Novel splice variants derived from the receptor tyrosine kinase superfamily are potential therapeutics for rheumatoid arthritis 英文参考文献.docVIP
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Novel splice variants derived from the receptor tyrosine kinase superfamily are potential therapeutics for rheumatoid arthritis 英文参考文献
Available online /content/10/4/R73
Research article
Open Access
Vol 10 No 4
Novel splice variants derived from the receptor tyrosine kinase
superfamily are potential therapeutics for rheumatoid arthritis
Pei Jin1, Juan Zhang1, Percy F Sumariwalla2, Irene Ni1, Brett Jorgensen1, Damian Crawford2,
Suzanne Phillips3, Marc Feldmann2, H Michael Shepard1 and Ewa M Paleolog2
1Receptor BioLogix, Inc., Palo Alto, CA 94303, USA
2Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College London, London W6 8LH, UK
3Gentris Corporation, Morrisville, NC 27560, USA
Corresponding author: Pei Jin, pjin@
Received: 13 May 2008 Revisions requested: 9 Jun 2008 Revisions received: 25 Jun 2008 Accepted: 1 Jul 2008 Published: 1 Jul 2008
Arthritis Research Therapy 2008, 10:R73 (doi:10.1186/ar2447)
This article is online at: /content/10/4/R73
? 2008 Jin et al.; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Introduction Despite the advent of biological therapies for the
treatment of rheumatoid arthritis, there is a compelling need to
develop alternative therapeutic targets for nonresponders to
existing treatments. Soluble receptors occur naturally in vivo,
such as the splice variant of the cell surface receptor for
vascular endothelial growth factor (VEGF) – a key regulator of
angiogenesis in rheumatoid arthritis. Bioinformatics analyses
predict that the majority of human genes undergo alternative
splicing, generating proteins – many of which may have
regulatory functions. The objective of the present study was to
identify alternative splice variants (ASV) from cell surface
receptor genes, and to determine whether the novel proteins
encoded exert therapeutic activity in an in
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