BDNF-TrkB signaling

Brain-derived neurotrophic factor (BDNF) is an important neurotrophin for the regulation of synaptic activity. BDNF-TrkB signaling, TrkB being the receptor of BDNF, is involved in transcription, translation, and trafficking of proteins in the various stages of synaptic development and evidence indicates that it also plays a significant role in synaptic plasticity, the ability of synapses to strengthen or weaken over time. Synaptic plasticity has been associated with learning and memory development. These functions are carried out through three pathways: mitogen-activated protein kinase (MAPK), phospholipase CG (PLC/PLCG), and phosphatidylinositol 3-kinase (PI3K). Pi3K and MAPK have crucial roles in the protein translation and transport caused by synaptic activity. PLCG regulates intracellular levels of Ca2+, which drives gene transcription through cyclic AMP. Evidence strongly indicates that abnormal levels of BDNF leads to significant developmental and neurodegenerative diseases by disrupting neural development and function. An understanding of how the BDNF-TrkB pathway regulates synaptic activity and plasticity is essential to an understanding of how we can effectively treat genetic disruptions of this pathway that lead to terrible neurodevelopmental diseases. Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP3676 CPTAC Assay Portal]

脑源性神经营养因子（BDNF）是调节突触活动的重要神经营养素。BDNF-TrkB信号通路，其中TrkB为BDNF的受体，参与突触发育各个阶段的蛋白质转录、翻译和转运，且有证据表明它在突触可塑性方面也发挥着显著作用，突触可塑性是指突触随时间推移而增强或减弱的能力。突触可塑性与学习和记忆的发展密切相关。这些功能通过三条途径实现：有丝分裂原激活蛋白激酶（MAPK）、磷脂酶CG（PLC/PLCG）和磷脂酰肌醇3激酶（PI3K）。PI3K和MAPK在突触活动引起的蛋白质翻译和转运中扮演着至关重要的角色。PLCG调节细胞内钙离子（Ca2+）的水平，通过环腺苷酸（cAMP）驱动基因转录。强有力的证据表明，BDNF水平的异常会导致神经发育和神经退行性疾病的发生，通过破坏神经发育和功能。了解BDNF-TrkB通路如何调节突触活动和可塑性对于理解如何有效治疗导致严重神经发育疾病的该通路遗传破坏至关重要。该通路上的蛋白质可通过[https://assays.cancer.gov/available_assays?wp_id=WP3676 CPTAC检测门户]进行靶向检测。