Eppig, J. T. et al. The Mouse Genome Database (MGD): from genes to mice—a community resource for mouse biology. Nucleic Acids Res. 33, D471-D475

The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.
Nucleic Acids Research (Impact Factor: 9.11). 02/2005; 33(Database issue):D471-5. DOI: 10.1093/nar/gki113
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The Mouse Genome Database (MGD) forms the core of the Mouse Genome Informatics (MGI) system (http://www.informatics.jax.org), a model organism database resource for the laboratory mouse. MGD provides essential integration of experimental knowledge for the mouse system with information annotated from both literature and online sources. MGD curates and presents consensus and experimental data representations of genotype (sequence) through phenotype information, including highly detailed reports about genes and gene products. Primary foci of integration are through representations of relationships among genes, sequences and phenotypes. MGD collaborates with other bioinformatics groups to curate a definitive set of information about the laboratory mouse and to build and implement the data and semantic standards that are essential for comparative genome analysis. Recent improvements in MGD discussed here include the enhancement of phenotype resources, the re-development of the International Mouse Strain Resource, IMSR, the update of mammalian orthology datasets and the electronic publication of classic books in mouse genetics.

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    • "The IMSR began as a collaboration between MRC Harwell and the Mouse Genome Database (MGD) at the Jackson Laboratory to provide the research community with a common site for finding mouse resources (Eppig and Strivens 1999). The IMSR has since grown to be a multi-institutional international collaboration supporting the research community that uses mouse as a model system for studying biology and disease (Eppig et al. 2005). The goal of the IMSR remains to provide a web searchable catalog to assist investigators in finding the mouse resources needed for their studies. "
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    ABSTRACT: The availability of and access to quality genetically defined, health-status known mouse resources is critical for biomedical research. By ensuring that mice used in research experiments are biologically, genetically, and health-status equivalent, we enable knowledge transfer, hypothesis building based on multiple data streams, and experimental reproducibility based on common mouse resources (reagents). Major repositories for mouse resources have developed over time and each has significant unique resources to offer. Here we (a) describe The International Mouse Strain Resource that offers users a combined catalog of worldwide mouse resources (live, cryopreserved, embryonic stem cells), with direct access to repository sites holding resources of interest and (b) discuss the commitment to nomenclature standards among resources that remain a challenge in unifying mouse resource catalogs.
    Mammalian Genome 09/2015; 26(9). DOI:10.1007/s00335-015-9600-0 · 3.07 Impact Factor
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    • "Rgs5LacZ mice, which have a nuclear localized β-galactosidase reporter gene knocked into exon 2 of the Rgs5 locus and mice have been backcrossed to a C57BL/6 background, were purchased (Deltagen [45]). To induce acute liver injury, mice were injected (i.p.) with 10 µl/g body weight CCl4 (Sigma-Aldrich) diluted 10% (v/v) in olive oil once. "
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    ABSTRACT: Liver fibrosis is mediated by hepatic stellate cells (HSCs), which respond to a variety of cytokine and growth factors to moderate the response to injury and create extracellular matrix at the site of injury. G-protein coupled receptor (GPCR)-mediated signaling, via endothelin-1 (ET-1) and angiotensin II (AngII), increases HSC contraction, migration and fibrogenesis. Regulator of G-protein signaling-5 (RGS5), an inhibitor of vasoactive GPCR agonists, functions to control GPCR-mediated contraction and hypertrophy in pericytes and smooth muscle cells (SMCs). Therefore we hypothesized that RGS5 controls GPCR signaling in activated HSCs in the context of liver injury. In this study, we localize RGS5 to the HSCs and demonstrate that Rgs5 expression is regulated during carbon tetrachloride (CCl4)-induced acute and chronic liver injury in Rgs5LacZ/LacZ reporter mice. Furthermore, CCl4 treated RGS5-null mice develop increased hepatocyte damage and fibrosis in response to CCl4 and have increased expression of markers of HSC activation. Knockdown of Rgs5 enhances ET-1-mediated signaling in HSCs in vitro. Taken together, we demonstrate that RGS5 is a critical regulator of GPCR signaling in HSCs and regulates HSC activation and fibrogenesis in liver injury.
    PLoS ONE 10/2014; 9(10):e108505. DOI:10.1371/journal.pone.0108505 · 3.23 Impact Factor
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    • "The sAC C1KO mice display male infertility (Esposito et al., 2004). Extensive phenotypic analysis revealed that female mice have increased circulating cholesterol and triglyceride and that both male and female mice have slightly elevated heart rates [as deposited in the Mouse Genome Database (Eppig et al., 2005)]. More recently, it was reported that an alternative start site upstream of exon 5 is used by somatic cells to produce yet another isoforms containing only one catalytic unit C2. "
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    ABSTRACT: The evolutionarily conserved soluble adenylyl cyclase (sAC, adcy10) was recently identified as a unique source of cAMP in the cytoplasm and the nucleus. Its activity is regulated by bicarbonate and fine-tuned by calcium. As such, and in conjunction with carbonic anhydrase (CA), sAC constitutes an HCO(-) 3/CO(-) 2/pH sensor. In both alpha-intercalated cells of the collecting duct and the clear cells of the epididymis, sAC is expressed at significant level and involved in pH homeostasis via apical recruitment of vacuolar H(+)-ATPase (VHA) in a PKA-dependent manner. In addition to maintenance of pH homeostasis, sAC is also involved in metabolic regulation such as coupling of Krebs cycle to oxidative phosphorylation via bicarbonate/CO2 sensing. Additionally, sAC also regulates CFTR channel and plays an important role in regulation of barrier function and apoptosis. These observations suggest that sAC, via bicarbonate-sensing, plays an important role in maintaining homeostatic status of cells against fluctuations in their microenvironment.
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