Research ExplorerPublicationsAssociation of human FOS promoter variants with the occurren...

Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study

Standard

Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study. / Huber, Rene; kirsten, Holger; Näkki, Annu; Pohlers, Dirk; Thude, Hansjörg; Eidner, Thorsten; Heinig, Matthias; Brand, Korbinian; Ahnert, Peter; Kinne, Raimund.

In: INT J MOL SCI, Vol. 20, No. 6, 19.03.2019.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Huber, R, kirsten, H, Näkki, A, Pohlers, D, Thude, H, Eidner, T, Heinig, M, Brand, K, Ahnert, P & Kinne, R 2019, 'Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study', INT J MOL SCI, vol. 20, no. 6. https://doi.org/10.3390/ijms20061382

APA

Huber, R., kirsten, H., Näkki, A., Pohlers, D., Thude, H., Eidner, T., Heinig, M., Brand, K., Ahnert, P., & Kinne, R. (2019). Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study. INT J MOL SCI, 20(6). https://doi.org/10.3390/ijms20061382

Vancouver

Huber R, kirsten H, Näkki A, Pohlers D, Thude H, Eidner T et al. Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study. INT J MOL SCI. 2019 Mar 19;20(6). https://doi.org/10.3390/ijms20061382

Bibtex

@article{22328db173c747b7bcd3585cd09576f8,
title = "Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study",
abstract = "Our aim was to analyse (i) the presence of single nucleotide polymorphisms (SNPs) in the JUN and FOS core promoters in patients with rheumatoid arthritis (RA), knee-osteoarthritis (OA), and normal controls (NC); (ii) their functional influence on JUN/FOS transcription levels; and (iii) their associations with the occurrence of RA or knee-OA. JUN and FOS promoter SNPs were identified in an initial screening population using the Non-Isotopic RNase Cleavage Assay (NIRCA); their functional influence was analysed using reporter gene assays. Genotyping was done in RA (n = 298), knee-OA (n = 277), and NC (n = 484) samples. For replication, significant associations were validated in a Finnish cohort (OA: n = 72, NC: n = 548). Initially, two SNPs were detected in the JUN promoter and two additional SNPs in the FOS promoter in perfect linkage disequilibrium (LD). JUN promoter SNP rs4647009 caused significant downregulation of reporter gene expression, whereas reporter gene expression was significantly upregulated in the presence of the FOS promoter SNPs. The homozygous genotype of FOS promoter SNPs showed an association with the susceptibility for knee-OA (odds ratio (OR) 2.12, 95% confidence interval (CI) 1.2⁻3.7, p = 0.0086). This association was successfully replicated in the Finnish Health 2000 study cohort (allelic OR 1.72, 95% CI 1.2⁻2.5, p = 0.006). FOS Promoter variants may represent relevant susceptibility markers for knee-OA.",
author = "Rene Huber and Holger kirsten and Annu N{\"a}kki and Dirk Pohlers and Hansj{\"o}rg Thude and Thorsten Eidner and Matthias Heinig and Korbinian Brand and Peter Ahnert and Raimund Kinne",
year = "2019",
month = mar,
day = "19",
doi = "10.3390/ijms20061382",
language = "English",
volume = "20",
journal = "INT J MOL SCI",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "6",

}

RIS

TY - JOUR

T1 - Association of human FOS promoter variants with the occurrence of knee-osteoarthritis in a case control association study

AU - Huber, Rene

AU - kirsten, Holger

AU - Näkki, Annu

AU - Pohlers, Dirk

AU - Thude, Hansjörg

AU - Eidner, Thorsten

AU - Heinig, Matthias

AU - Brand, Korbinian

AU - Ahnert, Peter

AU - Kinne, Raimund

PY - 2019/3/19

Y1 - 2019/3/19

N2 - Our aim was to analyse (i) the presence of single nucleotide polymorphisms (SNPs) in the JUN and FOS core promoters in patients with rheumatoid arthritis (RA), knee-osteoarthritis (OA), and normal controls (NC); (ii) their functional influence on JUN/FOS transcription levels; and (iii) their associations with the occurrence of RA or knee-OA. JUN and FOS promoter SNPs were identified in an initial screening population using the Non-Isotopic RNase Cleavage Assay (NIRCA); their functional influence was analysed using reporter gene assays. Genotyping was done in RA (n = 298), knee-OA (n = 277), and NC (n = 484) samples. For replication, significant associations were validated in a Finnish cohort (OA: n = 72, NC: n = 548). Initially, two SNPs were detected in the JUN promoter and two additional SNPs in the FOS promoter in perfect linkage disequilibrium (LD). JUN promoter SNP rs4647009 caused significant downregulation of reporter gene expression, whereas reporter gene expression was significantly upregulated in the presence of the FOS promoter SNPs. The homozygous genotype of FOS promoter SNPs showed an association with the susceptibility for knee-OA (odds ratio (OR) 2.12, 95% confidence interval (CI) 1.2⁻3.7, p = 0.0086). This association was successfully replicated in the Finnish Health 2000 study cohort (allelic OR 1.72, 95% CI 1.2⁻2.5, p = 0.006). FOS Promoter variants may represent relevant susceptibility markers for knee-OA.

AB - Our aim was to analyse (i) the presence of single nucleotide polymorphisms (SNPs) in the JUN and FOS core promoters in patients with rheumatoid arthritis (RA), knee-osteoarthritis (OA), and normal controls (NC); (ii) their functional influence on JUN/FOS transcription levels; and (iii) their associations with the occurrence of RA or knee-OA. JUN and FOS promoter SNPs were identified in an initial screening population using the Non-Isotopic RNase Cleavage Assay (NIRCA); their functional influence was analysed using reporter gene assays. Genotyping was done in RA (n = 298), knee-OA (n = 277), and NC (n = 484) samples. For replication, significant associations were validated in a Finnish cohort (OA: n = 72, NC: n = 548). Initially, two SNPs were detected in the JUN promoter and two additional SNPs in the FOS promoter in perfect linkage disequilibrium (LD). JUN promoter SNP rs4647009 caused significant downregulation of reporter gene expression, whereas reporter gene expression was significantly upregulated in the presence of the FOS promoter SNPs. The homozygous genotype of FOS promoter SNPs showed an association with the susceptibility for knee-OA (odds ratio (OR) 2.12, 95% confidence interval (CI) 1.2⁻3.7, p = 0.0086). This association was successfully replicated in the Finnish Health 2000 study cohort (allelic OR 1.72, 95% CI 1.2⁻2.5, p = 0.006). FOS Promoter variants may represent relevant susceptibility markers for knee-OA.

U2 - 10.3390/ijms20061382

DO - 10.3390/ijms20061382

M3 - SCORING: Journal article

VL - 20

JO - INT J MOL SCI

JF - INT J MOL SCI

SN - 1661-6596

IS - 6

ER -