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Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Catenins

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...

Notch Signaling Pathway

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...

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Related Experiment Video

Updated: May 20, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

Taking a bite out of Wnts.

Cortney M Bouldin¹, David Kimelman

¹Department of Biochemistry, University of Washington, Seattle, WA 98103-7350, USA.

|July 11, 2012

Summary

Researchers discovered a new protein, TIKI, that regulates head size in vertebrates. TIKI acts as a Wnt antagonist, revealing a novel mechanism controlling intercellular communication during embryonic development.

Area of Science:

Developmental biology
Molecular biology
Cell signaling

Background:

Intercellular communication via the Wnt signaling pathway is crucial for embryonic development.
Proper regulation of Wnt signaling is essential for vertebrate head formation.

Purpose of the Study:

To identify novel regulators of Wnt signaling involved in head development.
To elucidate the mechanism by which TIKI influences head size.

Main Methods:

The study utilized genetic screens and molecular assays.
Protein interaction studies were performed to understand TIKI's function.

Main Results:

A novel protein, TIKI, was identified as a key regulator of head size.

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The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

Published on: February 16, 2017

Studying Wnt Signaling During Patterning of Conducting Airways

Studying Wnt Signaling During Patterning of Conducting Airways

Published on: October 16, 2016

Related Experiment Videos

Last Updated: May 20, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

Published on: February 16, 2017

Studying Wnt Signaling During Patterning of Conducting Airways

Studying Wnt Signaling During Patterning of Conducting Airways

Published on: October 16, 2016

TIKI functions through a previously undescribed mechanism of Wnt antagonism.

TIKI directly impacts Wnt pathway activity during embryogenesis.

Conclusions:

TIKI represents a novel Wnt antagonist with a significant role in vertebrate head formation.
The discovery of TIKI provides new insights into the molecular mechanisms controlling embryonic development and Wnt signaling.