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RHAMM, a Receptor for Hyaluronan-Mediated Motility, Compensates for CD44 in Inflamed CD44-Knockout Mice: A Different Interpretation of Redundancy

Shlomo Nedvetzki, Erez Gonen, Nathalie Assayag, Reuven Reich, Richard O. Williams, Robin L. Thurmond, Jing-Feng Huang, Birgit A. Neudecker, Fu-Shang Wang, Eva A. Turley, David Naor and Philippa Marrack
Proceedings of the National Academy of Sciences of the United States of America
Vol. 101, No. 52 (Dec. 28, 2004), pp. 18081-18086
Stable URL: http://www.jstor.org/stable/3374197
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
RHAMM, a Receptor for Hyaluronan-Mediated Motility, Compensates for CD44
              in Inflamed CD44-Knockout Mice: A Different Interpretation of
              Redundancy
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Abstract

We report here that joint inflammation in collagen-induced arthritis is more aggravated in CD44-knockout mice than in WT mice, and we provide evidence for molecular redundancy as a causal factor. Furthermore, we show that under the inflammatory cascade, RHAMM (receptor for hyaluronan-mediated motility), a hyaluronan receptor distinct from CD44, compensates for the loss of CD44 in binding hyaluronic acid, supporting cell migration, up-regulating genes involved with inflammation (as assessed by microarrays containing 13,000 cDNA clones), and exacerbating collagen-induced arthritis. Interestingly, we further found that the compensation for loss of the CD44 gene does not occur because of enhanced expression of the redundant gene (RHAMM), but rather because the loss of CD44 allows increased accumulation of the hyaluronic acid substrate, with which both CD44 and RHAMM engage, thus enabling augmented signaling through RHAMM. This model enlightens several aspects of molecular redundancy, which is widely discussed in many scientific circles, but the processes are still ill defined.

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