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Wnt Signaling Overview

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Intracellular signaling pathways initiated by the growth factor Wnt play a number of important roles during embryonic development, and have more recently been linked to the function of synapses in the adult brain1. Wnt signaling is involved in the assembly of both the pre- and postsynaptic neuronal compartments as well as synaptic plasticity and maintenance. The Wnt inhibitor Dickkopf-1 (Dkk1) causes a dispersion of synaptic proteins that results in disassembly2.

With 19 genes encoding Wnt proteins and at least 15 different receptors and co-receptors identified to date, Wnt signaling is extremely complex. Extracellular Wnt binds to transmembrane cell surface receptors in the frizzled (Fz) and low-density lipoprotein-related protein (LRP) families. Activation of these receptors induces a hyperphosphorylation of Dishevelled (Dsh) proteins, resulting is one of three downstream signaling cascades: a “canonical” pathway that affects gene transcription through β-catenin, or two noncanonical, β-catenin-independent pathways that regulate the cytoskeleton and intracellular calcium levels1.

Synapse loss has emerged as an early pathological hallmark of the neurodegenerative disorder Alzheimer’s disease (AD) and is associated with cognitive decline in the illness3. The soluble form of amyloid-β (Aβ) may be to blame for this synapse loss, perhaps through a disruption of Wnt signaling2, 4. For example, the binding of soluble Aβ to Fz5 blocks Wnt signaling in vitro, and levels of Dkk1 are elevated in AD brains3, 5.

In addition to AD, Wnt signaling may have a hand in many other diseases of synaptic dysfunction, including Parkinson’s disease, schizophrenia, and autism. The knowledge that perturbation of Wnt signaling disrupts the integrity of synapses suggests that this pathway may be a therapeutic target for AD and other synaptic diseases6.

Detection of PKC-alpha in a FFPE section of mouse olfactory bulb by ICC-IF

Detection of mouse PKC-alpha (red) in FFPE olfactory bulb by IHC-IF. Antibody: Rabbit anti-PKC-alpha (A302-446A). Secondary: DyLight® 594 conjugated goat anti-rabbit (A120-201D4).  Counterstain: DAPI (blue).

Detection of mouse Nanog by WB of immunoprecipitates from F9 cells

Detection of mouse Nanog by WB of immunoprecipitates from F9 cells.  Antibodies: Rabbit anti-Nanog (A300-397A & A300-398A). Secondary: ReliaBLOT® reagents (WB120).



Below is the current listing of Bethyl antibodies involved in Wnt signaling pathway research:


Wnt Signaling


1. Niehrs C. 2012. The complex world of WNT receptor signaling. Nat Rev Mol Cell Biol. Dec;13(12):767-779.

2. Dickins EM, Salinas PC. 2013. Wnts in action: from synapse formation to synaptic maintenance. Front Cell Neurosci. Nov 5;7:162.

3. Purro SA, Galli S, Salinas PC. 2014. Dysfunction of Wnt signaling and synaptic disassembly in neurodegenerative diseases. J Mol Cell Biol. Feb;6(1):75-80.

4. Shankar GM, Bloodgood BL, Townsend M, Walsh DM, Selkoe DJ, Sabatini BL. 2007. Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway. J Neurosci. Mar 14;27(11):2866-2875.

5. Magdesian MH, Carvalho MM, Mendes FA, Saraiva LM, Juliano MA, Juliano L, Garcia-Abreu J, Ferreira ST. 2008. Amyloid-beta binds to the extracellular cysteine-rich domain of Frizzled and inhibits Wnt/beta-catenin signaling. J Biol Chem. Apr 4;283(14):9359-9368.

6. Nistic├▓ R, Pignatelli M, Piccinin S, Mercuri NB, Collingridge G. 2012. Targeting synaptic dysfunction in Alzheimer's disease therapy. Mol Neurobiol. Dec;46(3):572-587.

Contributed by Allison A. Curley, Ph.D.