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  • 1
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    Genetic dissection of an amygdala microcircuit that gates conditioned fear (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-12
    Description: The role of different amygdala nuclei (neuroanatomical subdivisions) in processing Pavlovian conditioned fear has been studied extensively, but the function of the heterogeneous neuronal subtypes within these nuclei remains poorly understood. Here we use molecular genetic approaches to map the functional connectivity of a subpopulation of GABA-containing neurons, located in the lateral subdivision of the central amygdala (CEl), which express protein kinase C-delta (PKC-delta). Channelrhodopsin-2-assisted circuit mapping in amygdala slices and cell-specific viral tracing indicate that PKC-delta(+) neurons inhibit output neurons in the medial central amygdala (CEm), and also make reciprocal inhibitory synapses with PKC-delta(-) neurons in CEl. Electrical silencing of PKC-delta(+) neurons in vivo suggests that they correspond to physiologically identified units that are inhibited by the conditioned stimulus, called CEl(off) units. This correspondence, together with behavioural data, defines an inhibitory microcircuit in CEl that gates CEm output to control the level of conditioned freezing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597095/" 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/PMC3597095/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haubensak, Wulf -- Kunwar, Prabhat S -- Cai, Haijiang -- Ciocchi, Stephane -- Wall, Nicholas R -- Ponnusamy, Ravikumar -- Biag, Jonathan -- Dong, Hong-Wei -- Deisseroth, Karl -- Callaway, Edward M -- Fanselow, Michael S -- Luthi, Andreas -- Anderson, David J -- 1 R01 MH085082-01A1/MH/NIMH NIH HHS/ -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 MH063912-09/MH/NIMH NIH HHS/ -- R01 MH063912-09S1/MH/NIMH NIH HHS/ -- R01 MH063912-10/MH/NIMH NIH HHS/ -- R01 MH085082/MH/NIMH NIH HHS/ -- R01 MH085082-01A1/MH/NIMH NIH HHS/ -- RC2 NS069464/NS/NINDS NIH HHS/ -- RC2 NS069464-01/NS/NINDS NIH HHS/ -- RC2 NS069464-02/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):270-6. doi: 10.1038/nature09553.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068836" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/anatomy & histology/cytology/enzymology/*physiology ; Animals ; Axonal Transport ; Cells, Cultured ; Conditioning, Classical/*physiology ; Fear/*physiology ; Female ; Freezing Reaction, Cataleptic ; Genetic Techniques ; Humans ; Male ; Mice ; Mice, Transgenic ; Neural Inhibition/*physiology ; Neural Pathways/cytology/enzymology/*physiology ; Neurons/enzymology/metabolism ; Protein Kinase C-delta/deficiency/genetics/metabolism ; Synapses/metabolism ; gamma-Aminobutyric Acid/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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  • 2
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    Scalable control of mounting and attack by Esr1+ neurons in the ventromedial hypothalamus (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-04-18
    Description: Social behaviours, such as aggression or mating, proceed through a series of appetitive and consummatory phases that are associated with increasing levels of arousal. How such escalation is encoded in the brain, and linked to behavioural action selection, remains an unsolved problem in neuroscience. The ventrolateral subdivision of the murine ventromedial hypothalamus (VMHvl) contains neurons whose activity increases during male-male and male-female social encounters. Non-cell-type-specific optogenetic activation of this region elicited attack behaviour, but not mounting. We have identified a subset of VMHvl neurons marked by the oestrogen receptor 1 (Esr1), and investigated their role in male social behaviour. Optogenetic manipulations indicated that Esr1(+) (but not Esr1(-)) neurons are sufficient to initiate attack, and that their activity is continuously required during ongoing agonistic behaviour. Surprisingly, weaker optogenetic activation of these neurons promoted mounting behaviour, rather than attack, towards both males and females, as well as sniffing and close investigation. Increasing photostimulation intensity could promote a transition from close investigation and mounting to attack, within a single social encounter. Importantly, time-resolved optogenetic inhibition experiments revealed requirements for Esr1(+) neurons in both the appetitive (investigative) and the consummatory phases of social interactions. Combined optogenetic activation and calcium imaging experiments in vitro, as well as c-Fos analysis in vivo, indicated that increasing photostimulation intensity increases both the number of active neurons and the average level of activity per neuron. These data suggest that Esr1(+) neurons in VMHvl control the progression of a social encounter from its appetitive through its consummatory phases, in a scalable manner that reflects the number or type of active neurons in the population.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4098836/" 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/PMC4098836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Hyosang -- Kim, Dong-Wook -- Remedios, Ryan -- Anthony, Todd E -- Chang, Angela -- Madisen, Linda -- Zeng, Hongkui -- Anderson, David J -- 1F32HD055198-01/HD/NICHD NIH HHS/ -- 1K99NS074077/NS/NINDS NIH HHS/ -- R01 MH085082/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 May 29;509(7502):627-32. doi: 10.1038/nature13169. Epub 2014 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Biology and Biological Engineering 156-29, California Institute of Technology, Pasadena, California 91125, USA [2] Howard Hughes Medical Institute, Pasadena, California 91125, USA. ; Computation and Neural Systems, California Institute of Technology, Pasadena, California 91125, USA. ; Division of Biology and Biological Engineering 156-29, California Institute of Technology, Pasadena, California 91125, USA. ; Allen Institute for Brain Science, Seattle, Washington 98103, USA. ; 1] Division of Biology and Biological Engineering 156-29, California Institute of Technology, Pasadena, California 91125, USA [2] Howard Hughes Medical Institute, Pasadena, California 91125, USA [3] Computation and Neural Systems, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739975" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Estrogen Receptor alpha/*metabolism ; Female ; Integrases/genetics/metabolism ; Male ; Mice ; Neurons/*metabolism ; Optogenetics ; Sexual Behavior, Animal/*physiology ; Ventromedial Hypothalamic Nucleus/*cytology/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Functional identification of an aggression locus in the mouse hypothalamus (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-11
    Description: Electrical stimulation of certain hypothalamic regions in cats and rodents can elicit attack behaviour, but the exact location of relevant cells within these regions, their requirement for naturally occurring aggression and their relationship to mating circuits have not been clear. Genetic methods for neural circuit manipulation in mice provide a potentially powerful approach to this problem, but brain-stimulation-evoked aggression has never been demonstrated in this species. Here we show that optogenetic, but not electrical, stimulation of neurons in the ventromedial hypothalamus, ventrolateral subdivision (VMHvl) causes male mice to attack both females and inanimate objects, as well as males. Pharmacogenetic silencing of VMHvl reversibly inhibits inter-male aggression. Immediate early gene analysis and single unit recordings from VMHvl during social interactions reveal overlapping but distinct neuronal subpopulations involved in fighting and mating. Neurons activated during attack are inhibited during mating, suggesting a potential neural substrate for competition between these opponent social behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075820/" 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/PMC3075820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Dayu -- Boyle, Maureen P -- Dollar, Piotr -- Lee, Hyosang -- Lein, E S -- Perona, Pietro -- Anderson, David J -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 10;470(7333):221-6. doi: 10.1038/nature09736.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, 1201 East California Boulevard, Pasadena, California 91125, USA. dayu.lin@nyumc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307935" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Electric Stimulation ; Electrophysiology ; Female ; Gene Expression Regulation ; Genes, fos/genetics ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neural Inhibition/genetics/physiology ; Neural Pathways/physiology ; Neurons/physiology ; Sexual Behavior, Animal/physiology ; Ventromedial Hypothalamic Nucleus/anatomy & ; histology/*cytology/metabolism/*physiology
    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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    Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Microtubules have pivotal roles in fundamental cellular processes and are targets of antitubulin chemotherapeutics. Microtubule-targeted agents such as Taxol and vincristine are prescribed widely for various malignancies, including ovarian and breast adenocarcinomas, non-small-cell lung cancer, leukaemias and lymphomas. These agents arrest cells in mitosis and subsequently induce cell death through poorly defined mechanisms. The strategies that resistant tumour cells use to evade death induced by antitubulin agents are also unclear. Here we show that the pro-survival protein MCL1 (ref. 3) is a crucial regulator of apoptosis triggered by antitubulin chemotherapeutics. During mitotic arrest, MCL1 protein levels decline markedly, through a post-translational mechanism, potentiating cell death. Phosphorylation of MCL1 directs its interaction with the tumour-suppressor protein FBW7, which is the substrate-binding component of a ubiquitin ligase complex. The polyubiquitylation of MCL1 then targets it for proteasomal degradation. The degradation of MCL1 was blocked in patient-derived tumour cells that lacked FBW7 or had loss-of-function mutations in FBW7, conferring resistance to antitubulin agents and promoting chemotherapeutic-induced polyploidy. Additionally, primary tumour samples were enriched for FBW7 inactivation and elevated MCL1 levels, underscoring the prominent roles of these proteins in oncogenesis. Our findings suggest that profiling the FBW7 and MCL1 status of tumours, in terms of protein levels, messenger RNA levels and genetic status, could be useful to predict the response of patients to antitubulin chemotherapeutics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wertz, Ingrid E -- Kusam, Saritha -- Lam, Cynthia -- Okamoto, Toru -- Sandoval, Wendy -- Anderson, Daniel J -- Helgason, Elizabeth -- Ernst, James A -- Eby, Mike -- Liu, Jinfeng -- Belmont, Lisa D -- Kaminker, Josh S -- O'Rourke, Karen M -- Pujara, Kanan -- Kohli, Pawan Bir -- Johnson, Adam R -- Chiu, Mark L -- Lill, Jennie R -- Jackson, Peter K -- Fairbrother, Wayne J -- Seshagiri, Somasekar -- Ludlam, Mary J C -- Leong, Kevin G -- Dueber, Erin C -- Maecker, Heather -- Huang, David C S -- Dixit, Vishva M -- CA043540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- England -- Nature. 2011 Mar 3;471(7336):110-4. doi: 10.1038/nature09779.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA. ingrid@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368834" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Transformation, Neoplastic/drug effects ; Drug Resistance, Neoplasm ; F-Box Proteins/genetics/*metabolism ; Fibroblasts ; Humans ; Mice ; Mitosis/drug effects ; Myeloid Cell Leukemia Sequence 1 Protein ; Paclitaxel/pharmacology ; Pharmacogenetics ; Phosphorylation/drug effects ; Polyploidy ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-bcl-2/deficiency/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Tubulin/*metabolism ; Tubulin Modulators/*pharmacology ; Ubiquitin-Protein Ligases/deficiency/genetics/*metabolism ; Vincristine/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-05
    Description: Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have broad therapeutic effects. Small molecule ATP-competitive RAF kinase inhibitors have potent antitumour effects on mutant BRAF(V600E) tumours but, in contrast to mitogen-activated protein kinase kinase (MEK) inhibitors, are not potent against RAS mutant tumour models, despite RAF functioning as a key effector downstream of RAS and upstream of MEK. Here we show that ATP-competitive RAF inhibitors have two opposing mechanisms of action depending on the cellular context. In BRAF(V600E) tumours, RAF inhibitors effectively block the mitogen-activated protein kinase (MAPK) signalling pathway and decrease tumour growth. Notably, in KRAS mutant and RAS/RAF wild-type tumours, RAF inhibitors activate the RAF-MEK-ERK pathway in a RAS-dependent manner, thus enhancing tumour growth in some xenograft models. Inhibitor binding activates wild-type RAF isoforms by inducing dimerization, membrane localization and interaction with RAS-GTP. These events occur independently of kinase inhibition and are, instead, linked to direct conformational effects of inhibitors on the RAF kinase domain. On the basis of these findings, we demonstrate that ATP-competitive kinase inhibitors can have opposing functions as inhibitors or activators of signalling pathways, depending on the cellular context. Furthermore, this work provides new insights into the therapeutic use of ATP-competitive RAF inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatzivassiliou, Georgia -- Song, Kyung -- Yen, Ivana -- Brandhuber, Barbara J -- Anderson, Daniel J -- Alvarado, Ryan -- Ludlam, Mary J C -- Stokoe, David -- Gloor, Susan L -- Vigers, Guy -- Morales, Tony -- Aliagas, Ignacio -- Liu, Bonnie -- Sideris, Steve -- Hoeflich, Klaus P -- Jaiswal, Bijay S -- Seshagiri, Somasekar -- Koeppen, Hartmut -- Belvin, Marcia -- Friedman, Lori S -- Malek, Shiva -- England -- Nature. 2010 Mar 18;464(7287):431-5. doi: 10.1038/nature08833. Epub 2010 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, South San Francisco, California 94080, USA. hatzivassiliou.georgia@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20130576" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Benzamides/pharmacology ; Cell Line ; Cell Membrane/drug effects/metabolism ; Cell Proliferation/drug effects ; Diphenylamine/analogs & derivatives/pharmacology ; Enzyme Activation/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Indenes/pharmacology ; Indoles/pharmacology ; MAP Kinase Signaling System/*drug effects ; Mice ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Neoplasms/drug therapy/enzymology/metabolism/*pathology ; Protein Kinase Inhibitors/*pharmacology/therapeutic use ; Protein Multimerization ; Protein Structure, Tertiary ; Protein Transport/drug effects ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins B-raf/antagonists & ; inhibitors/chemistry/genetics/metabolism ; Proto-Oncogene Proteins c-raf/deficiency/genetics/metabolism ; Pyrazoles/pharmacology ; Sulfonamides/pharmacology ; Xenograft Model Antitumor Assays ; raf Kinases/*antagonists & inhibitors/chemistry/genetics/*metabolism ; ras Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Genetic identification of C fibres that detect massage-like stroking of hairy skin in vivo (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-01
    Description: Stroking of the skin produces pleasant sensations that can occur during social interactions with conspecifics, such as grooming. Despite numerous physiological studies (reviewed in ref. 2), molecularly defined sensory neurons that detect pleasant stroking of hairy skin in vivo have not been reported. Previously, we identified a rare population of unmyelinated sensory neurons in mice that express the G-protein-coupled receptor MRGPRB4 (refs 5, 6). These neurons exclusively innervate hairy skin with large terminal arborizations that resemble the receptive fields of C-tactile (CT) afferents in humans. Unlike other molecularly defined mechanosensory C-fibre subtypes, MRGPRB4(+) neurons could not be detectably activated by sensory stimulation of the skin ex vivo. Therefore, we developed a preparation for calcium imaging in the spinal projections of these neurons during stimulation of the periphery in intact mice. Here we show that MRGPRB4(+) neurons are activated by massage-like stroking of hairy skin, but not by noxious punctate mechanical stimulation. By contrast, a different population of C fibres expressing MRGPRD was activated by pinching but not by stroking, consistent with previous physiological and behavioural data. Pharmacogenetic activation of Mrgprb4-expressing neurons in freely behaving mice promoted conditioned place preference, indicating that such activation is positively reinforcing and/or anxiolytic. These data open the way to understanding the function of MRGPRB4 neurons during natural behaviours, and provide a general approach to the functional characterization of genetically identified subsets of somatosensory neurons in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563425/" 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/PMC3563425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vrontou, Sophia -- Wong, Allan M -- Rau, Kristofer K -- Koerber, H Richard -- Anderson, David J -- 5P01NS-48499/NS/NINDS NIH HHS/ -- 5R01 NS023476/NS/NINDS NIH HHS/ -- P01 NS048499/NS/NINDS NIH HHS/ -- R01 NS023725/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jan 31;493(7434):669-73. doi: 10.1038/nature11810.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 156-29, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23364746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Profiling ; Mice ; Nerve Fibers, Unmyelinated/*metabolism ; Receptors, G-Protein-Coupled/*genetics/metabolism ; Sensory Receptor Cells/metabolism ; Skin/*innervation ; Touch/*genetics
    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 neuron-restrictive silencer factor (NRSF): a coordinate repressor of multiple neuron-specific genes (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-03
    Description: The neuron-restrictive silencer factor (NRSF) binds a DNA sequence element, called the neuron-restrictive silencer element (NRSE), that represses neuronal gene transcription in nonneuronal cells. Consensus NRSEs have been identified in 18 neuron-specific genes. Complementary DNA clones encoding a functional fragment of NRSF were isolated and found to encode a novel protein containing eight noncanonical zinc fingers. Expression of NRSF mRNA was detected in most nonneuronal tissues at several developmental stages. In the nervous system, NRSF mRNA was detected in undifferentiated neuronal progenitors, but not in differentiated neurons. NRSF represents the first example of a vertebrate silencer protein that potentially regulates a large battery of cell type-specific genes, and therefore may function as a master negative regulator of neurogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schoenherr, C J -- Anderson, D J -- NS23476/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1360-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871435" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cell Line ; Central Nervous System/chemistry/cytology/embryology ; DNA, Complementary/genetics ; DNA-Binding Proteins/analysis/chemistry/genetics/*physiology ; *Gene Expression Regulation ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Mice ; Molecular Sequence Data ; Nerve Growth Factors/genetics ; Nerve Tissue Proteins/genetics ; Neurons/chemistry ; *Regulatory Sequences, Nucleic Acid ; Repressor Proteins/physiology ; Sodium Channels/genetics ; Stem Cells/chemistry ; Synapsins/genetics ; Transcription Factors/analysis/chemistry/genetics/*physiology ; Transcription, Genetic ; Transfection ; Zinc Fingers
    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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