iScience· 2026Q1
Extracellular neuroligin-ICAM5 coupling drives dendritic growth via actin remodeling
- 2citations
- Q1SCImago
- 2026year
Short summary
Extracellular neuroligin (NLGN) binding to intercellular adhesion molecule-5 (ICAM5) directly drives dendritic growth by sustaining PAK-Cofilin signaling and F-actin organization in growth cones.
AI-generated from the title and abstract; the full text is not read.
Key points
- ICAM5 is a novel extracellular binding partner for all neuroligin isoforms.
- The NLGN-ICAM5 complex directly drives dendritic outgrowth.
- This complex does not contribute to synaptogenesis.
- ICAM5 sustains PAK-Cofilin signaling and F-actin organization in growth cones.
AI-generated from the title and abstract; the full text is not read.
Abstract
Neuroligins (NLGNs) organize neuronal connectivity by engaging a diverse set of interaction partners, yet how extracellular recognition couples to intracellular growth programs remains unclear. Using affinity proteomics, we identify intercellular adhesion molecule-5 (ICAM5), a cell-surface protein localized to dendritic filopodia, as a novel neuroligin interactor. Surface plasmon resonance and cell-based assays demonstrate direct binding between the ICAM5 and NLGN3 extracellular domains and reveal that ICAM5 engages all neuroligin isoforms. ICAM5 is required for NLGN-induced dendritic outgrowth, but the NLGN3–ICAM5 complex does not contribute to synaptogenesis. Mechanistically, ICAM5 sustains PAK–Cofilin signaling and F-actin organization in growth cones, positioning it as a downstream effector that links neuroligin engagement to actin remodeling. Together, these findings define a neuroligin–ICAM5 axis that couples extracellular recognition to intracellular actin remodeling to control neuronal structural development.
The authors' abstract, as published at the source. iScience, 2026 · DOI ↗
Continue with a free account
Ask the paper: 3 free questions a day about this paper; save it, get its citation, new summaries every day for your field. Takeaways are Premium.
Continue free on the webSign in with Google or Apple; no card needed. You come back to this paper.
On your phone:
Field: Cellular and Molecular Neuroscience
Cellular and Molecular NeuroscienceNeuroscience