Publication: Winding through the WNT pathway during cellular development and demise
Loading...
Date
2006
Authors
Li, F. ; Chong, Z.Z. ; Maiese, K.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
In slightly over a period of twenty years, our
comprehension of the cellular and molecular
mechanisms that govern the Wnt signaling pathway
continue to unfold. The Wnt proteins were initially
implicated in viral carcinogenesis experiments
associated with mammary tumors, but since this period
investigations focusing on the Wnt pathways and their
transmembrane receptors termed Frizzled have been
advanced to demonstrate the critical nature of Wnt for
the development of a variety of cell populations as well
as the potential of the Wnt pathway to avert apoptotic
injury. In particular, Wnt signaling plays a significant
role in both the cardiovascular and nervous systems
during embryonic cell patterning, proliferation,
differentiation, and orientation. Furthermore, modulation
of Wnt signaling under specific cellular influences can
either promote or prevent the early and late stages of
apoptotic cellular injury in neurons, endothelial cells,
vascular smooth muscle cells, and cardiomyocytes. A
number of downstream signal transduction pathways can
mediate the biological response of the Wnt proteins that
include Dishevelled, ß-catenin, intracellular calcium,
protein kinase C, Akt, and glycogen synthase kinase-3ß.
Interestingly, these cellular cascades of the Wnt-Frizzled pathways can participate in several neurodegenerative,
vascular, and cardiac disorders and may be closely
integrated with the function of trophic factors.
Identification of the critical elements that modulate the
Wnt-Frizzled signaling pathway should continue to
unlock the potential of Wnt pathway for the
development of new therapeutic options against
neurodegenerative and vascular diseases.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.