Dipeptidyl Peptidase IV Activity and/or Structure Homologs: Contributing Factors in the Pathogenesis of Rheumatoid Arthritis?

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Dipeptidyl Peptidase IV Activity and/or Structure Homologs: Contributing Factors in the Pathogenesis of Rheumatoid Arthritis?

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Title: Dipeptidyl Peptidase IV Activity and/or Structure Homologs: Contributing Factors in the Pathogenesis of Rheumatoid Arthritis?
Author: Sedo, Aleksi; Balaziova, Eva; Sedova, Liliana R; Duke-Cohan, Jonathan S.

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Citation: Sedo, Aleksi, Jonathan S. Duke-Cohan, Eva Balaziova, and Liliana R. Sedova. 2005. Dipeptidyl peptidase IV activity and/or structure homologs: Contributing factors in the pathogenesis of rheumatoid arthritis? Arthritis Research & Therapy 7(6): 253-269.
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Abstract: Several of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream of tumor necrosis factor-α as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1α and the neuropeptides vasoactive intestinal peptide (VIP) and substance P, have their biological half-lives controlled by dipeptidyl peptidase IV (DPPIV). Proteolysis by DPPIV regulates not only the half-life but also receptor preference and downstream signaling. In this article, we examine the role of DPPIV homologs, including CD26, the canonical DPPIV, and their substrates in the pathogenesis of rheumatoid arthritis. The differing specific activities of the DPPIV family members and their differential inhibitor response provide new insights into therapeutic design.
Published Version: doi:10.1186/ar1852
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297595/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:5358887
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