ArticleJournal of neurochemistry2020
Cathepsin B inhibition blocks neurite outgrowth in cultured neurons by regulating lysosomal trafficking and remodeling.
Article in Journal of neurochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Cathepsin B deficiency disrupts cortical development via PEG3, leading to depression-like behavior.Communications biology · 2025Article
- Cathepsin B modulates microglial migration and phagocytosis of amyloid β in Alzheimer's disease through PI3K-Akt signaling.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Muscle-brain crosstalk mediated by exercise-induced myokines - insights from experimental studies.Frontiers in physiology · 2024Review
- Genetic risk variants in New Yorkers of Puerto Rican and Dominican Republic heritage with Parkinson's disease.NPJ Parkinson's disease · 2023Article
- Integrative transcriptomic and network pharmacology analysis reveals the neuroprotective role of BYHWD through enhancing autophagy by inhibiting Ctsb in intracerebral hemorrhage mice.Chinese medicine · 2023Article
- Ar-turmerone inhibits the proliferation and mobility of glioma by downregulating cathepsin B.Aging · 2023Article
- Extralysosomal cathepsin B in central nervous system: Mechanisms and therapeutic implications.Brain pathology (Zurich, Switzerland) · 2022Review
- Cathepsin B p.Gly284Val Variant in Parkinson's Disease Pathogenesis.International journal of molecular sciences · 2022Article
- Quantitative proteomics and in-cell cross-linking reveal cellular reorganisation during early neuronal differentiation of SH-SY5Y cells.Communications biology · 2022Article
- The needs of a synapse-How local organelles serve synaptic proteostasis.The EMBO journal · 2022Review
- Molecular Features of CA-074 pH-Dependent Inhibition of Cathepsin B.Biochemistry · 2022Article
- Exercise and Dietary Factors Mediate Neural Plasticity Through Modulation of BDNF Signaling.Brain plasticity (Amsterdam, Netherlands) · 2022Review
- Muscle-to-Brain Signaling Via Myokines and Myometabolites.Brain plasticity (Amsterdam, Netherlands) · 2022Review
- Differential Expression and Distinct Roles of Proteinase-Activated Receptor 2 in Microglia and Neurons in Neonatal Mouse Brain After Hypoxia-Ischemic Injury.Molecular neurobiology · 2022Article
- Article
- Axonal Organelles as Molecular Platforms for Axon Growth and Regeneration after Injury.International journal of molecular sciences · 2021Review
- Exercise Factors Released by the Liver, Muscle, and Bones Have Promising Therapeutic Potential for Stroke.Frontiers in neurology · 2021Review
- Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Lysosomes are known to mediate neurite outgrowth in neurons. However, the principal lysosomal molecule controlling that outgrowth is unclear. We studied primary mouse neurons in vitro and found that they naturally develop neurite outgrowths over time and as they did so the lysosomal cysteine protease cathepsin B (CTSB) mRNA levels dramatically increased. Surprisingly, we found that treating those neurons with CA-074Me, which inhibits CTSB, prevented neurites. As that compound also inhibits another protease, we evaluated a N2a neuronal cell line in which the CTSB gene was deleted (CTSB knockout, KO) using CRISPR technology and induced their neurite outgrowth by treatment with retinoic acid. We found that CTSB KO N2a cells failed to produce neurite outgrowths but the wild-type (WT) did. CA-074Me is a cell permeable prodrug of CA-074, which is cell impermeable and a specific CTSB inhibitor. Neurite outgrowth was and was not suppressed in WT N2a cells treated with CA-074Me and CA-074, respectively. Lysosome-associated membrane glycoprotein 2-positive lysosomes traffic to the plasma cell membrane in WT but not in CTSB KO N
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.