Abstract

Animal models represent an invaluable tool, which must be judiciously used to provide the greatest benefit to human kind, due to their cost and time effectiveness. The CCN2 null mouse model described in this paper represents a new murine model of craniofacial development. This model is notable for its remarkably consistent phenotype and ease of colony care and propagation. The interaction of CCN2 with the TGF-β, BMP, FGF, EGF, Integrin, and WNT proteins is currently under investigated and signifies a plethora of research opportunities that may help elucidate novel therapeutic options for future patients. This paper presents a descriptive overview of the known craniofacial developmental abnormalities of this model as well as the known molecular signaling aberrances that provide clues to direct future investigative endeavors.

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