Human WNT7A (Protein Wnt-7a) ELISA Kit

Wnt7a has been reported to signal via the canonical pathway, but also in non-canonical pathways acting on the cytoskeleton. Since Wnt7a is expressed after neurulation, we set to investigate the effects of Wnt7a on brain regionalization. We engineered transgenic mouse embryos that, under control of the nestin second intron, overexpressed Wnt7a in neural stem/progenitor cells. Surprisingly, transgenic embryos failed to complete cranial neurulation due to reduced levels and an impaired distribution of actin microfilaments, beta-catenin, and N-cadherin at the neural tube adherens junctions. These transgenic embryos expressed high levels of Vangl2, an essential component of non-canonical Wnt signaling. In agreement with a disregulation of this pathway, aberrant spinal neurulation was detected in the transgenic embryos, revealing a novel function regulated by Wnts. Thus, our findings suggest that Wnt7a overexpression disrupts normal Wnt signaling in the neural tube, resulting in defective adherens junctions and neurulation. (c) 2005 Elsevier Inc. All rights reserved.

The various Wnt pathways that are related to upper limb anomalies are reviewed. Abnormalities in the Wnt7a pathway (located in the dorsal ectoderm) produce several clinically relevant conditions such as the palmar duplication syndrome, nail patella syndrome, ulnar ray deficiency, limb hypoplasia, polysyndactyly and the palmar nail syndrome. Abnormalities of the Wnt3/3a pathway (located in the apical ectodermal ridge) include tetra-amelia and loss of the distal phalanges/nails. Abnormalities of the Wnt5/5a pathway (located in the apical ectodermal ridge as well as in the mesoderm) will affect chondrogenesis of the developing limb and experimental Wnt5a(-/-) limbs have terminal adactyly. Chondrogenesis and limb muscle differentiation are both affected by several Wnt pathways and these will be reviewed in details. Abnormalities in LRP 5/6 (a co-receptor for Wnts) lead to congenital bone disease and Wnt4 is specifically involved in joint development. Finally, the relationship between the Wnt pathway and SALL4 (mutations of which cause Okihiro/Duane-radial ray deficiency in humans) are discussed.