hh.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • 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
Analysis of polymorphisms in the mediator complex subunit 13-like (Med13L) gene in the context of immune function and development of experimental arthritis
University of Copenhagen, Copenhagen, Denmark & Nordic Bioscience A/S, Copenhagen, Denmark.
University of Copenhagen, Copenhagen, Denmark & Novartis International AG, Copenhagen, Denmark.
Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.ORCID iD: 0000-0003-4360-7710
2018 (English)In: Archivum Immunologiae et Therapiae Experimentalis, ISSN 0004-069X, E-ISSN 1661-4917, Vol. 66, no 5, p. 365-377Article in journal (Refereed) Published
Abstract [en]

The Mediator complex subunit 13-like (MED13L) protein is part of the multi-protein mediator complex and plays an important role in gene transcription. Polymorphisms in the MED13L gene have been linked to congenital heart anomalies and intellectual disabilities. Despite recent evidence of indirect links of MED13L to cytokine release and inflammation, impact of genetic variations in MED13L on immune cells remains unexplored. The B10.RIII and RIIIS/J mouse strains vary in susceptibility to induced experimental autoimmune disease models. From sequencing data of the two mouse strains, we identified six polymorphisms in the coding regions of Med13l. By using congenic mice, we studied the effect of these polymorphisms on immune cell development and function along with susceptibility to collagen-induced arthritis, an animal model for Rheumatoid Arthritis (RA). Combining in vivo disease data, in vitro functional data, and computational analysis of the reported non-synonymous polymorphisms, we report that genetic polymorphisms in Med13l do not affect the immune phenotype in these mice and are predicted to be non-disease associated. © The Author(s) 2018

Place, publisher, year, edition, pages
Basel: Springer, 2018. Vol. 66, no 5, p. 365-377
Keywords [en]
MED13L, THRAP2, mediator complex, Collagen-induced arthritis, Rheumatoid Arthritis, congenic mice
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:hh:diva-36795DOI: 10.1007/s00005-018-0516-8PubMedID: 29951696Scopus ID: 2-s2.0-85049072770OAI: oai:DiVA.org:hh-36795DiVA, id: diva2:1209094
Note

This work was supported by The Danish Rheumatism Association, The AP Møller Research grant for Medical Science, and The Oticon foundation.

Available from: 2018-05-21 Created: 2018-05-21 Last updated: 2018-09-27Bibliographically approved

Open Access in DiVA

fulltext(1647 kB)1 downloads
File information
File name FULLTEXT01.pdfFile size 1647 kBChecksum SHA-512
2090e9aac90fe6b6d657d2dc8f6b6f62ea0778ae1aaefee17791067f17c161078a2a11be11af92717ffde8beb19ad24db0457fb8984fe9e94e8998de4c5a7367
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMedScopus

Authority records BETA

Andersson, Åsa

Search in DiVA

By author/editor
Andersson, Åsa
By organisation
The Rydberg Laboratory for Applied Sciences (RLAS)
In the same journal
Archivum Immunologiae et Therapiae Experimentalis
Immunology in the medical area

Search outside of DiVA

GoogleGoogle Scholar
Total: 1 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 16 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • 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