ArticleCurrent biology : CB2014
The CNK2 scaffold interacts with vilse and modulates Rac cycling during spine morphogenesis in hippocampal neurons.
Article in Current biology : CB, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- ARHGAP39 plays an essential role in anxiety-like behavior and stress response.Translational psychiatry · 2026Article
- Identification of Houge type of X-linked syndromic mental retardation caused by CNKSR2 truncated variants.Italian journal of pediatrics · 2025Article
- Loss of Arhgap39 facilitates cell migration and invasion in murine hepatocellular cancer cells.Oncology research · 2025Article
- A homozygous variant in ARHGAP39 is associated with lethal cerebellar vermis hypoplasia in a consanguineous Saudi family.Scientific reports · 2024Article
- Knockdown of Porf-2 restores visual function after optic nerve crush injury.Cell death & disease · 2023Article
- CNK2 promotes cancer cell motility by mediating ARF6 activation downstream of AXL signalling.Nature communications · 2023Article
- ARHGAP39 is a prognostic biomarker involved in immune infiltration in breast cancer.BMC cancer · 2023Article
- Brain-specific deletion of GIT1 impairs cognition and alters phosphorylation of synaptic protein networks implicated in schizophrenia susceptibility.Molecular psychiatry · 2022Article
- Physiological and Pathological Roles of the Cytohesin Family in Neurons.International journal of molecular sciences · 2022Review
- Review
- Rac-maninoff and Rho-vel: The symphony of Rho-GTPase signaling at excitatory synapses.Small GTPases · 2022Article
- Case report: Phenotype expansion and analysis ofFrontiers in neurology · 2022Article
- Cnksr2 Loss in Mice Leads to Increased Neural Activity and Behavioral Phenotypes of Epilepsy-Aphasia Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- CNKSR2-related neurodevelopmental and epilepsy disorder: a cohort of 13 new families and literature review indicating a predominance of loss of function pathogenic variants.BMC medical genomics · 2021Review
- Synaptic Protein Phosphorylation Networks Are Associated With Electroacupuncture-Induced Circadian Control in the Suprachiasmatic Nucleus.Frontiers in genetics · 2021Article
- Psychomotor development and attention problems caused by a splicing variant of CNKSR2.BMC medical genomics · 2020Article
- Molecular architecture of postsynaptic Interactomes.Cellular signalling · 2020Review
- Article
- Exons deletion of CNKSR2 gene identified in X-linked syndromic intellectual disability.BMC medical genetics · 2020Article
- Disease-associated synaptic scaffold protein CNK2 modulates PSD size and influences localisation of the regulatory kinase TNIK.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Protein scaffolds play an important role in signal transduction, functioning to facilitate protein interactions and localize key pathway components to specific signaling sites. Connector enhancer of KSR-2 (CNK2) is a neuronally expressed scaffold recently implicated in nonsyndromic, X-linked intellectual disability (NS-XLID) [1-3]. NS-XLID patients have deficits in cognitive function and their neurons often exhibit dendritic spine abnormalities [4], suggesting a role for CNK2 in synaptic signaling and/or spine formation. To gain insight regarding how CNK2 might contribute to these processes, we used mass spectrometry to identify proteins that interact with the endogenous CNK2 scaffold. Here, we report that the major binding partner of CNK2 is Vilse/ARHGAP39 and that CNK2 complexes are enriched for proteins involved in Rac/Cdc42 signaling, including Rac1 itself, α-PIX and β-PIX, GIT1 and GIT2, PAK3 and PAK4, and members of the cytohesin family. Binding between CNK2 and Vilse was found to be constitutive, mediated by the WW domains of Vilse and a proline motif in CNK2. Through mutant analysis, protein depletion and rescue experiments, we identify CNK2 as a spatial modulator of Rac cycling during spine morphogenesis and find that the interaction with Vilse is critical for maintaining RacGDP/GTP levels at a balance required for spine formation.
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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.