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  • 1
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    alpha-Klotho as a regulator of calcium homeostasis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: alpha-klotho was identified as a gene associated with premature aging-like phenotypes characterized by short lifespan. In mice, we found the molecular association of alpha-Klotho (alpha-Kl) and Na+,K+-adenosine triphosphatase (Na+,K+-ATPase) and provide evidence for an increase of abundance of Na+,K+-ATPase at the plasma membrane. Low concentrations of extracellular free calcium ([Ca2+]e) rapidly induce regulated parathyroid hormone (PTH) secretion in an alpha-Kl- and Na+,K+-ATPase-dependent manner. The increased Na+ gradient created by Na+,K+-ATPase activity might drive the transepithelial transport of Ca2+ in cooperation with ion channels and transporters in the choroid plexus and the kidney. Our findings reveal fundamental roles of alpha-Kl in the regulation of calcium metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imura, Akihiro -- Tsuji, Yoshihito -- Murata, Miyahiko -- Maeda, Ryota -- Kubota, Koji -- Iwano, Akiko -- Obuse, Chikashi -- Togashi, Kazuya -- Tominaga, Makoto -- Kita, Naoko -- Tomiyama, Ken-ichi -- Iijima, Junko -- Nabeshima, Yoko -- Fujioka, Makio -- Asato, Ryo -- Tanaka, Shinzo -- Kojima, Ken -- Ito, Juichi -- Nozaki, Kazuhiko -- Hashimoto, Nobuo -- Ito, Tetsufumi -- Nishio, Takeshi -- Uchiyama, Takashi -- Fujimori, Toshihiko -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1615-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569864" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/cerebrospinal fluid/*metabolism ; Cell Membrane/enzymology/metabolism ; Choroid Plexus/metabolism ; Cytoplasm/enzymology/metabolism ; Endoplasmic Reticulum/metabolism ; Endosomes/metabolism ; Enzyme Inhibitors/pharmacology ; Feedback, Physiological ; Glucuronidase/genetics/metabolism/*physiology ; Golgi Apparatus/metabolism ; HeLa Cells ; *Homeostasis ; Humans ; Ion Transport ; Kidney/enzymology/metabolism ; Mice ; Ouabain/pharmacology ; Parathyroid Glands/enzymology/metabolism ; Parathyroid Hormone/secretion ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Developmentally regulated activation of a SINE B2 repeat as a domain boundary in organogenesis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: The temporal and spatial regulation of gene expression in mammalian development is linked to the establishment of functional chromatin domains. Here, we report that tissue-specific transcription of a retrotransposon repeat in the murine growth hormone locus is required for gene activation. This repeat serves as a boundary to block the influence of repressive chromatin modifications. The repeat element is able to generate short, overlapping Pol II-and Pol III-driven transcripts, both of which are necessary and sufficient to enable a restructuring of the regulated locus into nuclear compartments. These data suggest that transcription of interspersed repetitive sequences may represent a developmental strategy for the establishment of functionally distinct domains within the mammalian genome to control gene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lunyak, Victoria V -- Prefontaine, Gratien G -- Nunez, Esperanza -- Cramer, Thorsten -- Ju, Bong-Gun -- Ohgi, Kenneth A -- Hutt, Kasey -- Roy, Rosa -- Garcia-Diaz, Angel -- Zhu, Xiaoyan -- Yung, Yun -- Montoliu, Lluis -- Glass, Christopher K -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, 9500 Gilman Drive, Room 345, La Jolla, CA 92093-0648, USA. vlunyak@uscd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromatin Immunoprecipitation ; DNA Polymerase II/metabolism ; DNA Polymerase III/metabolism ; *Gene Expression Regulation, Developmental ; Growth Hormone/*genetics ; Histones/metabolism ; *Insulator Elements ; Methylation ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Organogenesis ; Pituitary Gland/*embryology/metabolism ; *Short Interspersed Nucleotide Elements ; *Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Blastocyst axis is specified independently of early cell lineage but aligns with the ZP shape (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: The mechanisms controlling the establishment of the embryonic-abembryonic (E-Ab) axis of the mammalian blastocyst are controversial. We used in vitro time-lapse imaging and in vivo lineage labeling to provide evidence that the E-Ab axis of the mouse blastocyst is generated independently of early cell lineage. Rather, both the boundary between two-cell blastomeres and the E-Ab axis of the blastocyst align relative to the ellipsoidal shape of the zona pellucida (ZP), an extraembryonic structure. Lack of correlation between cell lineage and the E-Ab axis can be explained by the rotation of the embryo within the ZP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurotaki, Yoko -- Hatta, Kohei -- Nakao, Kazuki -- Nabeshima, Yo-Ichi -- Fujimori, Toshihiko -- New York, N.Y. -- Science. 2007 May 4;316(5825):719-23. Epub 2007 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology/physiology ; Blastocyst Inner Cell Mass ; Blastomeres/*physiology ; Body Patterning ; Cell Lineage ; Cell Movement ; Cell Nucleus/physiology ; *Embryonic Development ; Green Fluorescent Proteins ; Image Processing, Computer-Assisted ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Fluorescence ; Motion Pictures as Topic ; Rotation ; Zona Pellucida/physiology/*ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: During pregnancy, maternal pancreatic islets grow to match dynamic physiological demands, but the mechanisms regulating adaptive islet growth in this setting are poorly understood. Here we show that menin, a protein previously characterized as an endocrine tumor suppressor and transcriptional regulator, controls islet growth in pregnant mice. Pregnancy stimulated proliferation of maternal pancreatic islet beta-cells that was accompanied by reduced islet levels of menin and its targets. Transgenic expression of menin in maternal beta-cells prevented islet expansion and led to hyperglycemia and impaired glucose tolerance, hallmark features of gestational diabetes. Prolactin, a hormonal regulator of pregnancy, repressed islet menin levels and stimulated beta-cell proliferation. These results expand our understanding of mechanisms underlying diabetes pathogenesis and reveal potential targets for therapy in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karnik, Satyajit K -- Chen, Hainan -- McLean, Graeme W -- Heit, Jeremy J -- Gu, Xueying -- Zhang, Andrew Y -- Fontaine, Magali -- Yen, Michael H -- Kim, Seung K -- T32DK007217-32/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes, Gestational/*etiology/metabolism ; Female ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Obesity/metabolism ; Pregnancy ; Prolactin/metabolism ; Proto-Oncogene Proteins/*physiology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Regulation of the germinal center response by microRNA-155 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: MicroRNAs are small RNA species involved in biological control at multiple levels. Using genetic deletion and transgenic approaches, we show that the evolutionarily conserved microRNA-155 (miR-155) has an important role in the mammalian immune system, specifically in regulating T helper cell differentiation and the germinal center reaction to produce an optimal T cell-dependent antibody response. miR-155 exerts this control, at least in part, by regulating cytokine production. These results also suggest that individual microRNAs can exert critical control over mammalian differentiation processes in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thai, To-Ha -- Calado, Dinis Pedro -- Casola, Stefano -- Ansel, K Mark -- Xiao, Changchun -- Xue, Yingzi -- Murphy, Andrew -- Frendewey, David -- Valenzuela, David -- Kutok, Jeffery L -- Schmidt-Supprian, Marc -- Rajewsky, Nikolaus -- Yancopoulos, George -- Rao, Anjana -- Rajewsky, Klaus -- AI064345/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):604-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Cell Differentiation ; Cells, Cultured ; Cytokines/biosynthesis ; Germinal Center/*immunology ; Immunoglobulin G/analysis ; Lymphocyte Activation ; Lymphotoxin-alpha/biosynthesis ; Lymphotoxin-beta/biosynthesis ; Mice ; Mice, Knockout ; Mice, Transgenic ; MicroRNAs/genetics/*physiology ; Nitrophenols/immunology ; Peyer's Patches/immunology ; Phenylacetates ; Somatic Hypermutation, Immunoglobulin ; Spleen/immunology ; T-Lymphocytes/cytology/*immunology/metabolism ; Th1 Cells/cytology/immunology ; Th2 Cells/cytology/immunology ; Tumor Necrosis Factor-alpha/biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Requirement of inositol pyrophosphates for full exocytotic capacity in pancreatic beta cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-24
    Description: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Sparse optical microstimulation in barrel cortex drives learned behaviour in freely moving mice (2007)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2007
    Description: Electrical microstimulation can establish causal links between the activity of groups of neurons and perceptual and cognitive functions. However, the number and identities of neurons microstimulated, as well as the number of action potentials evoked, are difficult to ascertain. To address these issues we introduced the light-gated algal channel channelrhodopsin-2 (ChR2) specifically into a small fraction of layer 2/3 neurons of the mouse primary somatosensory cortex. ChR2 photostimulation in vivo reliably generated stimulus-locked action potentials at frequencies up to 50 Hz. Here we show that naive mice readily learned to detect brief trains of action potentials (five light pulses, 1 ms, 20 Hz). After training, mice could detect a photostimulus firing a single action potential in approximately 300 neurons. Even fewer neurons (approximately 60) were required for longer stimuli (five action potentials, 250 ms). Our results show that perceptual decisions and learning can be driven by extremely brief epochs of cortical activity in a sparse subset of supragranular cortical pyramidal neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425380/" 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/PMC3425380/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huber, Daniel -- Petreanu, Leopoldo -- Ghitani, Nima -- Ranade, Sachin -- Hromadka, Tomas -- Mainen, Zach -- Svoboda, Karel -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jan 3;451(7174):61-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18094685" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology/radiation effects ; Algal Proteins/genetics/metabolism ; Animals ; Behavior, Animal/*physiology/*radiation effects ; Cerebral Cortex/cytology/*physiology/*radiation effects ; Electric Stimulation ; Learning/*physiology/radiation effects ; Mice ; Movement/*physiology ; Optics and Photonics ; Photic Stimulation ; Pyramidal Cells/metabolism/radiation effects ; Rhodopsins, Microbial/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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  • 10
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    Positive regulation of Itk PH domain function by soluble IP4 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Pleckstrin homology (PH) domain-mediated protein recruitment to cellular membranes is of paramount importance for signal transduction. The recruitment of many PH domains is controlled through production and turnover of their membrane ligand, phosphatidylinositol 3,4,5-trisphosphate (PIP3). We show that phosphorylation of the second messenger inositol 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) establishes another mode of PH domain regulation through a soluble ligand. At physiological concentrations, IP4 promoted PH domain binding to PIP3. In primary mouse CD4+CD8+ thymocytes, this was required for full activation of the protein tyrosine kinase Itk after T cell receptor engagement. Our data suggest that IP4 establishes a feedback loop of phospholipase C-gamma1 activation through Itk that is essential for T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yina H -- Grasis, Juris A -- Miller, Andrew T -- Xu, Ruo -- Soonthornvacharin, Stephen -- Andreotti, Amy H -- Tsoukas, Constantine D -- Cooke, Michael P -- Sauer, Karsten -- AR048848/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):886-9. Epub 2007 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412921" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; *Amino Acid Motifs ; Animals ; Diglycerides/metabolism ; Feedback, Physiological ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol Phosphates/*metabolism/pharmacology ; Lymphopoiesis ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Organ Culture Techniques ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C gamma/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Receptors, Antigen, T-Cell/immunology ; Second Messenger Systems ; Signal Transduction ; Solubility ; T-Lymphocytes/cytology/immunology/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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