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Mus musculus strain:A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HILtJ,CAST/EiJ, PWK/PhJ, WSB/EiJ

ABSTRACT: RNA-Seq of CC Founder Islets

PROVIDER: PRJNA588047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10413300.fastq.gz	Fastqsanger.gz
	SRR10413301.fastq.gz	Fastqsanger.gz
	SRR10413302.fastq.gz	Fastqsanger.gz
	SRR10413303.fastq.gz	Fastqsanger.gz
	SRR10413304.fastq.gz	Fastqsanger.gz

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Mus musculus strain:A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HILtJ,CAST/EiJ, PWK/PhJ, and WSB/EiJ

Project description:RNA-Seq of hippocampus in Collaborative Cross Founder Mice

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Mus musculus strain:A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HILtJ,CAST/EiJ, PWK/PhJ, and WSB/EiJ

Project description:Mus musculus strain:A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HILtJ,CAST/EiJ, PWK/PhJ, and WSB/EiJ Raw sequence reads

| PRJNA588046 | ENA

Influenza H3N2 infection of the Collaborative Cross founder strains reveals highly divergent host responses and identifies a unique phenotype in CAST/EiJ mice (blood)

Project description:To determine if genetic background can modulate severity of an infection, we studied the host responses to influenza infections in the eight genetically highly diverse Collaborative Cross (CC) founder mice. The CC founder (C57BL/6J, 129S1/SvlmJ, CAST/EiJ, PWK/PhJ) were intranasally infected with influenza A/HK/01/68 (H3N2) with 20Î¼l virus solution (1x101 ffu) or mock infected (with PBS). After infection lung was collected at different time points (mock_d3), d3, d5).

2015-12-31 | E-GEOD-74073 | biostudies-arrayexpress

Influenza H3N2 infection of the Collaborative Cross founder strains reveals highly divergent host responses and identifies a unique phenotype in CAST/EiJ mice (lung)

2015-12-31 | E-GEOD-74074 | biostudies-arrayexpress

Influenza H3N2 infection of the Collaborative Cross founder strains reveals highly divergent host responses and identifies a unique phenotype in CAST/EiJ mice (lung)

2015-12-31 | GSE74074 | GEO

Influenza H3N2 infection of the Collaborative Cross founder strains reveals highly divergent host responses and identifies a unique phenotype in CAST/EiJ mice (blood)

2015-12-31 | GSE74073 | GEO

NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in mice.

Project description:Introduction of genes targeted in 129/Sv embryonic stem (ES) cells into NOD mice brings about linked genes that may modulate type 1 diabetes. Our objective was to identify 129S1/SvJ non-MHC regions contributing type 1 diabetes resistance or susceptibility in backcross to NOD/LtJ.After congenic transfer of the NOD H2(g7) haplotype onto 129S1/Sv, 310 females were produced by NOD x (NOD x 129.H2(g7))F1 backcross (N2). A genome scan for quantitative trait locus (QTL) affecting clinical diabetes, age of diabetes onset, and insulitis severity was performed using subphenotype characteristics to improve power and resolution for detection of diabetes susceptibility loci.Thirty-six of 310 (11.6%) N2 females developed type 1 diabetes between 14 and 40 weeks. Significant evidence of linkage for only a single previously reported Idd complex locus (Idd10/17/18, chromosome [Chr] 3) was indicated for clinical diabetes. The quantitative traits of insulitis either alone or combined with age at type 1 diabetes onset were significantly linked to known Idd regions on Chr 1 (Idd5 region), Chr 4 (Idd9 region), Chr 8 (Idd22), Chr 11 (Idd4.3), and proximal Chr 17 (Idd16 region). Significant 129S1/Sv resistance contributions were identified on Chr 1, 15 (two loci), and 19, with suggestive evidence for additional novel 129/Sv resistance QTL on Chr 5 and 17 and susceptibility on Chr 2.The 129S1/SvJ genome harbors collections of both known and potentially novel non-MHC Idd loci. Investigators targeting 129/Sv genes mapping within chromosomal regions reported herein or elsewhere in the genome need to exclude potential contributions from linked Idd loci by generating a NOD.129 control strain expressing the nontargeted allele.

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Candidate genes for obesity revealed from a C57BL/6J x 129S1/SvImJ intercross.

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Deficits across multiple behavioral domains align with susceptibility to stress in 129S1/SvImJ mice.

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