Mouse chromosome 4

Blank, Robert D.; Eppig, Janan T.; Fiedorek, Fred T.; Frankel, Wayne N.; Friedman, Jeffrey M.; Hüppi, Konrad; Jackson, Ian J.; Mock, Beverly A.

doi:10.1007/bf00656486

Cited by 25 publications

(8 citation statements)

References 117 publications

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“…The data in Fig. 4 (34), placing it close to the complement 8-beta gene (C8b). It is also apparently close to the obese-diabetes syndrome mutant gene db.…”

Section: Discussionmentioning

confidence: 73%

“…If such a mutant is subsequently identified and mapped to chromosome 4, the possible association with Diol should be apparent. The position of Diol in chromosome 4 of the mouse allows the prediction that the human homolog of Diol will map to HSA I p (34). The segment of chromosome 4 homologous to HSA lp extends proximally from Jun (position 44) to Skv (position 77) distally, and therefore represents one of the largest uninterrupted regions of conserved linkage between the two species.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Physiological and genetic analyses of inbred mouse strains with a type I iodothyronine 5' deiodinase deficiency.

Berry¹,

Grieco²,

Taylor³

et al. 1993

J. Clin. Invest.

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Inbred mouse strains differ in their capacity to deiodinate iododioxin and iodothyronines, with strains segregating into high or low activity groups. Metabolism of iododioxin occurs via the type I iodothyronine 5'deiodinase (51DI), one of two enzymes that metabolize thyroxine (T4) to 3,5,3'-triiodothyronine (T3). Recombinant inbred strains derived from crosses between high and low activity strains exhibit segregation characteristic of a single allele difference. Hepatic and renal 5DI mRNA in a high (C57BL/6J) and low (C3H/HeJ) strain paralleled enzyme activity and concentration, in agreement with a recent report. 5DI-deficient mice had twofold higher serum free T4 but normal free T3 and thyrotropin. Brown adipose tissue 51DII was invariant between the two strains. Southern analyses using a 51DI probe identified a restriction fragment length variant that segregated with 51DI activity in 33 of 35 recombinant inbred strains derived from four different pairs of high and low activity parental strains. Recombination frequencies using previously mapped loci allowed assignment of the 5DI gene to mouse chromosome 4 and identified its approximate chromosomal position. We propose the symbol Diol to denote the mouse 51)I gene. Conserved linkage between this segment of mouse chromosome 4 and human HSAlp predicts this location for human Diol. (J. Clin. Invest. 1993. 92:1517-1528

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“…The data in Fig. 4 (34), placing it close to the complement 8-beta gene (C8b). It is also apparently close to the obese-diabetes syndrome mutant gene db.…”

Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Physiological and genetic analyses of inbred mouse strains with a type I iodothyronine 5' deiodinase deficiency.

Berry¹,

Grieco²,

Taylor³

et al. 1993

J. Clin. Invest.

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“…To this end, we have mapped OBR physically by radiation hybrid (RH) mapping and placement on a contig composed of 10 adjacent yeast artificial chromosomes (YACs) and 5 P1 artificial chromosome (PACs). The location of the human homolog of Obr was predicted to be on lp based on conserved linkage of most of the telomeric half of mouse chromosome 4 with human lp (Blank et al 1991;Abbott et al 1992). Although OBR does map to lp, there has been an apparent rearrangement of the order of these genes in humans relative to that observed in mice and rats.…”

mentioning

confidence: 99%

Mapping of the OB receptor to 1p in a region of nonconserved gene order from mouse and rat to human.

Chung

Power-Kehoe²,

Chua³

et al. 1996

Genome Res.

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As part of an effort to identify informative molecular markers for genetic analysis of human pedigrees segregating for obesity, we have developed a genetic map of human lp in the region of the OB receptor (OBR), the gene that is defective in murine diabetes [Obr db) and rat Zucker fatty [Obr re) mutations located on mid-chromosome 4 and chromosome 5, respectively. OBR was mapped 0.9 cR centromeric to WI-9515 and 2.2 cR telomeric of WI-7249 by radiation hybrid [RH) mapping. Ten yeast artificial chromosomes (YACs) containing OBR were identified, confirming the location of OBR centromeric to WI-9515 and telomeric to WI-7249. Additionally, five PI artificial chromosomes [PACs) were identified that comprised a contiguous series of overlapping clones spanning the length of OBR. WI-5182 was contained within the two PACs that are 3' of OBR. Using a panel of 68 individuals from a single three-generation family and an additional nuclear family, we have mapped 18 polymorphic markers including phosphoglucomutase 1 [PGMI), which is centromeric to Obrdb/Ob~, and DIS~5, which is telomeric to ObrdblObr ~a in the mouse and rat. The following composite map integrates these radiation hybrid, genetic, and physical maps:

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“…The Glur-l locus is localized to a region of mouse chromosome 11 in which the recessive vibrator (vb), shaker-2 (sh-2), tipsy (ti), and spasmodic (spd) mutations have been mapped (67)(68)(69)(70). Glur-2 maps to the region of mouse chromosome 3 that contains the spastic (sp) mutation; and Glur-7 maps to the region of mouse chromosome 4 that contains the clasper (cla) mutation (69,(71)(72)(73)(74). As indicated by their distinct names, these mice exhibit motor signs, such as various tremors and spasms.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal localization of glutamate receptor genes: relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans.

Gregor

Reeves

Jabs

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Receptors for the major excitatory neurotransmitter glutamate may play key roles in neurodegeneration. The mouse Glur-5 gene maps to chromosome 16 between App and Sod-1. The homologous human GLUR5 gene maps to the corresponding region of human chromosome 21, which contains the locus for familial amyotrophic lateral sclerosis. This location, and other features, render GLUR5 a possible candidate gene for familial amyotrophic lateral sclerosis. In addition, dosage imbalance of GLUR5 may have a role in the trisomy 21 (Down syndrome). Further characterization of the murine glutamate receptor family includes mapping of Glur-1 to the same region as neurological mutants spasmodic, shaker-2, tipsy, and vibrator on chromosome 11; Glur-2 near spastic on chromosome 3; Glur-6 near waltzer and Jackson circler on chromosome 10; and Glur-7 near clasper on chromosome 4.

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Mouse chromosome 4

Cited by 25 publications

References 117 publications

Physiological and genetic analyses of inbred mouse strains with a type I iodothyronine 5' deiodinase deficiency.

Physiological and genetic analyses of inbred mouse strains with a type I iodothyronine 5' deiodinase deficiency.

Mapping of the OB receptor to 1p in a region of nonconserved gene order from mouse and rat to human.

Chromosomal localization of glutamate receptor genes: relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans.

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