Publications by authors named "R W Burt"
The MYST family histone acetyltransferase gene, KAT6B (MYST4, MORF, QKF) is mutated in two distinct human congenital disorders characterised by intellectual disability, facial dysmorphogenesis and skeletal abnormalities; the Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome and Genitopatellar syndrome. Despite its requirement in normal skeletal development, the cellular and transcriptional effects of KAT6B in skeletogenesis have not been thoroughly studied. Here, we show that germline deletion of the Kat6b gene in mice causes premature ossification in vivo, resulting in shortened craniofacial elements and increased bone density, as well as shortened tibias with an expanded pre-hypertrophic layer, as compared to wild type controls.
View Article and Find Full Text PDFCorrigendum: Organotypic culture of neonatal murine inner ear explants.
Front Cell Neurosci
November 2024
[This corrects the article DOI: 10.3389/fncel.2019.
View Article and Find Full Text PDFArticle Synopsis
- Cancer-associated fibroblasts (CAFs) in B-cell precursor acute lymphoblastic leukemia (B-ALL) originate from bone marrow-derived mesenchymal stromal cells (MSCs) and are influenced by reactive oxygen species from chemotherapy.
- The study shows that exposure of MSCs to B-ALL cells or their secretions initiates the CAF formation, marked by a strong interferon pathway response.
- A key finding is that leukemia cell-derived mitochondrial double-stranded RNA (dsRNA) stimulates MSCs to transition into CAFs, and disrupting dsRNA can block this process, revealing a new way cancer cells interact with their environment.
Article Synopsis
- Identification of stearoyl-CoA desaturase (SCD) as a key therapeutic target in improving the outcomes of acute myeloid leukemia (AML) patients, showing its role across different mutational backgrounds.
- Inhibition of SCD using the drug SSI-4 induces lipotoxicity, leading to cell death in AML models both in lab conditions and in living organisms.
- The study suggests that combining SCD inhibition with standard chemotherapy enhances the effectiveness of treatment, emphasizing the need for predictive biomarkers and combination therapies for optimal results.