Publications by authors named "P ESTEVE"

Nucleosomes are non-uniformly distributed across eukaryotic genomes, with stretches of 'open' chromatin strongly associated with transcriptionally active promoters and enhancers. Understanding chromatin accessibility patterns in normal tissue and how they are altered in pathologies can provide critical insights to development and disease. With the advent of high-throughput sequencing, a variety of strategies have been devised to identify open regions across the genome, including DNase-seq, MNase-seq, FAIRE-seq, ATAC-seq, and NicE-seq.

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While studying myoblast methylomes and transcriptomes, we found that had a remarkable preference for expression in both myoblasts and cerebellum. To understand how widespread such a relationship was and its epigenetic and biological correlates, we systematically looked for genes with similar transcription profiles and analyzed their DNA methylation and chromatin state and accessibility profiles in many different cell populations. Twenty genes were expressed preferentially in myoblasts and cerebellum (Myob/Cbl genes).

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Article Synopsis
  • Somatic mutations accumulate in cells as they age, leading to clonal expansion, especially in hematopoietic cells, where certain gene mutations increase the likelihood of clonal hematopoiesis (CH).
  • The study focuses on SRCAP mutations in hematopoietic stem cells, which enhance their survival and proliferation, particularly after chemotherapy treatment with doxorubicin.
  • SRCAP is linked to DNA repair and chromatin remodeling, and its mutations promote a specific expansion of lymphoid cells by altering how DNA is repaired and how certain histones are regulated.
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Microbiota dysbiosis and metabolic syndrome, consequences of a non-adequate diet, generate a feedback pathogenic state implicated in Alzheimer's disease development. The lower production of short chain fatty acids (SCFAs) under dysbiosis status leads to lipid homeostasis deregulation and decreases Angptl4 release and AMPK activation in the adipose tissue, promoting higher lipid storage (adipocyte hypertrophy) and cholesterol levels. Also, low SCFA generation reduces GPR41 and GPR43 receptor activation at the adipose tissue (increasing leptin release and leptin receptor resistance) and intestinal levels, reducing the release of GLP-1 and YPP.

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