Phone 615.343.4922
Office 4110 MRBIII
Nashville, TN 37232-8240
Email chin.chiang@vanderbilt.edu
Figure 3. Ventral midbrain is specified but cannot be maintained in the Shh-/- mouse.  From "Ventral specification and perturbed boundary formation in the mouse midbrain in the absence of Hedgehog signaling."


 

The Chiang laboratory is interested in the mechanism of Sonic hedgehog (Shh) signaling in development and disease. Mutations in Shh and genes encoding Shh signaling components have been associated with many clinical disorders found in humans including polydactyly, holoprosencephaly and various forms of cancer.  Mouse models involving the Hh pathway have provided lab members with several novel insights, including the role of Sonic hedgehog (Shh) in the specification and patterning of distinct neuronal subtypes in the spinal cord, how the Shh signaling gradient is interpreted in anterior-posterior patterning of the limb, and finally, how the Shh signaling gradient is regulated during embryonic development. The Chiang lab's current research is focused on the Gli3 transcription factor, a critical regulator of Shh signaling, in the pathogenesis of human diseases.  Lab members are currently using a combination of molecular, biochemical and genetic approaches to unravel the functions of Gli3 protein and to establish that specific clinical phenotypes are associated with distinct GLI3 functions.

 

For more information about Dr. Chiang visit his Vanderbilt Faculty Page or Lab Website

RECENT PUBLICATIONS

Ventral specification and perturbed boundary formation in the mouse midbrain in the absence of Hedgehog signaling.  Developmental Dynamics (2008) 237: 1359-1372

PREVIOUS PUBLICATIONS
 

 

 

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Last modified: Friday, May 17, 2008 by Kim.Kane@vanderbilt.edu