ArticleCell death and differentiation2020
Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Single-cell Transcriptomics Reveals that the SORBS1/FBXO22/BAG3 Axis Drives Astrocyte Senescence via Calcium Signaling and Affects Alzheimer's Disease-Related Neuronal Damage.Neuromolecular medicine · 2026Article
- Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease.Obesity pillars · 2025Article
- Pure Hereditary Spastic Paraplegia in a Patient With a Novel Heterozygous KIDINS220 Gene Mutation.Cureus · 2024Article
- Article
- Modulating TRPV4 Channel Activity in Pro-Inflammatory Macrophages within the 3D Tissue Analog.Biomedicines · 2024Article
- Multiubiquitination of TRPV4 reduces channel activity independent of surface localization.The Journal of biological chemistry · 2022Article
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- Gm364 coordinates MIB2/DLL3/Notch2 to regulate female fertility through AKT activation.Cell death and differentiation · 2022Article
- SINO Syndrome Causative KIDINS220/ARMS Gene Regulates Adipocyte Differentiation.Frontiers in cell and developmental biology · 2021Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Through their ability to modulate synaptic transmission, glial cells are key regulators of neuronal circuit formation and activity. Kidins220/ARMS (kinase-D interacting substrate of 220 kDa/ankyrin repeat-rich membrane spanning) is one of the key effectors of the neurotrophin pathways in neurons where it is required for differentiation, survival, and plasticity. However, its role in glial cells remains largely unknown. Here, we show that ablation of Kidins220 in primary cultured astrocytes induced defects in calcium (Ca
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Registered trials
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