Wnt Signaling and Genetic Bone Diseases

Abstract

The Wnt signal transduction plays a vital role in regulating development throughout the animal kingdom. The Wnt signal transduction is complex, including Wnt ligands, receptors, coreceptors, transducers, transcription factors, antagonists, agonists and their modulators, and target genes. It is classified into β-catenindependent canonical and independent non-canonical Wnt (mainly planar cell polarity and Wnt/Ca 2+) signaling pathways. Wnt signaling pathway is causative to multiple human diseases. Gene mutations from the components of WNT signaling machinery have been identified to relate with low or high bone mass diseases, such as osteogenesis imperfecta, Robinow syndrome, osteoporosis-pseudoglioma syndrome, and sclerosteosis. In this review, we provide an update of the Wnt signaling pathway and the bone diseases caused by the aberrant components of the pathways.

Comprehensive bioinformatic analysis of Wnt1 and Wnt1-associated diseases

“…Wnts are secreted lipid-modified glycoproteins that transmit a signal through one more of different signaling pathways including canonical Wnt-β-catenin signaling and non-canonical pathways. Aberrant components of Wnt signaling are related to various human diseases, including genetic diseases and complex diseases such as cancer (1,2). Wnt1, the first member of the Wnt family to be identified, is a gene that was activated by integration of mouse mammary tumor virus (MMTV) proviral DNA in virally induced breast tumors in 1982 (3).…”