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(Circulation Research. 2005;96:274.)
© 2005 American Heart Association, Inc.

Editorials

Wnt, a Driver of Myocardialization?

Maurice J.B. van den Hoff, Antoon F.M. Moorman

From the Molecular and Experimental Cardiology Group, Department of Anatomy and Embryology, Academic Medical Center, Meibergdreef 15, 1105AZ Amsterdam, The Netherlands

Correspondence to Dr Maurice J.B. van den Hoff, Department of Anatomy and Embryology, Academic Medical Center, Meibergdreef 15, 1105AZ Amsterdam, The Netherlands. E-mail m.j.vandenhoff@amc.uva.nl

See related article, pages 292–299

Key Words: Lp mouse • Wnt growth factors • signal transduction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In this current issue of Circulation Research, Phillips and coworkers¹ carefully analyze the cardiovascular defect observed in the naturally occurring Loop-tail (Lp) mouse strain, which is best known for its severe neural tube defects.² The genetic alteration in the Lp mouse was identified several years ago by two independent groups and appears to be a missense mutation in the Van Gogh–like 2 (VANGL2) gene (S464N).^3,4 Moreover, a second mouse strain was identified with another mutation in the VANGL2 gene (D255E) which has a similar phenotype.⁵ Vangl2 encodes a 521-aa protein which is predicted to contain four transmembrane regions, both the N and C termini protruding into the cytoplasm, and a C-terminal PDZ domain. The ancestral gene, Van Gogh (VANG), was initially identified in Drosophila as a regulator of cell/tissue polarity during development. Cell polarization is coordinated not only by Vang/Vangl but also by other components of the Wnt-Frizzled signaling pathway (see reviews^6,7). Which Wnt growth factors are involved in triggering the signal transduction is not yet known, though Wnt11 is a potential candidate based on zebrafish studies.⁸ In vertebrates a second homologue of Vang was cloned, which is referred to as Van Gogh–like 1. Vangl1 and 2 are structurally similar. In vitro assays showed that both Vangl1 and 2 are able to directly interact through their PDZ domain with all three known members of the Wnt intracellular signal transducer Deshevelled (Dvl). Moreover, both known Vangl2 mutations were found to disrupt binding to . . . [Full Text of this Article]

Related Article:

Vangl2 Acts via RhoA Signaling to Regulate Polarized Cell Movements During Development of the Proximal Outflow Tract

Helen M. Phillips, Jennifer N. Murdoch, Bill Chaudhry, Andrew J. Copp, and Deborah J. Henderson
Circ. Res. 2005 96: 292-299. [Abstract] [Full Text] [PDF]