help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
This version published online on March 29, 2007
Endocrinology, doi:10.1210/en.2006-1372
A more recent version of this article appeared on June 1, 2007
This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
148/6/2630    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Glass, D. A.
Right arrow Articles by Karsenty, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Glass, D. A., II
Right arrow Articles by Karsenty, G.

Submitted on October 6, 2006
Accepted on November 20, 2006

In vivo analysis of Wnt signaling in bone

Donald A. Glass II and Gerard Karsenty*

Medical Scientist Training Program, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030; Department of Genetics and Development, Columbia University Medical Center, 701 West 168th Street, Room 1602A, New York, NY 10032

* To whom correspondence should be addressed. E-mail: gk2172{at}columbia.edu.

Bone remodeling requires osteoblasts and osteoclasts working in concert to maintain a constant bone mass. The dysregulation of signaling pathways that affect osteoblast or osteoclast differentiation or function leads to either osteopenia or high bone mass. The discovery that activating and inactivating mutations in Lrp5, a putative Wnt coreceptor, led to high bone mass and low bone mass in humans, respectively, generated a tremendous amount of interest in the possible role of the Wnt signaling pathway in the regulation of bone remodeling. A number of mouse models have been generated to study a collection of Wnt signaling molecules that have been identified as regulators of bone mass. These mouse models help establish the canonical Wnt signaling pathway as a major regulator of chondrogenesis, osteoblastogenesis and osteoclastogenesis. This review will summarize these advances.
Key words: Wnt • osteoblast • osteoclast • beta-catenin • Lrp5 • bone remodeling




This article has been cited by other articles:


Home page
 Integr. Comp. Biol.Home page
K. M. Middleton, S. A. Kelly, and T. Garland Jr
Selective breeding as a tool to probe skeletal response to high voluntary locomotor activity in mice
Integr. Comp. Biol., June 18, 2008; (2008) icn057v1.
[Abstract] [Full Text] [PDF]

Home page
 IBMS BoneKEyHome page
D. A. Towler
Vascular Calcification: A Perspective On An Imminent Disease Epidemic
IBMS BoneKEy, February 1, 2008; 5(2): 41 - 58.
[Abstract] [Full Text] [PDF]

Home page
 DevelopmentHome page
P. Hayward, T. Kalmar, and A. Martinez Arias
Wnt/Notch signalling and information processing during development
Development, February 1, 2008; 135(3): 411 - 424.
[Abstract] [Full Text] [PDF]

Home page
 IBMS BoneKEyHome page
T. J. Martin and K. W. Ng
New Agents for the Treatment of Osteoporosis
IBMS BoneKEy, November 1, 2007; 4(11): 287 - 298.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2007 by The Endocrine Society