ArticleFrontiers in cellular neuroscience2019
Loss of TrkB Signaling Due to Status Epilepticus Induces a proBDNF-Dependent Cell Death.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- The genetic landscape and phenotypic spectrum of GAA-FGF14 ataxia in China: a large cohort study.EBioMedicine · 2024Article
- Bispecific antibody shuttles targeting CD98hc mediate efficient and long-lived brain delivery of IgGs.Cell chemical biology · 2024Article
- Post-mortem detection of neuronal and astroglial biochemical markers in serum and urine for diagnostics of traumatic brain injury.International journal of legal medicine · 2023Article
- Genetic knockout ofFrontiers in cellular neuroscience · 2023Article
- Injection of Anti-proBDNF Attenuates Hippocampal-Dependent Learning and Memory Dysfunction in Mice With Sepsis-Associated Encephalopathy.Frontiers in neuroscience · 2021Article
- p75NTR/proBDNF Modulates Basal Cell Carcinoma (BCC) Immune Microenvironment via Necroptosis Signaling Pathway.Journal of immunology research · 2021Article
- Neural Stem Cells and Cannabinoids in the Spotlight as Potential Therapy for Epilepsy.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotrophins (NTs) are secretory proteins that bind to target receptors and influence many cellular functions, such as cell survival and cell death in neurons. The mammalian NT brain-derived neurotrophic factor (matBDNF) is the C-terminal mature form released by cleavage from the proBDNF precursor. The binding of matBDNF to the tyrosine kinase receptor B (TrkB) activates different signaling cascades and leads to neuron survival and plasticity, while the interaction of proBDNF with the p75 NT receptor (p75NTR)/sortilin receptor complex has been highly involved in apoptosis. Many studies have demonstrated that prolonged seizures such as
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