Mouse chromosome 3

Meisler, Miriam H.; Seldin, Michael F.

doi:10.1007/bf00656485

Cited by 6 publications

(6 citation statements)

References 76 publications

(45 reference statements)

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“…Haplotype analysis of 53 animals and minimization of crossover frequency was used to deduce the gene order and genetic distance (cM): Crh, The map constructed from these data (Fig. 2) is consistent with the location presented for Car-2, II-2, and Gba on the consensus map (Meisler and Seldin 1991), although these genes have not been previously localized relative to one another. Three carbonic anhydrase genes have been localized in close proximity on human Chr 8 and mouse Chr 3 (Beechey et al 1990;Eicher et al 1976;Nakai et al 1987).…”

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confidence: 60%

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Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

et al. 1993

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confidence: 60%

“…Two mutations are located on proximal mouse Chr 3, cocoa (coa) and subtle gray (sut) (Meisler and Seldin 1991). The phenotypes of these two mutants do not correlate with those suggested for CRH deficiency from human and animals studies.…”

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confidence: 89%

Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

et al. 1993

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“…Thus, CD1 molecules were classified as a member of MHC class Ib family. However, unlike most of MHC class Ib genes, CD1 genes map outside of MHC both in humans and mice (8,9), and they are significantly divergent from other class I genes. The sequence homology between CD1 and other class I molecules is only 25-30% (5).…”

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confidence: 99%

Comparative Contribution of CD1 on the Development of CD4+ and CD8+ T Cell Compartments

Wang

Chun

Wang

2000

The Journal of Immunology

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CD1 molecules are MHC class I-like glycoproteins whose expression is essential for the development of a unique subset of T cells, the NK T cells. To evaluate to what extent CD1 contributes to the development of CD4+ and CD8+ T cells, we generated CD1oIIo and CD1oTAPo mice and compared the generation of T cells in these double-mutant mice and IIo or TAPo mice. FACS analysis showed that the number of CD4+ T cells in CD1oIIo mice was reduced significantly compared with the corresponding population in IIo mice. Both CD4+ NK1.1+ and the CD4+ NK1.1− population were reduced in CD1oIIo mice, suggesting that CD1 can select not only CD4+ NK1.1+ T cells but also some NK1.1− CD4+ T cells. Functional analysis showed that the residual CD4+ cells in CD1oIIo can secrete large amounts of IFN-γ and a significant amount of IL-4 during primary stimulation with anti-CD3, suggesting that this population may be enriched for NK T cells restricted by other class I molecules. In contrast to the CD4+ population, no significant differences in the CD8+ T cell compartment can be detected between TAPo and CD1oTAPo mice in all lymphoid tissues tested, including intestinal intraepithelial lymphocytes. Our data suggest that, unlike other MHC class I molecules, CD1 does not contribute in a major way to the development of CD8+ T cells.

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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 3

Cited by 6 publications

References 76 publications

Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

Corticotropin-releasing hormone (Crh) maps to mouse Chromosome 3

Comparative Contribution of CD1 on the Development of CD4+ and CD8+ T Cell Compartments

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

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