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  • Mice  (446)
  • 2010-2014  (446)
  • 2010  (446)
  • 1
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    A population-specific HTR2B stop codon predisposes to severe impulsivity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency 〉 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" 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/PMC3183507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, Laura -- Doly, Stephane -- Kaprio, Jaakko -- Yuan, Qiaoping -- Tikkanen, Roope -- Paunio, Tiina -- Zhou, Zhifeng -- Wedenoja, Juho -- Maroteaux, Luc -- Diaz, Silvina -- Belmer, Arnaud -- Hodgkinson, Colin A -- Dell'osso, Liliana -- Suvisaari, Jaana -- Coccaro, Emil -- Rose, Richard J -- Peltonen, Leena -- Virkkunen, Matti -- Goldman, David -- AA-09203/AA/NIAAA NIH HHS/ -- AA-12502/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z01 AA000301-10/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, Maryland 20852, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Case-Control Studies ; Cell Line ; Female ; Finland ; Founder Effect ; Gene Expression Regulation ; Gene Knockout Techniques ; Genotype ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mice, 129 Strain ; Mice, Knockout ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Receptor, Serotonin, 5-HT2B/*genetics/*metabolism ; Testosterone/blood/cerebrospinal fluid
    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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    mTORC1 controls fasting-induced ketogenesis and its modulation by ageing (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: The multi-component mechanistic target of rapamycin complex 1 (mTORC1) kinase is the central node of a mammalian pathway that coordinates cell growth with the availability of nutrients, energy and growth factors. Progress has been made in the identification of mTORC1 pathway components and in understanding their functions in cells, but there is relatively little known about the role of the pathway in vivo. Specifically, we have little knowledge regarding the role mTOCR1 has in liver physiology. In fasted animals, the liver performs numerous functions that maintain whole-body homeostasis, including the production of ketone bodies for peripheral tissues to use as energy sources. Here we show that mTORC1 controls ketogenesis in mice in response to fasting. We find that liver-specific loss of TSC1 (tuberous sclerosis 1), an mTORC1 inhibitor, leads to a fasting-resistant increase in liver size, and to a pronounced defect in ketone body production and ketogenic gene expression on fasting. The loss of raptor (regulatory associated protein of mTOR, complex 1) an essential mTORC1 component, has the opposite effects. In addition, we find that the inhibition of mTORC1 is required for the fasting-induced activation of PPARalpha (peroxisome proliferator activated receptor alpha), the master transcriptional activator of ketogenic genes, and that suppression of NCoR1 (nuclear receptor co-repressor 1), a co-repressor of PPARalpha, reactivates ketogenesis in cells and livers with hyperactive mTORC1 signalling. Like livers with activated mTORC1, livers from aged mice have a defect in ketogenesis, which correlates with an increase in mTORC1 signalling. Moreover, we show that the suppressive effects of mTORC1 activation and ageing on PPARalpha activity and ketone production are not additive, and that mTORC1 inhibition is sufficient to prevent the ageing-induced defect in ketogenesis. Thus, our findings reveal that mTORC1 is a key regulator of PPARalpha function and hepatic ketogenesis and suggest a role for mTORC1 activity in promoting the ageing of the liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sengupta, Shomit -- Peterson, Timothy R -- Laplante, Mathieu -- Oh, Stephanie -- Sabatini, David M -- CA103866/CA/NCI NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-04/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 23;468(7327):1100-4. doi: 10.1038/nature09584.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179166" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Fasting/*metabolism ; *Gene Expression Regulation ; Humans ; Ketone Bodies/*biosynthesis/metabolism ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multiprotein Complexes ; Nuclear Receptor Co-Repressor 1/metabolism ; PPAR alpha/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; TOR Serine-Threonine Kinases
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    The histone variant macroH2A suppresses melanoma progression through regulation of CDK8 (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Cancer is a disease consisting of both genetic and epigenetic changes. Although increasing evidence demonstrates that tumour progression entails chromatin-mediated changes such as DNA methylation, the role of histone variants in cancer initiation and progression currently remains unclear. Histone variants replace conventional histones within the nucleosome and confer unique biological functions to chromatin. Here we report that the histone variant macroH2A (mH2A) suppresses tumour progression of malignant melanoma. Loss of mH2A isoforms, histone variants generally associated with condensed chromatin and fine-tuning of developmental gene expression programs, is positively correlated with increasing malignant phenotype of melanoma cells in culture and human tissue samples. Knockdown of mH2A isoforms in melanoma cells of low malignancy results in significantly increased proliferation and migration in vitro and growth and metastasis in vivo. Restored expression of mH2A isoforms rescues these malignant phenotypes in vitro and in vivo. We demonstrate that the tumour-promoting function of mH2A loss is mediated, at least in part, through direct transcriptional upregulation of CDK8. Suppression of CDK8, a colorectal cancer oncogene, inhibits proliferation of melanoma cells, and knockdown of CDK8 in cells depleted of mH2A suppresses the proliferative advantage induced by mH2A loss. Moreover, a significant inverse correlation between mH2A and CDK8 expression levels exists in melanoma patient samples. Taken together, our results demonstrate that mH2A is a critical component of chromatin that suppresses the development of malignant melanoma, a highly intractable cutaneous neoplasm.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057940/" 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/PMC3057940/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapoor, Avnish -- Goldberg, Matthew S -- Cumberland, Lara K -- Ratnakumar, Kajan -- Segura, Miguel F -- Emanuel, Patrick O -- Menendez, Silvia -- Vardabasso, Chiara -- Leroy, Gary -- Vidal, Claudia I -- Polsky, David -- Osman, Iman -- Garcia, Benjamin A -- Hernando, Eva -- Bernstein, Emily -- 5P30CA016087-27/CA/NCI NIH HHS/ -- CA109388/CA/NCI NIH HHS/ -- R21 CA150117/CA/NCI NIH HHS/ -- R21 CA150117-01/CA/NCI NIH HHS/ -- R21 CA150117-02/CA/NCI NIH HHS/ -- R21CA150117/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1105-9. doi: 10.1038/nature09590.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin-Dependent Kinase 8/*metabolism ; Disease Progression ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HCT116 Cells ; Histones/deficiency/genetics/*metabolism ; Humans ; Melanoma/*pathology/physiopathology ; Melanoma, Experimental ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology/physiopathology ; Rats ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cortical representations of olfactory input by trans-synaptic tracing (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: In the mouse, each class of olfactory receptor neurons expressing a given odorant receptor has convergent axonal projections to two specific glomeruli in the olfactory bulb, thereby creating an odour map. However, it is unclear how this map is represented in the olfactory cortex. Here we combine rabies-virus-dependent retrograde mono-trans-synaptic labelling with genetics to control the location, number and type of 'starter' cortical neurons, from which we trace their presynaptic neurons. We find that individual cortical neurons receive input from multiple mitral cells representing broadly distributed glomeruli. Different cortical areas represent the olfactory bulb input differently. For example, the cortical amygdala preferentially receives dorsal olfactory bulb input, whereas the piriform cortex samples the whole olfactory bulb without obvious bias. These differences probably reflect different functions of these cortical areas in mediating innate odour preference or associative memory. The trans-synaptic labelling method described here should be widely applicable to mapping connections throughout the mouse nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073090/" 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/PMC3073090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyamichi, Kazunari -- Amat, Fernando -- Moussavi, Farshid -- Wang, Chen -- Wickersham, Ian -- Wall, Nicholas R -- Taniguchi, Hiroki -- Tasic, Bosiljka -- Huang, Z Josh -- He, Zhigang -- Callaway, Edward M -- Horowitz, Mark A -- Luo, Liqun -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 NS050835/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 14;472(7342):191-6. doi: 10.1038/nature09714. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HHMI/Department of Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179085" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/anatomy & histology/cytology/physiology ; Animals ; Axons/physiology ; Bias (Epidemiology) ; Brain Mapping ; HEK293 Cells ; Humans ; Mice ; Mice, Transgenic ; *Neuroanatomical Tract-Tracing Techniques ; Odors/analysis ; Olfactory Bulb/anatomy & histology/cytology/physiology ; Olfactory Pathways/anatomy & histology/*cytology/*physiology ; Olfactory Perception/genetics/*physiology ; Olfactory Receptor Neurons/cytology/physiology ; Rabies virus/physiology ; Synapses/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Preplay of future place cell sequences by hippocampal cellular assemblies (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: During spatial exploration, hippocampal neurons show a sequential firing pattern in which individual neurons fire specifically at particular locations along the animal's trajectory (place cells). According to the dominant model of hippocampal cell assembly activity, place cell firing order is established for the first time during exploration, to encode the spatial experience, and is subsequently replayed during rest or slow-wave sleep for consolidation of the encoded experience. Here we report that temporal sequences of firing of place cells expressed during a novel spatial experience occurred on a significant number of occasions during the resting or sleeping period preceding the experience. This phenomenon, which is called preplay, occurred in disjunction with sequences of replay of a familiar experience. These results suggest that internal neuronal dynamics during resting or sleep organize hippocampal cellular assemblies into temporal sequences that contribute to the encoding of a related novel experience occurring in the future.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104398/" 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/PMC3104398/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dragoi, George -- Tonegawa, Susumu -- P50 MH058880/MH/NIMH NIH HHS/ -- P50 MH058880-06/MH/NIMH NIH HHS/ -- P50 MH058880-07/MH/NIMH NIH HHS/ -- P50 MH058880-08/MH/NIMH NIH HHS/ -- P50 MH058880-09/MH/NIMH NIH HHS/ -- P50 MH058880-10/MH/NIMH NIH HHS/ -- P50-MH58880/MH/NIMH NIH HHS/ -- R01 MH078821/MH/NIMH NIH HHS/ -- R01 MH078821-13/MH/NIMH NIH HHS/ -- R01 MH078821-14/MH/NIMH NIH HHS/ -- R01 MH078821-15/MH/NIMH NIH HHS/ -- R01 MH078821-16/MH/NIMH NIH HHS/ -- R01 MH078821-17/MH/NIMH NIH HHS/ -- R01-MH078821/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jan 20;469(7330):397-401. doi: 10.1038/nature09633. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Picower Institute for Learning and Memory, RIKEN-MIT Center for Neural Circuit Genetics, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. gdragoi@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179088" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bayes Theorem ; Eating ; Food ; Hippocampus/*cytology/*physiology ; Memory/physiology ; Mice ; Mice, Inbred C57BL ; *Models, Neurological ; Neurons/*physiology ; Orientation/physiology ; Rest/physiology ; Sleep/physiology ; Space Perception/physiology ; Time Factors
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Behavioural neuroscience: A gene for impulsivity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelsoe, John R -- England -- Nature. 2010 Dec 23;468(7327):1049-50. doi: 10.1038/4681049a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crime/statistics & numerical data ; Finland ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mutation/genetics ; Receptor, Serotonin, 5-HT2B/*genetics ; Violence/statistics & numerical data
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    The assembly of a GTPase-kinase signalling complex by a bacterial catalytic scaffold (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-21
    Description: The fidelity and specificity of information flow within a cell is controlled by scaffolding proteins that assemble and link enzymes into signalling circuits. These circuits can be inhibited by bacterial effector proteins that post-translationally modify individual pathway components. However, there is emerging evidence that pathogens directly organize higher-order signalling networks through enzyme scaffolding, and the identity of the effectors and their mechanisms of action are poorly understood. Here we identify the enterohaemorrhagic Escherichia coli O157:H7 type III effector EspG as a regulator of endomembrane trafficking using a functional screen, and report ADP-ribosylation factor (ARF) GTPases and p21-activated kinases (PAKs) as its relevant host substrates. The 2.5 A crystal structure of EspG in complex with ARF6 shows how EspG blocks GTPase-activating-protein-assisted GTP hydrolysis, revealing a potent mechanism of GTPase signalling inhibition at organelle membranes. In addition, the 2.8 A crystal structure of EspG in complex with the autoinhibitory Ialpha3-helix of PAK2 defines a previously unknown catalytic site in EspG and provides an allosteric mechanism of kinase activation by a bacterial effector. Unexpectedly, ARF and PAKs are organized on adjacent surfaces of EspG, indicating its role as a 'catalytic scaffold' that effectively reprograms cellular events through the functional assembly of GTPase-kinase signalling complex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3675890/" 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/PMC3675890/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selyunin, Andrey S -- Sutton, Sarah E -- Weigele, Bethany A -- Reddick, L Evan -- Orchard, Robert C -- Bresson, Stefan M -- Tomchick, Diana R -- Alto, Neal M -- 1R01AI083359-01/AI/NIAID NIH HHS/ -- 5T32AI007520-12/AI/NIAID NIH HHS/ -- R01 AI083359/AI/NIAID NIH HHS/ -- R01 AI083359-01/AI/NIAID NIH HHS/ -- T32 AI007520/AI/NIAID NIH HHS/ -- T32 AI007520-12/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Jan 6;469(7328):107-11. doi: 10.1038/nature09593. Epub 2010 Dec 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8816, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21170023" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factors/chemistry/*metabolism ; Allosteric Regulation ; Animals ; *Biocatalysis ; Biological Transport ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Endoplasmic Reticulum/metabolism ; Enzyme Activation ; Escherichia coli O157/*chemistry/metabolism ; Escherichia coli Proteins/chemistry/*metabolism ; Golgi Apparatus/metabolism ; Guanosine Triphosphate/chemistry/metabolism ; Humans ; Hydrolysis ; Intracellular Membranes/metabolism ; Mice ; Models, Molecular ; Protein Binding ; Protein Conformation ; Protein Interaction Mapping ; Protein Unfolding ; Rats ; *Signal Transduction ; Two-Hybrid System Techniques ; p21-Activated Kinases/chemistry/*metabolism
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  • 8
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    Spatially asymmetric reorganization of inhibition establishes a motion-sensitive circuit (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-21
    Description: Spatial asymmetries in neural connectivity have an important role in creating basic building blocks of neuronal processing. A key circuit module of directionally selective (DS) retinal ganglion cells is a spatially asymmetric inhibitory input from starburst amacrine cells. It is not known how and when this circuit asymmetry is established during development. Here we photostimulate mouse starburst cells targeted with channelrhodopsin-2 (refs 6-8) while recording from a single genetically labelled type of DS cell. We follow the spatial distribution of synaptic strengths between starburst and DS cells during early postnatal development before these neurons can respond to a physiological light stimulus, and confirm connectivity by monosynaptically restricted trans-synaptic rabies viral tracing. We show that asymmetry develops rapidly over a 2-day period through an intermediate state in which random or symmetric synaptic connections have been established. The development of asymmetry involves the spatially selective reorganization of inhibitory synaptic inputs. Intriguingly, the spatial distribution of excitatory synaptic inputs from starburst cells is significantly more symmetric than that of the inhibitory inputs at the end of this developmental period. Our work demonstrates a rapid developmental switch from a symmetric to asymmetric input distribution for inhibition in the neural circuit of a principal cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonehara, Keisuke -- Balint, Kamill -- Noda, Masaharu -- Nagel, Georg -- Bamberg, Ernst -- Roska, Botond -- England -- Nature. 2011 Jan 20;469(7330):407-10. doi: 10.1038/nature09711. Epub 2010 Dec 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21170022" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Amacrine Cells/metabolism/physiology/radiation effects ; Animals ; Female ; Light ; Male ; Mice ; *Models, Neurological ; *Motion ; Motion Perception/*physiology ; Neural Inhibition/*physiology ; Neural Pathways/*physiology ; Neuroanatomical Tract-Tracing Techniques ; Photic Stimulation ; Rabies virus/genetics/isolation & purification/physiology ; Retina/cytology/growth & development/*physiology ; Retinal Ganglion Cells/physiology ; Rhodopsin/genetics/metabolism ; Synapses/metabolism
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  • 9
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    Neuroscience: Angelman syndrome connections (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheiffele, Peter -- Beg, Asim A -- England -- Nature. 2010 Dec 16;468(7326):907-8. doi: 10.1038/468907a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164477" target="_blank"〉PubMed〈/a〉
    Keywords: Angelman Syndrome/complications/*genetics/*pathology/physiopathology ; Animals ; Autistic Disorder/genetics/physiopathology ; Dendrites/metabolism/pathology ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Learning Disorders/complications/genetics/physiopathology ; Mice ; Nerve Net/metabolism/*pathology ; Phosphorylation ; Synapses/metabolism/pathology ; Ubiquitin-Protein Ligases/deficiency/*genetics/metabolism
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    CRTC3 links catecholamine signalling to energy balance (2010)
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    Publication Date: 2010-12-18
    Description: The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of beta-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in lipolysis and fatty-acid oxidation. Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Here we show that the cAMP response element binding (CREB) coactivator Crtc3 promotes obesity by attenuating beta-adrenergic receptor signalling in adipose tissue. Crtc3 was activated in response to catecholamine signals, when it reduced adenyl cyclase activity by upregulating the expression of Rgs2, a GTPase-activating protein that also inhibits adenyl cyclase activity. As a common human CRTC3 variant with increased transcriptional activity is associated with adiposity in two distinct Mexican-American cohorts, these results suggest that adipocyte CRTC3 may play a role in the development of obesity in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025711/" 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/PMC3025711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Youngsup -- Altarejos, Judith -- Goodarzi, Mark O -- Inoue, Hiroshi -- Guo, Xiuqing -- Berdeaux, Rebecca -- Kim, Jeong-Ho -- Goode, Jason -- Igata, Motoyuki -- Paz, Jose C -- Hogan, Meghan F -- Singh, Pankaj K -- Goebel, Naomi -- Vera, Lili -- Miller, Nina -- Cui, Jinrui -- Jones, Michelle R -- CHARGE Consortium -- GIANT Consortium -- Chen, Yii-Der I -- Taylor, Kent D -- Hsueh, Willa A -- Rotter, Jerome I -- Montminy, Marc -- M01 RR000425-36/RR/NCRR NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- N01 HC095159/HC/NHLBI NIH HHS/ -- N01-HC95159/HC/NHLBI NIH HHS/ -- N02 HL64278/HL/NHLBI NIH HHS/ -- N02-HL64278/HL/NHLBI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-09/DK/NIDDK NIH HHS/ -- P30-DK063491/DK/NIDDK NIH HHS/ -- R01 DK033651/DK/NIDDK NIH HHS/ -- R01 DK049777/DK/NIDDK NIH HHS/ -- R01 DK049777-18/DK/NIDDK NIH HHS/ -- R01 DK079888/DK/NIDDK NIH HHS/ -- R01 DK079888-05/DK/NIDDK NIH HHS/ -- R01 HL071205/HL/NHLBI NIH HHS/ -- R01 HL071205-05/HL/NHLBI NIH HHS/ -- R01 HL088457/HL/NHLBI NIH HHS/ -- R01 HL088457-04/HL/NHLBI NIH HHS/ -- R01-DK049777/DK/NIDDK NIH HHS/ -- R01-DK083834/DK/NIDDK NIH HHS/ -- R01-DK79888/DK/NIDDK NIH HHS/ -- R01-HL088457/HL/NHLBI NIH HHS/ -- R01-L071205/PHS HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- R37 DK083834-26/DK/NIDDK NIH HHS/ -- R37 DK083834-27/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Dec 16;468(7326):933-9. doi: 10.1038/nature09564.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164481" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/drug effects/metabolism ; Adipose Tissue/drug effects/metabolism ; Animals ; Body Temperature ; Catecholamines/*metabolism ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/antagonists & inhibitors/metabolism ; Dietary Fats/pharmacology ; *Energy Metabolism/genetics ; Female ; Genome-Wide Association Study ; Humans ; Insulin Resistance ; Mexican Americans/genetics ; Mice ; Obesity/chemically induced/genetics/metabolism ; Phosphorylation ; RGS Proteins/biosynthesis/genetics ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/drug effects/*physiology ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
    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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