Schizophrenia-associated NRXN1 deletions induce developmental-timing- and cell-type-specific vulnerabilities in human brain organoids
Abstract De novo mutations and copy number deletions in NRXN1 (2p16.3) pose a significant risk for schizophrenia (SCZ). It is unclear how NRXN1 deletions impact cortical development in a cell type-specific manner and disease background modulates these phenotypes. Here, we leveraged human pluripotent...
Αποθηκεύτηκε σε:
| Κύριοι συγγραφείς: | , , , , , , , , , , |
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| Μορφή: | Artigo |
| Γλώσσα: | Inglês |
| Έκδοση: |
Nature Portfolio
2023-06-01
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| Σειρά: | Nature Communications |
| Διαθέσιμο Online: | https://doi.org/10.1038/s41467-023-39420-6 |
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