Publications by authors named "F Boussin"

The lateral wall of the mouse subventricular zone harbors neural stem cells (NSC, B cells) which generate proliferating transient-amplifying progenitors (TAP, C cells) that ultimately give rise to neuroblasts (NB, A cells). Molecular profiling at the single-cell level struggles to distinguish these different cell types. Here, we combined transcriptome analyses of FACS-sorted cells and single-cell RNAseq to demonstrate the existence of an abundant, clonogenic and multipotent population of immature neuroblasts (iNB cells) at the transition between TAP and migrating NB (mNB).

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The stem cell niche plays a crucial role in the decision to either self-renew or differentiate. Recent observations lead to the hypothesis that O supply by blood and local O tension could be key components of the testicular niche of spermatogonial stem cells (SSCs). In this study, we investigated the impact of different hypoxic conditions (3.

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Article Synopsis
  • - XLF/Cernunnos is part of a key DNA repair system called classical non-homologous end-joining (cNHEJ), which helps fix DNA double-strand breaks.
  • - Research on Xlf-/- mice shows they experience neurodevelopmental delays, behavioral changes, and microcephaly, similar to humans with cNHEJ deficiencies; this is linked to increased neural cell apoptosis and premature neurogenesis.
  • - The study finds that XLF is crucial for normal brain development by maintaining balanced divisions of neural progenitors, and disruption of this can lead to developmental issues and stress-related pathologies.
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Cancer stem cells (CSCs) serve an essential role in failure of conventional antitumor therapy. In breast cancer, CD24/CD44 phenotype and high aldehyde dehydrogenase activity are associated with CSC subtypes. Furthermore, CD24/CD44 pattern is also characteristic of mesenchymal cells generated by epithelial‑mesenchymal transition (EMT).

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We developed an separation of function mouse line to overcome the embryonic lethality of Xrcc4-deficient mice. XRCC4 protein does not interact with Xlf, thus obliterating XRCC4-Xlf filament formation while preserving the ability to stabilize DNA ligase IV. X4 mice, which are DNA repair deficient, phenocopy the (known as -/-) setting with a minor impact on the development of the adaptive immune system.

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