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  • 1
    Electronic Resource
    Electronic Resource
    Genetic Regulation of Susceptibility and Severity of Demyelination (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 540 (1988), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1988.tb27230.x
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  • 2
    Electronic Resource
    Electronic Resource
    GHRH receptor of little mice contains a missense mutation in the extracellular domain that disrupts receptor function (1993)
    [s.l.] : Nature Publishing Group
    Nature genetics 4 (1993), S. 227-232 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The growth hormone–releasing hormone receptor (GHRHR) is a member of the family of G protein–coupled receptors that is expressed on pituitary somatotrope cells and mediates the actions of GHRH in stimulating growth hormone (GH) synthesis and secretion. We report that the Ghrhr gene is ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0793-227
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  • 3
    Electronic Resource
    Electronic Resource
    Mapping of mouse gamma crystallin genes on chromosome 1 (1988)
    Springer
    Biochemical genetics 26 (1988), S. 557-570 
    Details
    ISSN: 1573-4927
    Keywords: mouse ; gamma crystallin ; gene mapping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Restriction fragments analysis of DNA from mouse-hamster somatic-cell hybrid clones revealed that a mouse gamma crystallin cDNA hybridized to genomic sequences located on mouse chromosome 1. Identification of restriction fragment length polymorphisms (RFLPs) in the gamma crystallin sequences of inbred strains of mice permitted the further localization of the gamma crystallin genes (Cryg) to the proximal region of chromosome 1 closely linked to the loci encoding isocitrate dehydrogenase (Idh-1), a low molecular weight (LM) crystallin protein polymorphism (Len-1), and fibronectin (Fn-1). A single recombinant was observed betweenLen-1 and an RFLP in the gamma crystallin gene family, consistent with the hypothesis thatLen-1 is one of the several structural loci encoding gamma crystallin genes.Len-1 is probably located on the centromeric end of theCryg gene family. Linkage ofIdh-1, Cryg, andFn-1 in mice extends the syntenic relationship of those loci to the human, bovine, and rodent genomes and may define a chromosomal region that is generally conserved among mammals. The map position ofCryg, near the eye lens obsolescence (Elo) locus, was confirmed by the discovery that the restriction fragment patterns of gamma crystallin sequences differed between strain C3H/HeJ and the congenic anophthalmic mutant strain, C3H.Elo. Therefore, the gamma crystallin genes were contransferred with the mutantElo gene in the derivation of C3H.Elo. The results establish that LEN-1 is a marker for the gamma crystallin gene family, position the gamma crystallin gene family relative to other markers on mouse chromosome 1, and provide additional evidence that theElo mutation is encoded at a locus closely linked to the gamma crystallin gene cluster. This study found no evidence of recombination hot spots within the gamma crystallin gene cluster.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02399601
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  • 4
    Electronic Resource
    Electronic Resource
    Mapping of mouse gamma crystallin genes on chromosome 1 (1988)
    Springer
    Biochemical genetics 26 (1988), S. 557-570 
    Details
    ISSN: 1573-4927
    Keywords: mouse ; gamma crystallin ; gene mapping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Restriction fragments analysis of DNA from mouse-hamster somatic-cell hybrid clones revealed that a mouse gamma crystallin cDNA hybridized to genomic sequences located on mouse chromosome 1. Identification of restriction fragment length polymorphisms (RFLPs) in the gamma crystallin sequences of inbred strains of mice permitted the further localization of the gamma crystallin genes (Cryg) to the proximal region of chromosome 1 closely linked to the loci encoding isocitrate dehydrogenase (Idh-1), a low molecular weight (LM) crystallin protein polymorphism (Len-1), and fibronectin (Fn-1). A single recombinant was observed betweenLen-1 and an RFLP in the gamma crystallin gene family, consistent with the hypothesis thatLen-1 is one of the several structural loci encoding gamma crystallin genes.Len-1 is probably located on the centromeric end of theCryg gene family. Linkage ofIdh-1, Cryg, andFn-1 in mice extends the syntenic relationship of those loci to the human, bovine, and rodent genomes and may define a chromosomal region that is generally conserved among mammals. The map position ofCryg, near the eye lens obsolescence (Elo) locus, was confirmed by the discovery that the restriction fragment patterns of gamma crystallin sequences differed between strain C3H/HeJ and the congenic anophthalmic mutant strain, C3H.Elo. Therefore, the gamma crystallin genes were contransferred with the mutantElo gene in the derivation of C3H.Elo. The results establish that LEN-1 is a marker for the gamma crystallin gene family, position the gamma crystallin gene family relative to other markers on mouse chromosome 1, and provide additional evidence that theElo mutation is encoded at a locus closely linked to the gamma crystallin gene cluster. This study found no evidence of recombination hot spots within the gamma crystallin gene cluster.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00553779
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  • 5
    Electronic Resource
    Electronic Resource
    Microcephalic cerebrum with hypomyelination in the congenital goiter mouse (cog) (1992)
    Springer
    Neurochemical research 17 (1992), S. 1037-1040 
    Details
    ISSN: 1573-6903
    Keywords: Congenital Goiter Mouse (cog) ; microcephalic cerebrum ; hypomyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 2′,3′-Cyclic nucleotide 3′-phosphohydrolase activity in the cerebrum of the congenital goiter mouse (cog/cog) is reduced in comparison with the normal heterozygote (cog/+). The weight of thecog/cog cerebrum and cerebellum were significantly less than those of the normal controls, 89.0% less for the cerebrum, and 81.1% less for the cerebellum. However, no differences were observed with regard to DNA and RNA content and the RNA/DNA ratio. The results of this study indicate that hypomyelination in the congenital goiter mouse is restricted to the cerebrum, and is not related to arrested glial proliferation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966833
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  • 6
    Electronic Resource
    Electronic Resource
    Quantitative trait loci for bone density in C57BL/6J and CAST/EiJ inbred mice (1999)
    Springer
    Mammalian genome 10 (1999), S. 1043-1049 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Genetic analyses for loci regulating bone mineral density have been conducted in a cohort of F2 mice derived from intercross matings of (C57BL/6J × CAST/EiJ)F1 parents. Femurs were isolated from 714 4-month-old females when peak adult bone density had been achieved. Bone mineral density (BMD) data were obtained by peripheral quantitative computed tomography (pQCT), and genotype data were obtained by Polymerase Chain Reaction (PCR) assays for polymorphic markers carried in genomic DNA of each mouse. Genome-wide scans for co-segregation of genetic marker data with high or low BMD revealed loci on eight different chromosomes, four of which (Chrs 1, 5, 13, and 15) achieved conservative statistical criteria for suggestive, significant, or highly significant linkage with BMD. These four quantitative trait loci (QTLs) were confirmed by a linear regression model developed to describe the main effects; none of the loci exhibited significant interaction effects by ANOVA. The four QTLs have been named Bmd1 (Chr 1), Bmd2 (Chr 5), Bmd3 (Chr 13), and Bmd4 (Chr 15). Additive effects were observed for Bmd1, recessive for Bmd3, and dominant effects for Bmd2 and Bmd4. The current large size of the QTL regions (6→31 cM) renders premature any discussion of candidate genes at this time. Fine mapping of these QTLs is in progress to refine their genetic positions and to evaluate human homologies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359901159
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  • 7
    Electronic Resource
    Electronic Resource
    Defective thyroid ontogenesis in fetal hypothyroid (hyt/hyt) mice (1982)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 202 (1982), S. 387-393 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Thyroid glands of fetal hypothyroid (hyt/hyt) mice were studied to determine the effects of the mutant gene during embyrogenesis. Comparisons of mutant and normal thyroids were made with respect to morphology, iodine-concentrating ability, and glandular thyroxine (T4) content at day 18 of gestation. Fetal hyt/hyt thyroid tissue was properly located, but incompletely differentiated. The mutant thyroid was characterized microscopically by small, poorly developed follicles with colloid diminished in PAS-staining properties. The mutant glands' ability to concentrate iodine was found to be only 5-16% of that exhibited by normal glands. When litters contained both mutant and normal offspring, the differential iodine-concentrating ability allowed fetuses to be separated into two distinct, nonoverlapping populations. The distribution of fetal mice into high or low iodine-concentrating groups agreed closely with predicted frequencies for normal and mutant phenotypes. Thyroid content of T4 in mutant mice was found to be approximately equal to that found in age-matched normal controls.The poorly developed morphology and deficient iodine-concentrating ability of fetal thyroids from day 18 hyt/hyt mice indicated that the mutant gene acts during the ontogeny of this gland. Although such data are not available on human fetuses affected by thyroid dysgenesis, postnatal hyt/hyt mice display characteristics similar to those of infants born with this form of congenital primary hypothyroidism. Thus, elucidation of the site of mutant gene action in the mouse should contribute to our knowledge of disturbed fetal thyroid development and its implications in the adult mammal.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092020311
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