour suppressor gene BRCA1 lead to breast and/or ovarian cancer. Here we show that loss of Brca1 in mice results in transcriptional de-repression of the tandemly repeated satellite DNA. Brca1 deficiency is accompanied by a reduction of condensed DNA regions in the genome and loss of ubiquitylation of histone H2A at satellite repeats. BRCA1 binds to satellite DNA regions and ubiquitylates H2A in vivo. Ectopic expression of H2A fused to ubiquitin reverses the effects of BRCA1 loss, indicating that BRCA1 maintains heterochromatin structure via ubiquitylation of histone H2A. Satellite DNA de-repression was also observed in mouse and human BRCA1-deficient breast cancers. Ectopic expression of satellite DNA can phenocopy BRCA1 loss in centrosome amplification, cell-cycle checkpoint defects, DNA damage and genomic instability. We propose that the role of BRCA1 in maintaining global heterochromatin integrity accounts for many of its tumour suppressor functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240576/" 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/PMC3240576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Quan -- Pao, Gerald M -- Huynh, Alexis M -- Suh, Hoonkyo -- Tonnu, Nina -- Nederlof, Petra M -- Gage, Fred H -- Verma, Inder M -- NS50217/NS/NINDS NIH HHS/ -- NS52842/NS/NINDS NIH HHS/ -- R01 NS050217/NS/NINDS NIH HHS/ -- R01 NS050217-05/NS/NINDS NIH HHS/ -- R01 NS052842/NS/NINDS NIH HHS/ -- R01 NS052842-04/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Sep 7;477(7363):179-84. doi: 10.1038/nature10371.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21901007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/deficiency/genetics/*metabolism ; Breast/cytology ; Breast Neoplasms/*genetics/pathology ; Cell Line, Tumor ; Cells, Cultured ; DNA, Satellite/genetics ; Epithelial Cells/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Genes, BRCA1/*physiology ; Genomic Instability/genetics ; HeLa Cells ; Heterochromatin/*genetics/*metabolism ; Histones/metabolism ; Humans ; Mice ; Ovarian Neoplasms/genetics ; RNA, Messenger/genetics ; Transcription, Genetic/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitinated Proteins/metabolism ; Ubiquitination
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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