ArticleCell death and differentiation2012
Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 73 citations in OpenAlex.
- A non-canonical ARMS-GABARAP interaction modulates dendritic spine formation and synaptic development.The EMBO journal · 2026Article
- Transcriptomic analysis reveals liver lncRNA-mRNA regulatory networks mediating Nicol1-induced growth and reproduction in golden pompano (Trachinotus ovatus).BMC genomics · 2025Article
- KIDINS220 Variant Associated With Hypoplasia of the Corpus Callosum and Aqueduct Stenosis.Prenatal diagnosis · 2025Article
- Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease.Obesity pillars · 2025Article
- Matrix stiffness regulates nucleus pulposus cell glycolysis by MRTF-A-dependent mechanotransduction.Bone research · 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
- Novel autosomal recessive SINO syndrome-associatedHeliyon · 2024Article
- 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
- The genetic basis of hydrocephalus: genes, pathways, mechanisms, and global impact.Fluids and barriers of the CNS · 2024Review
- Alterations in KIDINS220/ARMS Expression Impact Sensory Processing and Social Behavior in Adult Mice.International journal of molecular sciences · 2024Article
- Article
- Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024Review
- 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
- Designing a Novel Monitoring Approach for the Effects of Space Travel on Astronauts' Health.Life (Basel, Switzerland) · 2023Article
- Pre- and Postnatal Characterization of Autosomal RecessiveMolecular syndromology · 2022Article
- 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
- SINO Syndrome Causative KIDINS220/ARMS Gene Regulates Adipocyte Differentiation.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Signaling downstream of receptor tyrosine kinases controls cell differentiation and survival. How signals from different receptors are integrated is, however, still poorly understood. In this work, we have identified Kidins220 (Kinase D interacting substrate of 220 kDa)/ARMS (Ankyrin repeat-rich membrane spanning) as a main player in the modulation of neurotrophin and vascular endothelial growth factor (VEGF) signaling in vivo, and a primary determinant for neuronal and cardiovascular development. Kidins220(-/-) embryos die at late stages of gestation, and show extensive cell death in the central and peripheral nervous systems. Primary neurons from Kidins220(-/-) mice exhibit reduced responsiveness to brain-derived neurotrophic factor, in terms of activation of mitogen-activated protein kinase signaling, neurite outgrowth and potentiation of excitatory postsynaptic currents. In addition, mice lacking Kidins220 display striking cardiovascular abnormalities, possibly due to impaired VEGF signaling. In support of this hypothesis, we demonstrate that Kidins220 constitutively interacts with VEGFR2. These findings, together with the data presented in the accompanying paper, indicate that Kidins220 mediates the integration of several growth factor receptor pathways during development, and mediates the activation of distinct downstream cascades according to the location and timing of stimulation.
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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.