Molecular Biology of the Cell track citations

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

MBC in Press, published online ahead of print October 31, 2007
Mol. Biol. Cell 10.1091/mbc.E07-07-0682

A more recent version of this article appeared on January 1, 2008
This Article
Right arrow Full Text (PDF)
Right arrow Supplemental Materials
Right arrow All Versions of this Article:
E07-07-0682v1
19/1/78    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sakaguchi, M.
Right arrow Articles by Huh, N.-h.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sakaguchi, M.
Right arrow Articles by Huh, N.-h.

Submitted on July 19, 2007
Revised on October 10, 2007
Accepted on October 18, 2007

S100A11, an Dual Mediator for Growth Regulation of Human Keratinocytes

Masakiyo Sakaguchi,* Hiroyuki Sonegawa,* Hitoshi Murata,*{dagger} Midori Kitazoe,{dagger} Jun-ichiro Futami,{dagger} Ken Kataoka,* Hidenori Yamada,{dagger} and Nam-ho Huh*

*Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikatachou, Okayama 700-8558, Japan; {dagger}Department of Bioscience and Biotechnology, Okayama University Graduate School of Natural Science and Technology, Tsushimanaka, Okayama 700-8530, Japan

Monitoring Editor: M. Bishr Omary

We previously revealed a novel signal pathway involving S100A11 for inhibition of the growth of normal human keratinocytes (NHK) caused by high Ca++ or TGF{beta} (ProNAS USA, 102:13921–13926, 2005). Exposure to either agent resulted in transfer of S100A11 to nuclei, where it induced p21WAF1. On the other hand, S100A11 has been shown to be overexpressed in many human cancers. To address this apparent discrepancy, we analyzed possible new functions of S100A11 and provide herewith evidence that 1) S100A11 is actively secreted by NHK, 2) extracellular S100A11 acts on NHK to enhance the production of EGF family proteins, resulting in growth stimulation, 3) RAGE (receptor for advanced glycation endproducts), NF-{kappa}B, Akt, and CREB are involved in the S100A11-triggered signal transduction, and 4) production and secretion of S100A11 are markedly enhanced in human squamous cancer cells. These findings indicate that S100A11 plays an dual role in growth regulation of epithelial cells.

Address correspondence to: Nam-ho Huh (namu{at}md.okayama-u.ac.jp)




This article has been cited by other articles:


Home page
 Mol. Biol. CellHome page
U. Murzik, P. Hemmerich, S. Weidtkamp-Peters, T. Ulbricht, W. Bussen, J. Hentschel, F. von Eggeling, and C. Melle
Rad54B Targeting to DNA Double-Strand Break Repair Sites Requires Complex Formation with S100A11
Mol. Biol. Cell, July 1, 2008; 19(7): 2926 - 2935.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2007 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.