Wnt/β‐catenin signaling in brain development and mental disorders: keeping TCF7L2 in mind
| Autor: | Nikola Brozko, Chaitali Chakraborty, Marcin Andrzej Lipiec, Łukasz M. Szewczyk, Andrzej Nagalski, Kamil Koziński, Joanna Bem, Marta Barbara Wiśniewska |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Beta-catenin
Neurogenesis Biophysics Wnt pathway Context (language use) brain development Review Article Biochemistry 03 medical and health sciences oligodendrogenesis Structural Biology thalamus Translational Research Genetics medicine Animals Humans postmitotic differentiation Enhancer Molecular Biology Transcription factor Wnt Signaling Pathway beta‐catenin 030304 developmental biology 0303 health sciences biology habenula Mental Disorders 030302 biochemistry & molecular biology Wnt signaling pathway Brain Cell Biology medicine.disease TCF7L2 Mood disorders biology.protein Neuroscience Transcription Factor 7-Like 2 Protein |
| Zdroj: | Febs Letters |
| ISSN: | 1873-3468 0014-5793 |
| Popis: | Canonical Wnt signaling, which is transduced by β-catenin and lymphoid enhancer factor 1/T cell-specific transcription factors (LEF1/TCFs), regulates many aspects of metazoan development and tissue renewal. Although much evidence has associated canonical Wnt/β-catenin signaling with mood disorders, the mechanistic links are still unknown. Many components of the canonical Wnt pathway are involved in cellular processes that are unrelated to classical canonical Wnt signaling, thus further blurring the picture. The present review critically evaluates the involvement of classical Wnt/β-catenin signaling in developmental processes that putatively underlie the pathology of mental illnesses. Particular attention is given to the roles of LEF1/TCFs, which have been discussed surprisingly rarely in this context. Highlighting recent discoveries, we propose that alterations in the activity of LEF1/TCFs, and particularly of transcription factor 7-like 2 (TCF7L2), result in defects previously associated with neuropsychiatric disorders, including imbalances in neurogenesis and oligodendrogenesis, the functional disruption of thalamocortical circuitry and dysfunction of the habenula. |
| Databáze: | OpenAIRE |
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