ReviewFrontiers in cellular neuroscience2016
Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.
Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Extended genome-wide association study employing the African genome resources panel identifies novel susceptibility loci for Alzheimer's disease in individuals of African ancestry.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Pooled it
- A non-canonical ARMS-GABARAP interaction modulates dendritic spine formation and synaptic development.The EMBO journal · 2026Article
- KIDINS220 and InsP8 safeguard the stepwise regulation of phosphate exporter XPR1.Molecular cell · 2025Article
- Kidins220-deficient hydrocephalus mice exhibit altered glial phenotypes and AQP4 differential regulation in the retina and optic nerve, with preserved retinal ganglion cell survival.Fluids and barriers of the CNS · 2025Article
- A novelFrontiers in neuroscience · 2025Article
- NEXMIF Combined with KIDINS220 Gene Mutation Caused Neurodevelopmental Disorder and Epilepsy: One Case Report.Actas espanolas de psiquiatria · 2024Article
- Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.Science advances · 2024Article
- Increased burden of rare protein-truncating variants in constrained, brain-specific and synaptic genes in extremely impulsively violent males with antisocial personality disorder.Genes, brain, and behavior · 2024Article
- Article
- Neuronal Scaffold Protein ARMS Interacts with Synaptotagmin-4 C2AB through the Ankyrin Repeat Domain with an Unexpected Mode.International journal of molecular sciences · 2023Article
- Kidins220 sets the threshold for survival of neural stem cells and progenitors to sustain adult neurogenesis.Cell death & disease · 2023Article
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- Kidins220 deficiency causes ventriculomegaly via SNX27-retromer-dependent AQP4 degradation.Molecular psychiatry · 2021Article
- Autosomal recessive variants iniScience · 2021Article
- Article
- Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.Cell death and differentiation · 2020Article
- 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
- Kidins220 and tumour development: Insights into a complexity of cross-talk among signalling pathways (Review).International journal of molecular medicine · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The correct functioning of the nervous system depends on the exquisitely fine control of neuronal excitability and synaptic plasticity, which relies on an intricate network of protein-protein interactions and signaling that shapes neuronal homeostasis during development and in adulthood. In this complex scenario, Kinase D interacting substrate of 220 kDa/ankyrin repeat-rich membrane spanning (Kidins220/ARMS) acts as a multi-functional scaffold protein with preferential expression in the nervous system. Engaged in a plethora of interactions with membrane receptors, cytosolic signaling components and cytoskeletal proteins, Kidins220/ARMS is implicated in numerous cellular functions including neuronal survival, neurite outgrowth and maturation and neuronal activity, often in the context of neurotrophin (NT) signaling pathways. Recent studies have highlighted a number of cell- and context-specific roles for this protein in the control of synaptic transmission and neuronal excitability, which are at present far from being completely understood. In addition, some evidence has began to emerge, linking alterations of Kidins220 expression to the onset of various neurodegenerative diseases and neuropsychiatric disorders. In this review, we present a concise summary of our fragmentary knowledge of Kidins220/ARMS biological functions, focusing on the mechanism(s) by which it controls various aspects of neuronal activity. We have tried, where possible, to discuss the available evidence in the wider context of NT-mediated regulation, and to outline emerging roles of Kidins220/ARMS in human pathologies.
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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.