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http://dx.doi.org/10.1172/JCI185824 | DOI Listing |
J Clin Invest
October 2024
Division of Infectious Diseases, and.
Front Immunol
April 2022
Department of Pharmacology and Physiology, Université de Montréal, Institute for Research in Immunology and Cancer, QC, Canada.
Early T-cell development is precisely controlled by E proteins, that indistinguishably include HEB/TCF12 and E2A/TCF3 transcription factors, together with NOTCH1 and pre-T cell receptor (TCR) signalling. Importantly, perturbations of early T-cell regulatory networks are implicated in leukemogenesis. NOTCH1 gain of function mutations invariably lead to T-cell acute lymphoblastic leukemia (T-ALL), whereas inhibition of E proteins accelerates leukemogenesis.
View Article and Find Full Text PDFmSphere
December 2021
Department of Microbiology, Ramón y Cajal University Hospital and Ramón y Cajal Health Research Institute (IRYCIS), Madrid, Spain.
This is a longitudinal study comprising 649 Escherichia coli isolates representing all 7,165 E. coli bloodstream infection (BSI) episodes recorded in a hospital (1996 to 2016). Strain analysis included clonal identification (phylogenetic groups/subgroups, STc131 subclades, pulsed-field gel electrophoresis [PFGE], and whole-genome sequencing [WGS]), antibiotic susceptibility (13 antibiotics), and virulence-associated genes (VAGs; 29 genes).
View Article and Find Full Text PDFAdv Cancer Res
September 2020
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel. Electronic address:
Growth factors and their receptor tyrosine kinases (RTKs), a group of transmembrane molecules harboring cytoplasm-facing tyrosine-specific kinase functions, play essential roles in migration of multipotent cell populations and rapid proliferation of stem cells' descendants, transit amplifying cells, during embryogenesis and tissue repair. These intrinsic functions are aberrantly harnessed when cancer cells undergo intertwined phases of cell migration and proliferation during cancer progression. For example, by means of clonal expansion growth factors fixate the rarely occurring driver mutations, which initiate tumors.
View Article and Find Full Text PDFNat Commun
June 2019
Institut für Biologische Physik, Universität zu Köln, Zülpicherstr. 77, 50937, Köln, Germany.
The evolution of microbial and viral organisms often generates clonal interference, a mode of competition between genetic clades within a population. Here we show how interference impacts systems biology by constraining genetic and phenotypic complexity. Our analysis uses biophysically grounded evolutionary models for molecular phenotypes, such as fold stability and enzymatic activity of genes.
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