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Absence of association between the INSIG2 gene polymorphism (rs7566605) and obesity in the European Youth Heart Study (EYHS).

https://arctichealth.org/en/permalink/ahliterature95295
Source
Obesity (Silver Spring). 2009 Jul;17(7):1453-7
Publication Type
Article
Date
Jul-2009
Author
Vimaleswaran Karani S
Franks Paul W
Brage Soren
Sardinha Luis B
Andersen Lars B
Wareham Nicholas J
Ekelund Ulf
Loos Ruth J F
Author Affiliation
MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK.
Source
Obesity (Silver Spring). 2009 Jul;17(7):1453-7
Date
Jul-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Child
Cross-Sectional Studies
Denmark
Estonia
Europe
Female
Genetic Predisposition to Disease - genetics
Genotype
Humans
Intracellular Signaling Peptides and Proteins - genetics
Lipids - blood
Male
Membrane Proteins - genetics
Obesity - blood - ethnology - genetics
Polymorphism, Single Nucleotide - genetics
Waist Circumference - genetics
Abstract
The first genome-wide association study for BMI identified a polymorphism, rs7566605, 10 kb upstream of the insulin-induced gene 2 (INSIG2) transcription start site, as the most significantly associated variant in children and adults. Subsequent studies, however, showed inconsistent association of this polymorphism with obesity traits. This polymorphism has been hypothesized to alter INSIG2 expression leading to inhibition of fatty acid and cholesterol synthesis. Hence, we investigated the association of the INSIG2 rs7566605 polymorphism with obesity- and lipid-related traits in Danish and Estonian children (930 boys and 1,073 girls) from the European Youth Heart Study (EYHS), a school-based, cross-sectional study of pre- and early pubertal children. The association between the polymorphism and obesity traits was tested using additive and recessive models adjusted for age, age-group, gender, maturity and country. Interactions were tested by including the interaction terms in the model. Despite having sufficient power (98%) to detect the previously reported effect size for association with BMI, we did not find significant effects of rs7566605 on BMI (additive, P = 0.68; recessive, P = 0.24). Accordingly, the polymorphism was not associated with overweight (P = 0.87) or obesity (P = 0.34). We also did not find association with waist circumference (WC), sum of four skinfolds, or with total cholesterol, triglycerides, low-density lipoprotein, or high-density lipoprotein. There were no gender-specific (P = 0.55), age-group-specific (P = 0.63) or country-specific (P = 0.56) effects. There was also no evidence of interaction between genotype and physical activity (P = 0.95). Despite an adequately powered study, our findings suggest that rs7566605 is not associated with obesity-related traits and lipids in the EYHS.
PubMed ID
19197262 View in PubMed
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Association analysis of podocyte slit diaphragm genes as candidates for diabetic nephropathy.

https://arctichealth.org/en/permalink/ahliterature160579
Source
Diabetologia. 2008 Jan;51(1):86-90
Publication Type
Article
Date
Jan-2008
Author
P. Ihalmo
M. Wessman
M A Kaunisto
R. Kilpikari
M. Parkkonen
C. Forsblom
H. Holthöfer
P-H Groop
Author Affiliation
Folkhälsan Institute of Genetics, Folkhälsan Research Center, University of Helsinki, Helsinki, Finland.
Source
Diabetologia. 2008 Jan;51(1):86-90
Date
Jan-2008
Language
English
Publication Type
Article
Keywords
Actinin - genetics
Adult
Cross-Sectional Studies
Diabetes Mellitus, Type 1 - genetics
Diabetic Nephropathies - diagnosis - genetics
Female
Finland
Genetic Predisposition to Disease
Humans
Intracellular Signaling Peptides and Proteins - genetics
Male
Membrane Proteins - genetics
Podocytes - metabolism
Polymorphism, Single Nucleotide
Sialoglycoproteins - genetics
Abstract
The slit diaphragm is an adhesion and signalling protein complex linking the interdigitating podocyte foot processes in the kidney glomerulus, and mutations in slit diaphragm-associated genes result in severe proteinuria. Here we report a genetic association analysis of four slit diaphragm genes, LRRC7, KIRREL, NPHS2 and ACTN4, in a Finnish diabetic nephropathy cohort.
A total of 40 single nucleotide polymorphisms (SNPs) were genotyped in 1103 patients with type 1 diabetes. The patients were classified according to their renal status, and the genotype data were analysed in a cross-sectional case-control setting. To confirm positive associations, four SNPs were genotyped in 1,025 additional patients with type 1 diabetes.
No associations with diabetic nephropathy were observed for any of the analysed SNPs. The SNPs were not associated with the time from the onset of diabetes to the diagnosis of nephropathy or with glomerular filtration rate or AER as quantitative variables. In a sex-specific sub-analysis, the variants rs979972 and rs749701 in the first intron of ACTN4 were nominally associated with diabetic nephropathy in females, with odds ratios of 1.81 (95% CI 1.18-2.79, p = 0.007) and 1.93 (95% CI 1.26-2.96, p = 0.003) respectively.
Our study has not found any evidence that common variants in LRRC7, KIRREL, NPHS2 and ACTN4 contribute to susceptibility to diabetic nephropathy in Finnish patients with type 1 diabetes.
PubMed ID
17968527 View in PubMed
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Association of NFE2L2 and KEAP1 haplotypes with amyotrophic lateral sclerosis.

https://arctichealth.org/en/permalink/ahliterature257631
Source
Amyotroph Lateral Scler Frontotemporal Degener. 2014 Mar;15(1-2):130-7
Publication Type
Article
Date
Mar-2014
Author
Petra Bergström
Malin von Otter
Staffan Nilsson
Ann-Charloth Nilsson
Michael Nilsson
Peter M Andersen
Ola Hammarsten
Henrik Zetterberg
Author Affiliation
Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine, The Sahlgrenska Academy at the University of Gothenburg , Gothenburg , Sweden.
Source
Amyotroph Lateral Scler Frontotemporal Degener. 2014 Mar;15(1-2):130-7
Date
Mar-2014
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Aged
Aged, 80 and over
Amyotrophic Lateral Sclerosis - genetics
Bulbar Palsy, Progressive - genetics
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease - genetics
Haplotypes
Humans
Intracellular Signaling Peptides and Proteins - genetics
Male
Middle Aged
Muscular Atrophy, Spinal - genetics
NF-E2-Related Factor 2 - genetics
Polymorphism, Single Nucleotide - genetics
Promoter Regions, Genetic - genetics
Sweden
Abstract
Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron syndrome influenced by oxidative stress. The transcription factor Nrf2 and its repressor Keap1 constitute an important defence system in cellular protection against oxidative stress. Here we hypothesize that common genetic variations in the genes NFE2L2 and KEAP1, encoding Nrf2 and Keap1, may influence the risk and phenotype of ALS. Five hundred and twenty-two Swedish patients with sporadic ALS (SALS) and 564 Swedish control subjects were studied. Eight tag SNPs in NFE2L2 and three tag SNPs in KEAP1 were genotyped by allelic discrimination and three functional NFE2L2 promoter SNPs were genotyped by sequencing. One NFE2L2 haplotype (GGGAC) was associated with decreased risk of SALS (OR = 0.62 per allele, p = 0.003) and one haplotype in KEAP1 (CGG) was associated with later SALS onset (+3.4 years per allele, p = 0.015). When stratified by subgroup, one haplotype in NFE2L2, GAGCAGA including three functional promoter SNPs associated with high Nrf2 protein expression, was associated with 4.0 years later disease onset per allele in subgroup ALS (p = 0.008). In conclusion, these results suggest that variations in NFE2L2 and KEAP1, encoding two central proteins in cellular oxidative stress defence, may influence SALS pathogenesis.
PubMed ID
24102512 View in PubMed
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Azidothymidine and cisplatin increase p14ARF expression in OVCAR-3 ovarian cancer cell line.

https://arctichealth.org/en/permalink/ahliterature81725
Source
Toxicol Appl Pharmacol. 2006 Oct 1;216(1):89-97
Publication Type
Article
Date
Oct-1-2006
Author
Vaskivuo Liisa
Rysä Jaana
Koivuperä Johanna
Myllynen Päivi
Vaskivuo Tommi
Chvalova Katerina
Serpi Raisa
Savolainen Eeva-Riitta
Puistola Ulla
Vähäkangas Kirsi
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, FI-90014 Oulu, Finland.
Source
Toxicol Appl Pharmacol. 2006 Oct 1;216(1):89-97
Date
Oct-1-2006
Language
English
Publication Type
Article
Keywords
Antineoplastic Agents - pharmacology
Apoptosis - drug effects
Blotting, Western
Cell Line, Tumor
Cisplatin - pharmacology
DNA-Binding Proteins - genetics - metabolism
Dose-Response Relationship, Drug
Female
Gene Expression Regulation, Neoplastic - drug effects
HT29 Cells
Humans
Intracellular Signaling Peptides and Proteins - genetics - metabolism
Ovarian Neoplasms - genetics - metabolism - pathology
Proto-Oncogene Proteins c-mdm2 - genetics - metabolism
RNA, Messenger - genetics - metabolism
Reverse Transcriptase Inhibitors - pharmacology
Taxoids - pharmacology
Transcription Factors - genetics - metabolism
Tumor Suppressor Protein p14ARF - genetics - metabolism
Tumor Suppressor Protein p53 - genetics - metabolism
Zidovudine - pharmacology
ras Proteins - genetics - metabolism
Abstract
p14(ARF) tumor suppressor protein regulates p53 by interfering with mdm2-p53 interaction. p14(ARF) is activated in response to oncogenic stimuli but little is known of the responses of endogenous p14(ARF) to different types of cellular stress or DNA damage. Azidothymidine (AZT) is being tested in several clinical trials as an enhancer of anticancer chemotherapy. However, the knowledge of the relationship between AZT and cellular pathways, e.g. p53 pathway, is very limited. In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses. We found that endogenous p14(ARF) protein in OVCAR-3 cells is down-regulated by DTX but induced by AZT and a short CDDP pulse treatment. In HT-29 colon carcinoma cells with a mutated p53, all treatments down-regulated p14(ARF) protein. Both CDDP and AZT increased the expression of p14ARF mRNA in OVCAR-3 cells. Differences in cell death induced by these drugs did not explain the differences in protein and mRNA expressions. No increase in the level of either c-Myc or H-ras oncoproteins was seen in OVCAR-3 cells after AZT or CDDP-treatment. These results suggest that p14(ARF) can respond to DNA damage without oncogene activation in cell lines without functional p53.
PubMed ID
16797627 View in PubMed
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[Blau syndrome--a chronic granulomatous, genetic disease]

https://arctichealth.org/en/permalink/ahliterature80041
Source
Ugeskr Laeger. 2006 Oct 16;168(42):3612-4
Publication Type
Article
Date
Oct-16-2006
Author
Milman Nils
Byg Keld-Erik
Author Affiliation
H:S Rigshospitalet, Hjertecentret, Medicinsk Afdeling B, Afsnit for Lungetransplantation, København Ø. milman@rh.dk
Source
Ugeskr Laeger. 2006 Oct 16;168(42):3612-4
Date
Oct-16-2006
Language
Danish
Publication Type
Article
Keywords
Arthritis - diagnosis - drug therapy - genetics
Child, Preschool
Diagnosis, Differential
Erythema - diagnosis - drug therapy - genetics
Exanthema - diagnosis - drug therapy - genetics
Granuloma - diagnosis - drug therapy - genetics
Humans
Infant
Intracellular Signaling Peptides and Proteins - genetics
Mutation
Nod2 Signaling Adaptor Protein
Prognosis
Syndrome
Uveitis - diagnosis - drug therapy - genetics
Abstract
Blau syndrome is a rare hereditary granulomatous disease presenting in patients of young age with exanthema, granulomatous arthritis and uveitis. Genetic analysis has shown an autosomal dominant inheritance and a number of specific mutations on chromosome 16q in codon 334, of which the most predominant are R334W and R334Q. Blau syndrome exists in Caucasian, Asian and Afro-American families, and de novo mutations have been reported. The estimated minimum incidence in Denmark is 0.05 per 100,000 person-years. Blau syndrome has pathological, clinical and therapeutic features in common with sarcoidosis but rarely involves the lungs or other parenchymatous organs. Discrimination between Blau syndrome and early-onset sarcoidosis should rely on chromosome analysis.
PubMed ID
17069723 View in PubMed
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CARD15 mutations are rare in Swedish pediatric Crohn disease.

https://arctichealth.org/en/permalink/ahliterature29803
Source
J Pediatr Gastroenterol Nutr. 2005 Apr;40(4):456-60
Publication Type
Article
Date
Apr-2005
Author
Maja Ideström
Carlos Rubio
Fredrik Granath
Yigael Finkel
J-P Hugot
Author Affiliation
Department of Woman and Child Health, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. maja.idestrom@karolinska.se
Source
J Pediatr Gastroenterol Nutr. 2005 Apr;40(4):456-60
Date
Apr-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Child
Crohn Disease - genetics
DNA Mutational Analysis
Female
Gene Frequency
Genetic Predisposition to Disease - genetics
Genotype
Heterozygote
Humans
Intracellular Signaling Peptides and Proteins - genetics
Male
Mutation - genetics
Phenotype
Research Support, Non-U.S. Gov't
Retrospective Studies
Severity of Illness Index
Sweden
Abstract
BACKGROUND: An association between mutations in a gene involved in bacterial recognition by monocytes, CARD15/NOD2 and Crohn disease (CD) has been reported in studies of adults and children. The aim of this study was to investigate the presence of CARD15 mutations in Swedish children with CD and analyze genotype-phenotype correlations. PATIENTS AND METHODS: Fifty-eight children (62% boys) with CD diagnosed between 2.8 and 16.9 years (median 10.9 years), were reviewed. Histopathology, retrospective data collection and mutational analyses for the three main mutations R702W, G908R and 1007fs were independently performed. First-degree relatives were also genotyped. RESULTS: A CARD15 mutation was found in 8.6% (95% confidence interval, 2.9% to 19.0%), all of whom were heterozygotes, giving an overall allele frequency of 4.3% (95% confidence interval, 1.4-9.8). In 12%, all patients without mutations, a first-degree relative had CD. In four of five children, mutations were transferred from their healthy mothers. Granulomas at onset were found in 80% of patients with mutations and in 43% of those without (P = 0.17). No statistical association was found between mutation and phenotype regarding age at onset, anatomic location at onset or follow-up, severity of inflammation at onset, development of stenosis, perianal disease or extra intestinal manifestations. CONCLUSIONS: The frequency of CARD15 mutation in this Swedish pediatric CD population is lower than reported in a mixed adult and pediatric population. The genotype-phenotype correlations were non-significant although a trend was found between the presence of mutations and granuloma formation. Healthy heterozygote mothers conveyed the mutation to their children with CD.
PubMed ID
15795594 View in PubMed
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CARD15/NOD2 polymorphisms do not explain concordance of Crohn's disease in Swedish monozygotic twins.

https://arctichealth.org/en/permalink/ahliterature173960
Source
Dig Liver Dis. 2005 Oct;37(10):768-72
Publication Type
Article
Date
Oct-2005
Author
J. Halfvarson
F. Bresso
M. D'Amato
G. Järnerot
S. Pettersson
C. Tysk
Author Affiliation
Division of Gastroenterology, Department of Internal Medicine, Orebro University Hospital, 701 85 Orebro, Sweden. jonas.halfvarson@orebroll.se
Source
Dig Liver Dis. 2005 Oct;37(10):768-72
Date
Oct-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Arginine
Case-Control Studies
Child
Crohn Disease - genetics
Female
Frameshift Mutation
Gene Frequency
Genetic Predisposition to Disease
Genotype
Glycine
Humans
Intracellular Signaling Peptides and Proteins - genetics
Leucine
Male
Middle Aged
Nod2 Signaling Adaptor Protein
Polymorphism, Genetic
Sweden - epidemiology
Tryptophan
Twins, Monozygotic - genetics
Abstract
CARD15/NOD2 polymorphisms are associated with Crohn's disease. There is a high concordance for disease and disease phenotype in monozygotic twin pairs with Crohn's disease.
We studied CARD15/NOD2 polymorphisms in a Swedish, population-based cohort of monozygotic twins with Crohn's disease to assess whether these variants explain disease concordance.
Twenty-nine monozygotic twin pairs (concordant n=9, discordant n=20) with Crohn's disease and 192 healthy controls were investigated for the CARD15/NOD2 variants Arg702Trp, Gly908Arg and Leu1007fsinsC.
CARD15/NOD2 mutations were found in 5/38 (13%) twins with Crohn's disease, corresponding to a total allele frequency of 6.6%. Only 2/9 concordant twin pairs carried any of the variants and the remaining seven were wild type genotype. The total allele frequency was 4.4 times higher (95% confidence interval 1.0-21.5, p=0.06) in concordant twins than in discordant ones, 11.1% versus 2.5%. In healthy controls the total allele frequency was 2.6%.
CARD15/NOD2 polymorphisms contribute but do not alone explain concordance of Crohn's disease in monozygotic twins and, at least in a Swedish population, other polymorphisms are required. The low occurrence of CARD15/NOD2 mutations in the study and other Northern European populations suggests that these variants are of less importance in Northern Europe.
PubMed ID
16002353 View in PubMed
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CCDC26 rs4295627 polymorphism (8q24.21) and glioma risk: a meta-analysis.

https://arctichealth.org/en/permalink/ahliterature271704
Source
Genet Mol Res. 2015;14(4):12074-84
Publication Type
Article
Date
2015
Author
H W Lu
M. Huang
J H Wang
X L Sun
Y Q Ke
Source
Genet Mol Res. 2015;14(4):12074-84
Date
2015
Language
English
Publication Type
Article
Keywords
Brain Neoplasms - ethnology - genetics
Case-Control Studies
China
Glioma - ethnology - genetics
Humans
Intracellular Signaling Peptides and Proteins - genetics
Polymorphism, Single Nucleotide
Sweden
Abstract
The association between the CCDC26 rs4295627 single nucleotide polymorphism (SNP) and the glioma risk has been studied previously, but these studies have yielded conflicting results. The aim of the present study is to analyze this association more vigorously, by means of a meta-analysis. A comprehensive literature search was performed in databases PubMed and EMBASE. Six articles including 12 case-control studies in English with 11,368 controls and 5891 cases were eligible for the meta-analysis. We conducted subgroup analyses by the source of controls, ethnicity, and country. Our meta-analysis revealed that the rs4295627 SNP was associated with the glioma risk in a heterozygote model (TG versus TT: odds ratio = 1.35, 95% confidence interval = 1.26-1.45, P = 0.066). Moreover, our results suggested that the rs4295627 SNP was associated with a notably increased risk of glioma among Caucasians except for Swedes in 4 models (the homozygote model, recessive model, dominant model, and additive model). Nonetheless, in Sweden and China, the results showed no associations. No evidence of the publication bias was uncovered. Thus, our meta-analysis suggests that the rs4295627 SNP is associated with an increased risk of glioma. Additional studies are needed to derive more precise conclusion.
PubMed ID
26505354 View in PubMed
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Contribution of CARD15 variants in determining susceptibility to Crohn's disease in Sweden.

https://arctichealth.org/en/permalink/ahliterature169195
Source
Scand J Gastroenterol. 2006 Jun;41(6):700-5
Publication Type
Article
Date
Jun-2006
Author
Leif Törkvist
Colin L Noble
Mikael Lördal
Urban Sjöqvist
Ulrik Lindforss
Elaine R Nimmo
Richard K Russell
Robert Löfberg
Jack Satsangi
Author Affiliation
Department of Medical and Surgical Gastroenterology, Karolinska University Hospital, Stockholm, Sweden. leif.torkvist@ki.se
Source
Scand J Gastroenterol. 2006 Jun;41(6):700-5
Date
Jun-2006
Language
English
Publication Type
Article
Keywords
Alleles
Case-Control Studies
Crohn Disease - epidemiology - genetics
European Continental Ancestry Group
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Humans
Intracellular Signaling Peptides and Proteins - genetics
Male
Multivariate Analysis
Mutation
Nod2 Signaling Adaptor Protein
Sweden - epidemiology
Abstract
Crohn's disease (CD) is a chronic inflammatory bowel disorder caused by environmental and genetic factors. Mutations in the CARD15 gene have been associated with CD. No previous case-control CARD15 study has been performed in the Swedish population.
The study comprised of 321 individuals: 178 with CD and 143 healthy controls (HCs), all from Stockholm County. All were genotyped for the three main CD-associated CARD15 variants (R702W, G908R and 1007fs) and phenotypic associations were investigated.
The allele frequencies of the R702W variant (4.5% CD versus 0.7% HC, p=0.008, OR = 6.8) and the G908R variant (2.0% CD versus 0% HC, p=0.045) were more common in CD patients than in controls. No significant difference in1007fs variant allele frequency was found between CD patients and controls (2.0% CD versus 1.7% HC, p = 0.8, OR = 1.1). Carriage of CARD15 variants was more common in the CD patients than in controls (15.2% CD versus 4.2% HC, p = 0.001, OR = 4.1, population attributable risk (PAR) = 11.4%). Genotype-phenotype analysis demonstrated that CARD15 variants were associated with ileal disease (p=0.0006, OR = 9.3, CI = 2.2-34) and protective for colonic CD (p = 0.01, OR = 0.18). An association between CARD15 variants and ileal CD (p=0.004, OR = 6.6) was confirmed by multivariate analyses.
The CARD15 variants R702W and G908R, but not 1007fs, are associated with susceptibility to CD in Stockholm County. Genotype-phenotype analysis shows an association with ileal CD. The contribution of these CARD15 mutations in Swedish CD patients overall is low in relation to studies elsewhere in Central Europe and North America, but is consistent with emerging data from elsewhere in Scandinavia and in Northern Europe.
PubMed ID
16716969 View in PubMed
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Crohn's disease associated CARD15 (NOD2) variants are not involved in the susceptibility to type 1 diabetes.

https://arctichealth.org/en/permalink/ahliterature46977
Source
Mol Genet Metab. 2005 Nov;86(3):379-83
Publication Type
Article
Date
Nov-2005
Author
Pegah Ghandil
Claude Chelala
Danièle Dubois-Laforgue
Valérie Senée
Sophie Caillat-Zucman
Ingrid Kockum
Holgar Luthman
Jorn Nerup
Flemming Pociot
José Timsit
Cécile Julier
Author Affiliation
Genetics of Infectious and Autoimmune Diseases, INSERM U730, Institut Pasteur, Paris, France.
Source
Mol Genet Metab. 2005 Nov;86(3):379-83
Date
Nov-2005
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Crohn Disease - genetics
Denmark
Diabetes Mellitus, Type 1 - genetics
European Continental Ancestry Group
France
Genetic Predisposition to Disease
Humans
Intracellular Signaling Peptides and Proteins - genetics
Research Support, Non-U.S. Gov't
Sweden
Variation (Genetics)
Abstract
Three variants in the caspase recruitment domain 15/nucleotide-binding oligomerization domain 2 (CARD15/NOD2) gene have been shown to be associated with Crohn's disease (CD). There is a strong support for shared genetic determinants between various autoimmune and inflammatory diseases. In particular, linkage of type 1 diabetes (T1D) and other autoimmune and inflammatory diseases has been reported on chromosome 16, encompassing the region containing the CARD15 gene. We therefore considered this gene as a good candidate for the T1D locus mapped to this region, and we tested the three CARD15 variants in the susceptibility to T1D in two independent settings: family based association analysis in Scandinavian multiplex families that we previously showed to be linked to this region, and case/control association study in a large cohort of French diabetic patients. We found no evidence for association of these variants with T1D overall, nor in subgroups of patients with or without the major risk genotypes at HLA-DRB1, at insulin (INS), or positive or negative for autoantibodies specific to other autoimmune diseases. Our results do not support a role for CD-associated CARD15 variants in the susceptibility to T1D, and suggest that another gene is responsible for the shared susceptibility between autoimmune and inflammatory diseases mapping to this region.
PubMed ID
16198136 View in PubMed
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39 records – page 1 of 4.