ArticleThe Journal of biological chemistry2009
Interaction of Mint2 with TrkA is involved in regulation of nerve growth factor-induced neurite outgrowth.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Overexpression of Nogo-A changes nerve growth factor signaling dynamics in PC12 cells.Cellular signalling · 2025Article
- Interrogation and validation of the interactome of neuronal Munc18-interacting Mint proteins with AlphaFold2.The Journal of biological chemistry · 2024Article
- Article
- Exploratory locomotion, a predictor of addiction vulnerability, is oligogenic in rats selected for this phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Phosphorylation of multiple sites within an acidic region of Alcadein α is required for kinesin-1 association and Golgi exit of Alcadein α cargo.Molecular biology of the cell · 2017Article
- The Intersection of NGF/TrkA Signaling and Amyloid Precursor Protein Processing in Alzheimer's Disease Neuropathology.International journal of molecular sciences · 2017Review
- Association of TrkA and APP Is Promoted by NGF and Reduced by Cell Death-Promoting Agents.Frontiers in molecular neuroscience · 2017Article
- Syntaxin 8 modulates the post-synthetic trafficking of the TrkA receptor and inflammatory pain transmission.The Journal of biological chemistry · 2014Article
- TROY interacts with Rho guanine nucleotide dissociation inhibitor α (RhoGDIα) to mediate Nogo-induced inhibition of neurite outgrowth.The Journal of biological chemistry · 2013Article
- X11/Mint genes control polarized localization of axonal membrane proteins in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Extracellular pH and neuronal depolarization serve as dynamic switches to rapidly mobilize trkA to the membrane of adult sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Peripheral somatosensation: a touch of genetics.Current opinion in genetics & development · 2011Review
- Deletions flanked by breakpoints 3 and 4 on 15q13 may contribute to abnormal phenotypes.European journal of human genetics : EJHG · 2011Article
- MiR-21 plays an important role in radiation induced carcinogenesis in BALB/c mice by directly targeting the tumor suppressor gene Big-h3.International journal of biological sciences · 2011Article
- Expression and ultrastructural localization of Mint2 in the spinal cord of rats.Molecular biology reports · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TrkA receptor signaling is essential for nerve growth factor (NGF)-induced survival and differentiation of sensory neurons. To identify possible effectors or regulators of TrkA signaling, yeast two-hybrid screening was performed using the intracellular domain of TrkA as bait. We identified muc18-1-interacting protein 2 (Mint2) as a novel TrkA-binding protein and found that the phosphotyrosine binding domain of Mint2 interacted with TrkA in a phosphorylation- and ligand-independent fashion. Coimmunoprecipitation assays showed that endogenous TrkA interacted with Mint2 in rat tissue homogenates, and immunohistochemical evidence revealed that Mint2 and TrkA colocalized in rat dorsal root ganglion neurons. Furthermore, Mint2 overexpression inhibited NGF-induced neurite outgrowth in both PC12 and cultured dorsal root ganglion neurons, whereas inhibition of Mint2 expression by RNA interference facilitated NGF-induced neurite outgrowth. Moreover, Mint2 was found to promote the retention of TrkA in the Golgi apparatus and inhibit its surface sorting. Taken together, our data provide evidence that Mint2 is a novel TrkA-regulating protein that affects NGF-induced neurite outgrowth, possibly through a mechanism involving retention of TrkA in the Golgi apparatus.
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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.