Endoplasmic reticulum aminopeptidase-1 polymorphism increases the risk of rheumatoid arthritis

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dc.authoridAKBULUT, EKREM/0000-0002-7526-9835
dc.authoridOZTURK, Onur/0000-0003-3404-4135
dc.authorwosidAKBULUT, EKREM/Q-2765-2015
dc.authorwosidOZTURK, Onur/HLH-4990-2023
dc.contributor.authorAkbulut, Ekrem
dc.contributor.authorYildirim, Tulay
dc.contributor.authorOzturk, Onur
dc.date.accessioned2024-08-04T20:10:17Z
dc.date.available2024-08-04T20:10:17Z
dc.date.issued2022
dc.departmentİnönü Üniversitesien_US
dc.description.abstractObjectives Endoplasmic reticulum aminopeptidase-1 (ERAP1) polymorphic changes cause autoimmunity. To understand the contribution of ERAP1 to the occurrence of rheumatoid arthritis (RA) disease, we investigated the relationship between ERAP1 and RA. Methods This study was conducted with 201 patients and 171 healthy controls. The rs26653, rs27044, rs27582, rs28096, and rs30187 polymorphic regions of ERAP1 were investigated. The comparison was done with Arlequin software and logistic regression. Haplotypes were analyzed with Phylogenetic Network software. ERAP1 was modeled using Promod3. Topological changes in ERAP1 were analyzed with TM-Score. Results The results showed that rs26653G>C (p=0.002, OR=2.001, 95%CI=1.276-3.137), rs27044C>G (p=0.037, OR=1.583, 95%CI=1.028-2.440), rs27582G>A (p<0.05, OR=0.348, 95%CI=0.194-0.622) and rs30187C>T (p=0.006, OR=1.849, 95%CI=1.191-2.870) polymorphisms are associated with RA disease risk. The relationship between rs28096 polymorphism and RA disease risk could not be determined (p=0.509). The risk haplotype for rheumatoid arthritis was determined as [CGAAT]. It was determined that polymorphisms of ERAP1 cause changes in the entry pocket of substrate and ligand. Conclusions We report a haplotype [CGAAT] that is associated with RA risk from Turkey that has not been described before. These data will make important contributions to elucidating the molecular mechanism of RA.en_US
dc.description.sponsorshipMunzur University Research Budget [2017-DT]en_US
dc.description.sponsorshipThis study was supported by Munzur University Research Budget (2017-DT).en_US
dc.identifier.doi10.1515/tjb-2022-0007
dc.identifier.endpage473en_US
dc.identifier.issn0250-4685
dc.identifier.issn1303-829X
dc.identifier.issue4en_US
dc.identifier.scopus2-s2.0-85146382574en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage465en_US
dc.identifier.trdizinid1176439en_US
dc.identifier.urihttps://doi.org/10.1515/tjb-2022-0007
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/1176439
dc.identifier.urihttps://hdl.handle.net/11616/92695
dc.identifier.volume47en_US
dc.identifier.wosWOS:000772130800001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.publisherWalter De Gruyter Gmbhen_US
dc.relation.ispartofTurkish Journal of Biochemistry-Turk Biyokimya Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectautoimmunityen_US
dc.subjectERAP1en_US
dc.subjectgenetic predispositionen_US
dc.subjectpeptide presentationen_US
dc.subjectrheumatoid arthritisen_US
dc.titleEndoplasmic reticulum aminopeptidase-1 polymorphism increases the risk of rheumatoid arthritisen_US
dc.typeArticleen_US

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