umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Type 1 diabetes and the control of dexamethazone-induced apoptosis in mice maps to the same region on chromosome 6
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department for Cell and Molecular Biology, University of Umezå, Umeå, Sweden)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology. University of Umeå)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department for Cell and Molecular Biology, University of Umezå, Umeå, Sweden)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology. University of Umeå)
1995 (English)In: Genomics, ISSN 0888-7543, E-ISSN 1089-8646, Vol. 28, no 3, 398-404 p.Article in journal (Refereed) Published
Abstract [en]

Quantitative trait loci mapping was used to identify the chromosomal location of genes that contribute to increase the resistance to apoptosis induced in immature CD4+8+ thymocytes. An F2 intercross of the nonobese diabetic (NOD) mouse (displaying an apoptosis-resistance phenotype) and the C57BL/6 mouse (displaying a nonresistance phenotype) was phenotypically analyzed and genotyped for 32 murine microsatellite polymorphisms. Maximum likelihood methods identified a region on the distal part of chromosome 6 that is linked to dexamethazone-induced apoptosis (lod score = 3.46) and accounts for 14% of the phenotypic variation. This chromosomal region contains the diabetes susceptibility locus Idd6, suggesting that the apoptosis-resistance phenotype constitutes a pathogenesis factor in IDDM of NOD mice.

Place, publisher, year, edition, pages
Elsevier, 1995. Vol. 28, no 3, 398-404 p.
National Category
Basic Medicine
Research subject
Immunology
Identifiers
URN: urn:nbn:se:umu:diva-87505DOI: 10.1006/geno.1995.1167PubMedID: 7490073OAI: oai:DiVA.org:umu-87505DiVA: diva2:709597
Available from: 2014-04-02 Created: 2014-04-02 Last updated: 2017-12-05Bibliographically approved
In thesis
1. Cellular and genetic components in the development of IDDM in NOD mice.
Open this publication in new window or tab >>Cellular and genetic components in the development of IDDM in NOD mice.
1996 (English)Doctoral thesis, comprehensive summary (Other academic)
Place, publisher, year, edition, pages
Umeå: Umeå universitet, 1996. 80 p.
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 464
Keyword
non-obese diabetic, IgVh gene utilisation, immunoregulation, programmed cell death, genetic linkage analysis
National Category
Basic Medicine
Research subject
Immunology
Identifiers
urn:nbn:se:umu:diva-87787 (URN)91-7191-150-2 (ISBN)
Public defence
1996-03-22, Institutionen för Mikrobiologi, föreläsningssalen, Umeå universitet, Umeå, 09:30
Supervisors
Available from: 2014-04-11 Created: 2014-04-09 Last updated: 2014-04-11Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Penha-Gonçalves, CarlosLeijon, KristinaPersson, LindaHolmberg, Dan
By organisation
Department of Molecular Biology (Faculty of Medicine)
In the same journal
Genomics
Basic Medicine

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 42 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf