A5037610613- Protein Degradation and Inhibitors
- Ubiquitin and proteasome pathways
- Sarcoma Diagnosis and Treatment
- Cellular transport and secretion
- Chromatin Remodeling and Cancer
- CAR-T cell therapy research
- Multiple Myeloma Research and Treatments
- Cardiac tumors and thrombi
- Lipid Membrane Structure and Behavior
- Cancer, Lipids, and Metabolism
- Biochemical and Structural Characterization
- Genetics, Aging, and Longevity in Model Organisms
- Microtubule and mitosis dynamics
- Cardiac Ischemia and Reperfusion
- Pickering emulsions and particle stabilization
- Alzheimer's disease research and treatments
- Pancreatic function and diabetes
- Hippo pathway signaling and YAP/TAZ
- Genetics and Neurodevelopmental Disorders
- Endoplasmic Reticulum Stress and Disease
- Retinal Development and Disorders
- Supramolecular Self-Assembly in Materials
- Prion Diseases and Protein Misfolding
- Adipose Tissue and Metabolism
Genoway (France)
2023-2025
Centre National de la Recherche Scientifique
2009-2012
Inserm
2008-2012
Institut Jacques Monod
2007-2012
Université Paris Cité
2009-2012
Délégation Paris 7
2012
Sorbonne Paris Cité
2012
Abstract NUT carcinoma (NC) is an aggressive squamous defined by the BRD4–NUT fusion oncoprotein. Routinely effective systemic treatments are unavailable for most NC patients. The lack of adequate animal model precludes identifying and leveraging cell-extrinsic factors therapeutically in NC. Here, we created a genetically engineered mouse (GEMM) that forms Brd4::NUTM1 gene upon tamoxifen induction Sox2-driven Cre. displayed complete disease penetrance, with tumors arising from epithelium...
The accuracy of protein synthesis and its relation to ageing has been long-standing interest. To study whether spontaneous changes in the rate ribosomal error occur as a function age, we first determined that stop-codon readthrough is more sensitive read-out mistranslation due codon-anticodon mispairing than missense amino acid incorporation. Subsequently, developed knock-in mice for in-vivo detection using gain-of-function Kat2-TGA-Fluc reporter which combines fluorescent bioluminescent...
Abstract Mitochondrial dysfunction is a hallmark of aging and numerous age-related diseases. A wealth studies supports the accumulation mitochondrial DNA (mtDNA) mutations as contributing factor to in disease. One best models study relationship between mtDNA mutator mouse, which expresses proofreading-deficient version polymerase-γ (PolgA). Despite its groundbreaking contributions biology research, this model limited by whole-body mutations, prevents investigation tissue-specific differences...
<p>Supplementary Fig. S3. mNC-derived cell lines share transcriptional profiles with tumor tissues that are characterized by MYC pathway upregulation.</p>
<p>Supplementary Fig. S1. Creation of an inducible, highly penetrant genetically engineered mouse model NUT carcinoma.</p>
<p>Supplementary Fig. S5. H3K27me3 and H3K27ac domains are mutually exclusive.</p>
<div>Abstract<p>NUT carcinoma (NC) is an aggressive squamous defined by the BRD4–NUT fusion oncoprotein. Routinely effective systemic treatments are unavailable for most NC patients. The lack of adequate animal model precludes identifying and leveraging cell-extrinsic factors therapeutically in NC. Here, we created a genetically engineered mouse (GEMM) that forms <i>Brd4::NUTM1</i> gene upon tamoxifen induction <i>Sox2</i>-driven Cre. displayed complete...
<p>Supplementary Fig. S4. Large domains are larger in mNC samples.</p>
<p>Supplementary Fig. S4. Large domains are larger in mNC samples.</p>
<p>Supplementary Fig. S3. mNC-derived cell lines share transcriptional profiles with tumor tissues that are characterized by MYC pathway upregulation.</p>
<p>Supplementary Fig. S2. mNC tumors arise from esophagus.</p>