The 5-HT4 receptor interacts with adhesion molecule L1 to modulate morphogenic signaling in neurons
العنوان: | The 5-HT4 receptor interacts with adhesion molecule L1 to modulate morphogenic signaling in neurons |
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المؤلفون: | Simon Bennet Sonnenberg, Vladimir S. Naumenko, Daria Guseva, Christoph Göhr, Stephan C. Bischoff, Dalia Abdel Galil, Andre Zeug, Sophie Kristin Schade, Nataliya Gorinski, Jonah Rauer, Evgeni Ponimaskin |
المصدر: | Journal of Cell Science. 134 |
بيانات النشر: | The Company of Biologists, 2021. |
سنة النشر: | 2021 |
مصطلحات موضوعية: | 0303 health sciences, Dendritic spine, L1, Cell adhesion molecule, 5-HT4 receptor, Cell Biology, Adhesion, Biology, Cell biology, 03 medical and health sciences, 0302 clinical medicine, Förster resonance energy transfer, Signal transduction, 030217 neurology & neurosurgery, 5-HT receptor, 030304 developmental biology |
الوصف: | Morphological remodeling of dendritic spines is critically involved in memory formation and depends on adhesion molecules. Serotonin receptors are also implicated in this remodeling, though the underlying mechanisms remain enigmatic. Here, we uncovered a signaling pathway involving the adhesion molecule L1CAM (L1) and serotonin receptor 5-HT4 (5-HT4R, encoded by HTR4). Using Förster resonance energy transfer (FRET) imaging, we demonstrated a physical interaction between 5-HT4R and L1, and found that 5-HT4R–L1 heterodimerization facilitates mitogen-activated protein kinase activation in a Gs-dependent manner. We also found that 5-HT4R–L1-mediated signaling is involved in G13-dependent modulation of cofilin-1 activity. In hippocampal neurons in vitro, the 5-HT4R–L1 pathway triggers maturation of dendritic spines. Thus, the 5-HT4R–L1 signaling module represents a previously unknown molecular pathway regulating synaptic remodeling. |
تدمد: | 1477-9137 0021-9533 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::36ed5be1adc4115d6343cf25f2ec3e67 https://doi.org/10.1242/jcs.249193 |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi...........36ed5be1adc4115d6343cf25f2ec3e67 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 14779137 00219533 |
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