ArticleScientific reports2019
GAS2-like 1 coordinates cell division through its association with end-binding proteins.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- A comprehensive analysis of GAS2 family members identifies that GAS2L1 is a novel biomarker and promotes the proliferation of hepatocellular carcinoma.Discover oncology · 2024Article
- Emerging roles of centrosome cohesion.Open biology · 2022Review
- Integrative analysis regarding the correlation between GAS2 family genes and human glioma prognosis.Cancer medicine · 2021Article
- Growth arrest-specific 2 protein family: Structure and function.Cell proliferation · 2021Review
- The molecular structure of mammalian primary cilia revealed by cryo-electron tomography.Nature structural & molecular biology · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cell division involves the tightly coordinated rearrangement of actin and microtubules (MTs). We have previously shown that a member of the family of growth arrest-specific 2-like proteins, GAS2-like 1 (G2L1) regulates actin-MT crosstalk through its associations with plus-end microtubule tip-binding (EB) proteins. Here we show that G2L1 is involved in the regulation of cell division. We show that the depletion of G2L1 results in a reduction in the number of cells undergoing cell division and a significant proportion of those cells that do divide are either multinucleated, display deformed nuclei, or undergo cell division at a much slower rate. Exogenous expression of G2L1 mutants revealed that the association of G2L1 with EB1 is critical for regulated cell division and blocking this interaction inhibits cell division as observed in cells lacking G2L1. Taken together, our data suggest that G2L1 controls the precise regulation and successful progression of cell division through its binding to EB-proteins.
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