For the best experience on the Abcam website please upgrade to a modern browser such as Google Chrome
If you continue without changing your cookie settings, we'll assume you’re happy with this.
See how activation of the canonical and non-canonical Wnt signaling pathways lead to the regulation of numerous downstream targets.
Wnt signaling – an overview
The Wnt signaling pathway was discovered more than 35 years ago but still, researchers are making new exciting discoveries based on this pathway even today1. Wnt signaling is relevant for many fields of research including cell proliferation and differentiation in development, stem cell renewal, and cancer progression1,2. This is why it is important for many scientists to understand the core components of the pathway and what can go wrong to lead to disease progression1.
Canonical Wnt signaling
In this poster, you can see the downstream effects on the Wnt signaling components after binding of Wnt ligands to their Frizzled receptors. This activation is known to lead to accumulation of β-catenin which can enter the nucleus, activating transcription of Wnt-dependent genes eg c-myc. Conversely, you can also see the downstream consequence of Wnt inhibitors (eg DKK, WIF, and sFRP) binding to Frizzled receptors. This leads to the proteasomal degradation of β-catenin via ubiquitination.
Non-canonical Wnt signaling
This poster also covers non-canonical Wnt signaling – the planar cell polarity (PCP) and the Wnt/calcium pathways. Activation of the PCP pathway leads to activation of downstream MAPK signaling resulting in cell survival or gene repression. Alternatively, it may activate Rock/Rho signaling leading to cytoskeletal rearrangement. Non-canonical Wnt signaling can also go down the route of the Wnt/calcium pathway. You can see here how this pathway may also lead to cytoskeletal rearrangement and activation of Wnt/calcium-dependent genes.