ArticleMolecular biology of the cell2007
Kidins220/ARMS is transported by a kinesin-1-based mechanism likely to be involved in neuronal differentiation.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- Significantly higher rates of KIDINS220 polymorphisms in patients with obesity and end-stage renal disease.Obesity pillars · 2025Article
- Novel autosomal recessive SINO syndrome-associatedHeliyon · 2024Article
- Review
- Kinase D-interacting Substrate of 220 kDa Is Overexpressed in Gastric Cancer and Associated With Local Invasion.Cancer genomics & proteomics · 2023Article
- Neuronal Scaffold Protein ARMS Interacts with Synaptotagmin-4 C2AB through the Ankyrin Repeat Domain with an Unexpected Mode.International journal of molecular sciences · 2023Article
- Pre- and Postnatal Characterization of Autosomal RecessiveMolecular syndromology · 2022Article
- Molecular architecture of the autoinhibited kinesin-1 lambda particle.Science advances · 2022Article
- SINO Syndrome Causative KIDINS220/ARMS Gene Regulates Adipocyte Differentiation.Frontiers in cell and developmental biology · 2021Article
- Differential regulation of Kidins220 isoforms in Huntington's disease.Brain pathology (Zurich, Switzerland) · 2020Article
- LMTK2 binds to kinesin light chains to mediate anterograde axonal transport of cdk5/p35 and LMTK2 levels are reduced in Alzheimer's disease brains.Acta neuropathologica communications · 2019Article
- Kidins220 and tumour development: Insights into a complexity of cross-talk among signalling pathways (Review).International journal of molecular medicine · 2017Review
- MiR-4638-5p inhibits castration resistance of prostate cancer through repressing Kidins220 expression and PI3K/AKT pathway activity.Oncotarget · 2016Article
- Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.Frontiers in cellular neuroscience · 2016Review
- Rare variants in the neurotrophin signaling pathway implicated in schizophrenia risk.Schizophrenia research · 2015Article
- KIF5B transports BNIP-2 to regulate p38 mitogen-activated protein kinase activation and myoblast differentiation.Molecular biology of the cell · 2015Article
- Novel Kidins220/ARMS Splice Isoforms: Potential Specific Regulators of Neuronal and Cardiovascular Development.PloS one · 2015Article
- Ankyrin repeat-rich membrane spanning (ARMS)/Kidins220 scaffold protein regulates neuroblastoma cell proliferation through p21.Molecules and cells · 2014Article
- Protein kinase D: a new player among the signaling proteins that regulate functions in the nervous system.Neuroscience bulletin · 2014Review
- Kidins220/ARMS is expressed in neuroblastoma tumors and stabilizes neurotrophic signaling in a human neuroblastoma cell line.Pediatric research · 2013Article
- PI3K p110α/Akt signaling negatively regulates secretion of the intestinal peptide neurotensin through interference of granule transport.Molecular endocrinology (Baltimore, Md.) · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kinase D-interacting substrate of 220 kDa/ankyrin repeat-rich membrane spanning (Kidins220/ARMS) is a conserved membrane protein mainly expressed in brain and neuroendocrine cells, which is a downstream target of the signaling cascades initiated by neurotrophins and ephrins. We identified kinesin light chain 1 (KLC1) as a binding partner for Kidins220/ARMS by a yeast two-hybrid screen. The interaction between Kidins220/ARMS and the kinesin-1 motor complex was confirmed by glutathione S-transferase-pull-down and coimmunoprecipitation experiments. In addition, Kidins220/ARMS and kinesin-1 were shown to colocalize in nerve growth factor (NGF)-differentiated PC12 cells. Using Kidins220/ARMS and KLC1 mutants, we mapped the regions responsible for the binding to a short sequence of Kidins220/ARMS, termed KLC-interacting motif (KIM), which is sufficient for the interaction with KLC1. Optimal binding of KIM requires a region of KLC1 spanning both the tetratricopeptide repeats and the heptad repeats, previously not involved in cargo recognition. Overexpression of KIM in differentiating PC12 cells impairs the formation and transport of EGFP-Kidins220/ARMS carriers to the tips of growing neurites, leaving other kinesin-1 dependent processes unaffected. Furthermore, KIM overexpression interferes with the activation of the mitogen-activated protein kinase signaling and neurite outgrowth in NGF-treated PC12 cells. Our results suggest that Kidins220/ARMS-positive carriers undergo a kinesin-1-dependent transport linked to neurotrophin action.
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