ArticleThe EMBO journal2008
JNK phosphorylates synaptotagmin-4 and enhances Ca2+-evoked release.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- CaNeuromolecular medicine · 2025Article
- SYT4 Interacts with PSMC6 to Facilitate Malignant Progression in Gastric Carcinoma via Activating Wnt/β-catenin Signaling.International journal of biological sciences · 2025Article
- Follistatin Is a Novel Chemoattractant for Migration and Invasion of Placental Trophoblasts of Mice.Cells · 2022Article
- Regulation of BDNF Release by ARMS/Kidins220 through Modulation of Synaptotagmin-IV Levels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Capture of Dense Core Vesicles at Synapses by JNK-Dependent Phosphorylation of Synaptotagmin-4.Cell reports · 2017Article
- JNK Signaling: Regulation and Functions Based on Complex Protein-Protein Partnerships.Microbiology and molecular biology reviews : MMBR · 2016Review
- Injured astrocytes are repaired by Synaptotagmin XI-regulated lysosome exocytosis.Cell death and differentiation · 2016Article
- Synaptotagmin-7 phosphorylation mediates GLP-1-dependent potentiation of insulin secretion from β-cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release.Scientific reports · 2015Article
- Synaptotagmin IV acts as a multi-functional regulator of Ca2+-dependent exocytosis.Neurochemical research · 2011Review
- Hippocampal c-Jun-N-terminal kinases serve as negative regulators of associative learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+ influx induced by membrane depolarization triggers the exocytosis of secretory vesicles in various cell types such as endocrine cells and neurons. Peptidyl growth factors enhance Ca2+-evoked release, an effect that may underlie important adaptive responses such as the long-term potentiation of synaptic transmission induced by growth factors. Here, we show that activation of the c-Jun N-terminal kinase (JNK) plays an essential role in nerve growth factor (NGF) enhancement of Ca2+-evoked release in PC12 neuroendocrine cells. Moreover, JNK associated with phosphorylated synaptotagmin-4 (Syt 4), a key mediator of NGF enhancement of Ca2+-evoked release in this system. NGF treatment led to phosphorylation of endogenous Syt 4 at Ser135 and translocation of Syt 4 from immature to mature secretory vesicles in a JNK-dependent manner. Furthermore, mutation of Ser135 abrogated enhancement of Ca2+-evoked release by Syt 4. These results provide a molecular basis for the effect of growth factors on Ca2+-mediated secretion.
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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.