ArticleScientific reports2024
CRISPR/Cas9-mediated deletion of a GA-repeat in human GPM6B leads to disruption of neural cell differentiation from NT2 cells.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 10 citations in OpenAlex.
- Cell-type-specific architecture of the hypothalamus in a socially plastic vertebrate.bioRxiv : the preprint server for biology · 2026Article
- Tandem repeats in human brain evolution and disease susceptibility.Molecules and cells · 2026Review
- Pooled CRISPR screens with joint single-nucleus chromatin accessibility and transcriptome profiling.Nature biotechnology · 2025Article
- Minimal repeats are ubiquitous sites of crossover and recombination across the human genome.BMC genomics · 2025Article
- Modeling of cancer stem cells and the tumor microenvironment Via NT2/D1 cells to probe pathology and treatment for cancer and beyond.Discover oncology · 2025Review
- Glycoprotein M6B suppresses the maintenance of glioma stem cell stemness and proliferation via the integrin β1/β-catenin pathway.Frontiers in molecular biosciences · 2025Article
- Investigation of GPM6B as a novel therapeutic target in Osteoarthritis.Arthritis research & therapy · 2024Article
- A Hypermutable Region in the DISP2 Gene Links to Natural Selection and Late-Onset Neurocognitive Disorders in Humans.Molecular neurobiology · 2024Article
- The human SMAD9 (GCC) repeat links to natural selection and late-onset neurocognitive disorders.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
The human neuron-specific gene, GPM6B (Glycoprotein membrane 6B), is considered a key gene in neural cell functionality. This gene contains an exceptionally long and strictly monomorphic short tandem repeat (STR) of 9-repeats, (GA)9. STRs in regulatory regions, may impact on the expression of nearby genes. We used CRISPR-based tool to delete this GA-repeat in NT2 cells, and analyzed the consequence of this deletion on GPM6B expression. Subsequently, the edited cells were induced to differentiate into neural cells, using retinoic acid (RA) treatment. Deletion of the GA-repeat significantly decreased the expression of GPM6B at the RNA (p < 0.05) and protein (40%) levels. Compared to the control cells, the edited cells showed dramatic decrease of the astrocyte and neural cell markers, including GFAP (0.77-fold), TUBB3 (0.57-fold), and MAP2 (0.2-fold). Subsequent sorting of the edited cells showed an increased number of NES (p < 0.01), but a decreased number of GFAP (p < 0.001), TUBB3 (p < 0.05), and MAP2 (p < 0.01), compared to the control cells. In conclusion, CRISPR/Cas9-mediated deletion of a GA-repeat in human GPM6B, led to decreased expression of this gene, which in turn, disrupted differentiation of NT2 cells into neural cells.
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