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      A Digital Atlas of Ion Channel Expression Patterns in the Two-Week-Old Rat Brain

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          Abstract

          The approximately 350 ion channels encoded by the mammalian genome are a main pillar of the nervous system. We have determined the expression pattern of 320 channels in the two-week-old (P14) rat brain by means of non-radioactive robotic in situ hybridization. Optimized methods were developed and implemented to generate stringently coronal brain sections. The use of standardized methods permits a direct comparison of expression patterns across the entire ion channel expression pattern data set and facilitates recognizing ion channel co-expression. All expression data are made publically available at the Genepaint.org database. Inwardly rectifying potassium channels (Kir, encoded by the Kcnj genes) regulate a broad spectrum of physiological processes. Kcnj channel expression patterns generated in the present study were fitted with a deformable subdivision mesh atlas produced for the P14 rat brain. This co-registration, when combined with numerical quantification of expression strengths, allowed for semi-quantitative automated annotation of expression patterns as well as comparisons among and between Kcnj subfamilies. The expression patterns of Kcnj channel were also cross validated against previously published expression patterns of Kcnj channel genes.

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          The online version of this article (doi:10.1007/s12021-014-9247-0) contains supplementary material, which is available to authorized users.

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          Most cited references71

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          GenePaint.org: an atlas of gene expression patterns in the mouse embryo.

          High-throughput instruments were recently developed to determine gene expression patterns on tissue sections by RNA in situ hybridization. The resulting images of gene expression patterns, chiefly of E14.5 mouse embryos, are accessible to the public at http://www.genepaint.org. This relational database is searchable for gene identifiers and RNA probe sequences. Moreover, patterns and intensity of expression in approximately 100 different embryonic tissues are annotated and can be searched using a standardized catalog of anatomical structures. A virtual microscope tool, the Zoom Image Server, was implemented in GenePaint.org and permits interactive zooming and panning across approximately 15,000 high-resolution images.
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            ATP-sensitive potassium channelopathies: focus on insulin secretion.

            ATP-sensitive potassium (K(ATP)) channels, so named because they are inhibited by intracellular (ATP), play key physiological roles in many tissues. In pancreatic beta cells, these channels regulate glucose-dependent insulin secretion and serve as the target for sulfonylurea drugs used to treat type 2 diabetes. This review focuses on insulin secretory disorders, such as congenital hyperinsulinemia and neonatal diabetes, that result from mutations in K(ATP) channel genes. It also considers the extent to which defective regulation of K(ATP) channel activity contributes to the etiology of type 2 diabetes.
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              Inward rectifier potassium channels.

              The past three years have seen remarkable progress in research on the molecular basis of inward rectification, with significant implications for basic understanding and pharmacological manipulation of cellular excitability. Expression cloning of the first inward rectifier K channel (Kir) genes provided the necessary break-through that has led to isolation of a family of related clones encoding channels with the essential functional properties of classical inward rectifiers, ATP-sensitive K channels, and muscarinic receptor-activated K channels. High-level expression of cloned channels led to the discovery that classical inward so-called anomalous rectification is caused by voltage-dependent block of the channel by polyamines and Mg2+ ions, and it is now clear that a similar mechanism results in inward rectification of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-kainate receptor channels. Knowledge of the primary structures of Kir channels and the ability to mutate them also has led to the determination of many of the structural requirements of inward rectification.
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                Author and article information

                Contributors
                ++49-551-201-2701 , gregor.eichele@mpibpc.mpg.de
                Journal
                Neuroinformatics
                Neuroinformatics
                Neuroinformatics
                Springer US (Boston )
                1539-2791
                1559-0089
                7 October 2014
                7 October 2014
                2015
                : 13
                : 111-125
                Affiliations
                [ ]Department of Genes and Behavior, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Göttingen, Germany
                [ ]Life Sciences Computing, Texas Advanced Computing Center, 10100 Burnet Road, Austin, TX 78758 USA
                Article
                9247
                10.1007/s12021-014-9247-0
                4303740
                25284011
                cf62a321-fc3c-477a-965b-37c0b753ac5f
                © The Author(s) 2014

                Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                Categories
                Data Original Article
                Custom metadata
                © Springer Science+Business Media New York 2015

                Neurosciences
                ion channels,gene expression analysis,in situ hybridization,genepaint.org database,rat brain,digital atlas,subdivision mesh

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