ArticleThe EMBO journal2004
A unique pathway for sustained neurotrophin signaling through an ankyrin-rich membrane-spanning protein.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 142 citations in OpenAlex.
- A non-canonical ARMS-GABARAP interaction modulates dendritic spine formation and synaptic development.The EMBO journal · 2026Article
- Novel mouse line with D277N mutation in theFrontiers in cell and developmental biology · 2026Article
- Review
- Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.Science advances · 2024Article
- Alterations in KIDINS220/ARMS Expression Impact Sensory Processing and Social Behavior in Adult Mice.International journal of molecular sciences · 2024Article
- Article
- Morphogenetic theory of mental and cognitive disorders: the role of neurotrophic and guidance molecules.Frontiers in molecular neuroscience · 2024Review
- Kidins220 sets the threshold for survival of neural stem cells and progenitors to sustain adult neurogenesis.Cell death & disease · 2023Article
- Congenital hydrocephalus: new Mendelian mutations and evidence for oligogenic inheritance.Human genomics · 2023Article
- ARMS-NF-κB signaling regulates intracellular ROS to induce autophagy-associated cell death upon oxidative stress.iScience · 2023Article
- Pre- and Postnatal Characterization of Autosomal RecessiveMolecular syndromology · 2022Article
- Phosphate dysregulation via the XPR1-KIDINS220 protein complex is a therapeutic vulnerability in ovarian cancer.Nature cancer · 2022Article
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- Functional analysis of a novel fusion protein PAX5-KIDINS220 identified in a pediatric Ph-like ALL patient.International journal of hematology · 2020Article
- Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.Cell death and differentiation · 2020Article
- Differential regulation of Kidins220 isoforms in Huntington's disease.Brain pathology (Zurich, Switzerland) · 2020Article
- Excitotoxic targeting of Kidins220 to the Golgi apparatus precedes calpain cleavage of Rap1-activation complexes.Cell death & disease · 2019Article
- Targeting NMDA receptors in stroke: new hope in neuroprotection.Molecular brain · 2018Review
- Neurotrophin Signaling and Stem Cells-Implications for Neurodegenerative Diseases and Stem Cell Therapy.Molecular neurobiology · 2017Review
- Kidins220 and tumour development: Insights into a complexity of cross-talk among signalling pathways (Review).International journal of molecular medicine · 2017Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
A major question in cell biology is how molecular specificity is achieved by different growth factor receptors that activate apparently identical signaling events. For the neurotrophin family, a distinguishing feature is the ability to maintain a prolonged duration of signal transduction. However, the mechanisms by which neurotrophin receptors assemble such a sustained signaling complex are not understood. Here we report that an unusual ankyrin-rich transmembrane protein (ARMS+kidins220) is closely associated with Trk receptor tyrosine kinases, and not the EGF receptor. This association requires interactions between transmembrane domains of Trk and ARMS. ARMS is rapidly tyrosine phosphorylated after binding of neurotrophins to Trk receptors and provides a docking site for the CrkL-C3G complex, resulting in Rap1-dependent sustained ERK activation. Accordingly, disruption of Trk-ARMS or the ARMS-CrkL interaction with dominant-negative ARMS mutants, or treatment with small interference RNA against ARMS substantially reduce neurotrophin-elicited signaling to ERK, but without any effect upon Ras or Akt activation. These findings suggest that ARMS acts as a major and neuronal-specific platform for prolonged MAP kinase signaling by neurotrophins.
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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.