c-Abl Tyrosine Kinase Is Required for BDNF-Induced Dendritic Branching and Growth

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dc.contributor.authorChandia-Cristi, America
dc.contributor.authorStuardo, Nicolas
dc.contributor.authorTrejos, Cristian
dc.contributor.authorLeal, Nancy
dc.contributor.authorUrrutia, Daniela
dc.contributor.authorBronfman, Francisca C.
dc.contributor.authorRojas, Alejandra Alvarez
dc.date.accessioned2025-01-20T20:18:00Z
dc.date.available2025-01-20T20:18:00Z
dc.date.issued2023
dc.description.abstractBrain-derived neurotrophic factor (BDNF) induces activation of the TrkB receptor and several downstream pathways (MAPK, PI3K, PLC-gamma), leading to neuronal survival, growth, and plasticity. It has been well established that TrkB signaling regulation is required for neurite formation and dendritic arborization, but the specific mechanism is not fully understood. The non-receptor tyrosine kinase c-Abl is a possible candidate regulator of this process, as it has been implicated in tyrosine kinase receptors' signaling and trafficking, as well as regulation of neuronal morphogenesis. To assess the role of c-Abl in BDNF-induced dendritic arborization, wild-type and c-Abl-KO neurons were stimulated with BDNF, and diverse strategies were employed to probe the function of c-Abl, including the use of pharmacological inhibitors, an allosteric c-Abl activator, and shRNA to downregulates c-Abl expression. Surprisingly, BDNF promoted c-Abl activation and interaction with TrkB receptors. Furthermore, pharmacological c-Abl inhibition and genetic ablation abolished BDNF-induced dendritic arborization and increased the availability of TrkB in the cell membrane. Interestingly, inhibition or genetic ablation of c-Abl had no effect on the classic TrkB downstream pathways. Together, our results suggest that BDNF/TrkB-dependent c-Abl activation is a novel and essential mechanism in TrkB signaling.
dc.fuente.origenWOS
dc.identifier.doi10.3390/ijms24031944
dc.identifier.eissn1422-0067
dc.identifier.urihttps://doi.org/10.3390/ijms24031944
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/92434
dc.identifier.wosidWOS:000930923700001
dc.issue.numero3
dc.language.isoen
dc.revistaInternational journal of molecular sciences
dc.rightsacceso restringido
dc.subjectdendritic arborization
dc.subjectc-Abl
dc.subjectBDNF
dc.subjectTrkB pathway
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titlec-Abl Tyrosine Kinase Is Required for BDNF-Induced Dendritic Branching and Growth
dc.typeartículo
dc.volumen24
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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