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Canonical Wnt Signaling Pathway02:54

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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...
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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...
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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.
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Related Experiment Video

Updated: Jan 13, 2026

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SARS-CoV-2 Infection Influences Wnt/β-Catenin Pathway Components in Astrocytes.

KaReisha F Robinson1, Avantika I Ahiya1, Justin M Richner2

  • 1Department of Anatomy and Cell Biology, University of Illinois Chicago, Chicago, IL 60612, USA.

Pathogens (Basel, Switzerland)
|October 29, 2025
PubMed
Summary

SARS-CoV-2 infection alters Wnt/β-catenin pathway components in human astrocytes. This finding may explain neuroinflammation and cognitive issues seen in COVID-19 and Long COVID.

Keywords:
SARS-CoV-2Wnt/β-cateninastrocytes

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Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Molecular Biology

Background:

  • Neuroinflammation and cognitive impairment are observed in COVID-19 and Long COVID.
  • Cerebrovascular Wnt/β-catenin pathway suppression is linked to neuroinflammation in a COVID-19 mouse model.

Purpose of the Study:

  • To investigate if SARS-CoV-2 infection causes cell-autonomous changes in Wnt/β-catenin pathway components within astrocytes.
  • To explore the molecular mechanisms underlying SARS-CoV-2-induced neurological dysfunction.

Main Methods:

  • Utilized induced pluripotent stem cell (hiPSC)-derived human astrocytes (iAs).
  • Exposed iAs to SARS-CoV-2 (NY Iota strain) in vitro.
  • Quantified changes in Wnt/β-catenin pathway gene expression using real-time PCR.

Main Results:

  • SARS-CoV-2 successfully infected iAs in vitro.
  • Infection led to decreased Wnt3a, Wnt10b, β-catenin, and TCF3 transcripts.
  • Increased Wnt7b and CXCL10 transcripts were observed, suggesting a proinflammatory response.

Conclusions:

  • SARS-CoV-2 infection differentially impacts Wnt/β-catenin pathway components in astrocytes.
  • These molecular alterations in astrocytes may contribute to the neuroinflammation and cognitive deficits associated with COVID-19 and Long COVID.