Inger-Lise Mero
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Inger-Lise Mero has a total of 37 co-authors. Here are the top co-authors by number of shared publications:
- Anne Spurkland
Department of Molecular Medicine Institute of Basic Medical Sciences University of Oslo Oslo Norway
2 shared publications A Compston
Department of Neurology, Oslo University Hospital, Oslo, Norway
1 shared publicationAnnette Bang Oturai
Department of Neurology, Oslo University Hospital, Ullevål, Oslo, Norway
1 shared publicationAnu Kemppinen
Department of Neurology, Oslo University Hospital, Ullevål, Oslo, Norway
1 shared publicationB A Lie
Department of Neurology, Oslo University Hospital, Oslo, Norway
1 shared publicationB Skinningsrud
Department of Neurology, Oslo University Hospital, Oslo, Norway
1 shared publication
Latest Publications
- 23 December 2010
- Published by Springer Nature in Genes & Immunity
- Vol. 12 (3) , 191-198
Exploring the CLEC16A gene reveals a MS-associated variant with correlation to the relative expression of CLEC16A isoforms in thymus
Genomewide association studies have implicated the CLEC16A gene in several autoimmune diseases, including multiple sclerosis (MS) and type 1 diabetes. However, the most associated single-nucleotide polymorphism (SNP) varies, and causal variants are still to be defined. In MS, two SNPs in partial linkage disequilibrium with each other, rs6498169 and rs12708716, have been validated at genomewide significance level. To explore the CLEC16A association in MS in more detail, we genotyped 57 SNPs in 807 Norwegian MS patients and 1027 Norwegian controls. Six highly associated SNPs emerged and were then replicated in two large independent sample sets (Norwegian and British), together including 1153 MS trios, 2308 MS patients and 4044 healthy controls. In combined analyses, SNP rs12708716 gave the strongest association signal in MS (P=5.3 × 10−8, odds ratio 1.18, 95% confidence interval=1.11–1.25), and was found to be superior to the other SNP associations in conditional logistic regression analyses. Expression analysis revealed that rs12708716 genotype was significantly associated with the relative expression levels of two different CLEC16A transcripts in thymus (P=0.004), but not in blood, possibly implying a thymus- or cell-specific splice regulation.
- 23 December 2010
- Published by Springer Nature in Genes & Immunity
- Vol. 12 (3) , 191-198
Exploring the CLEC16A gene reveals a MS-associated variant with correlation to the relative expression of CLEC16A isoforms in thymus
Genomewide association studies have implicated the CLEC16A gene in several autoimmune diseases, including multiple sclerosis (MS) and type 1 diabetes. However, the most associated single-nucleotide polymorphism (SNP) varies, and causal variants are still to be defined. In MS, two SNPs in partial linkage disequilibrium with each other, rs6498169 and rs12708716, have been validated at genomewide significance level. To explore the CLEC16A association in MS in more detail, we genotyped 57 SNPs in 807 Norwegian MS patients and 1027 Norwegian controls. Six highly associated SNPs emerged and were then replicated in two large independent sample sets (Norwegian and British), together including 1153 MS trios, 2308 MS patients and 4044 healthy controls. In combined analyses, SNP rs12708716 gave the strongest association signal in MS (P=5.3 × 10−8, odds ratio 1.18, 95% confidence interval=1.11–1.25), and was found to be superior to the other SNP associations in conditional logistic regression analyses. Expression analysis revealed that rs12708716 genotype was significantly associated with the relative expression levels of two different CLEC16A transcripts in thymus (P=0.004), but not in blood, possibly implying a thymus- or cell-specific splice regulation.
- 4 November 2009
- Published by Springer Nature in European Journal of Human Genetics
- Vol. 18 (4) , 502-504
A rare variant of the TYK2 gene is confirmed to be associated with multiple sclerosis
A rare functional variant within the TYK2 gene (rs34536443) has been reported as protective in multiple sclerosis (MS) in recent studies. However, because of the low frequency of the minor allele (minor allele frequency=0.04), genome-wide significant association has been hard to establish. We genotyped 5429 Nordic MS cases and 6167 healthy controls for this TYK2 non-synonymous single-nucleotide polymorphism (ns-SNP), and combined the Nordic genotype data with raw genotypes from previous studies. The combined Nordic analysis showed significant association with MS (P=5 × 10−4, odds ratio (OR) 0.78), and by mega-analysis of 10 642 MS patients, 10 620 controls and 2110 MS trios, the association at genome-wide significance level (P=5.08 × 10−9, OR 0.77) was shown.
- 4 November 2009
- Published by Springer Nature in European Journal of Human Genetics
- Vol. 18 (4) , 502-504
A rare variant of the TYK2 gene is confirmed to be associated with multiple sclerosis
A rare functional variant within the TYK2 gene (rs34536443) has been reported as protective in multiple sclerosis (MS) in recent studies. However, because of the low frequency of the minor allele (minor allele frequency=0.04), genome-wide significant association has been hard to establish. We genotyped 5429 Nordic MS cases and 6167 healthy controls for this TYK2 non-synonymous single-nucleotide polymorphism (ns-SNP), and combined the Nordic genotype data with raw genotypes from previous studies. The combined Nordic analysis showed significant association with MS (P=5 × 10−4, odds ratio (OR) 0.78), and by mega-analysis of 10 642 MS patients, 10 620 controls and 2110 MS trios, the association at genome-wide significance level (P=5.08 × 10−9, OR 0.77) was shown.