Publications by authors named "Ramy Ragheb"

Article Synopsis
  • Enhancers interact with transcription factors, chromatin regulators, and non-coding RNA to influence gene expression, particularly during cell differentiation.
  • The study examines 3D genome structures of mouse embryonic stem cells transitioning from pluripotency to neuroectodermal differentiation, revealing significant reorganization of chromosome interactions.
  • This reorganization leads to the creation of multiway hubs that connect enhancers and promoters from distant chromosomal regions, implicating these structural changes in the regulation of gene expression and the establishment of new cell identities.
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Article Synopsis
  • As cells transition from a pluripotent state to a specific lineage, they must activate lineage-specific genes while silencing pluripotency-associated genes, and the NuRD complex plays a crucial role in this process.
  • The NuRD complex helps control nucleosome density to enable proper gene expression and minimize unwanted transcription in undifferentiated cells.
  • Research indicates that NuRD doesn't silence all genes, but rather keeps certain genes poised for activation when cells exit pluripotency, thereby guiding proper lineage commitment and maintaining stability between different cellular states.
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Differentiation of mammalian pluripotent cells involves large-scale changes in transcription and, among the molecules that orchestrate these changes, chromatin remodellers are essential to initiate, establish and maintain a new gene regulatory network. The Nucleosome Remodelling and Deacetylation (NuRD) complex is a highly conserved chromatin remodeller which fine-tunes gene expression in embryonic stem cells. While the function of NuRD in mouse pluripotent cells has been well defined, no study yet has defined NuRD function in human pluripotent cells.

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In mammals, both sterile wounding and infection induce inflammation and activate the innate immune system, and the combination of both challenges may lead to severe health defects, revealing the importance of the balance between the intensity and resolution of the inflammatory response for the organism's fitness. Underlying mechanisms remain however elusive. Using Drosophila, we show that, upon infection with the entomopathogenic bacterium Pseudomonas entomophila (Pe), a sterile wounding induces a reduced resistance and increased host mortality.

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