Abstract:
OBJECTIVE:To describe the relationship between the two mechanisms involved in sIL6R generation in rheumatoid arthritis (RA). METHOD:RA patients were selected from a group of subjects genotyped for the rs8192284 SNP, located at the proteolytic cleavage site of IL-6R. sIL6R and protease levels (ADAM17) were measured and the contribution of alternative splicing in the generation of sIL-6R was evaluated through qRT-PCR. RESULT:Increased sIL-6R plasma levels and expression of spliced isoform generating sIL-6R are genotype dependent. ADAM17 concentrations were independent of the genotype studied. CONCLUSION:Alternative splicing and proteolytic cleavage participate in sIL-6R generation in RA. The rs8192284 polymorphism determines the sIL-6R plasma level through differential proteolytic rupture controlled by ADAM17.
journal_name
Cytokinejournal_title
Cytokineauthors
Lamas JR,Rodríguez-Rodríguez L,Tornero-Esteban P,Villafuertes E,Hoyas J,Abasolo L,Varadé J,Alvarez-Lafuente R,Urcelay E,Fernández-Gutiérrez Bdoi
10.1016/j.cyto.2012.12.025subject
Has Abstractpub_date
2013-03-01 00:00:00pages
720-3issue
3eissn
1043-4666issn
1096-0023pii
S1043-4666(13)00004-5journal_volume
61pub_type
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