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Träfflista för sökning "WFRF:(Becker Nikolaus) ;lar1:(gu)"

Sökning: WFRF:(Becker Nikolaus) > Göteborgs universitet

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1.
  • Grotz, Wolfgang, et al. (författare)
  • Sleep apnea - Treatment improves hypertension
  • 2006
  • Ingår i: Medizinische Klinik. - : Springer Science and Business Media LLC. - 0723-5003 .- 1615-6722. ; 101:11, s. 880-885
  • Forskningsöversikt (refereegranskat)
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2.
  • Weinstock, Joshua S, et al. (författare)
  • Aberrant activation of TCL1A promotes stem cell expansion in clonal haematopoiesis.
  • 2023
  • Ingår i: Nature. - 1476-4687. ; 616:7958, s. 755-763
  • Tidskriftsartikel (refereegranskat)abstract
    • Mutations in a diverse set of driver genes increase the fitness of haematopoietic stem cells (HSCs), leading to clonal haematopoiesis1. These lesions are precursors for blood cancers2-6, but the basis of their fitness advantage remains largely unknown, partly owing to a paucity of large cohorts in which the clonal expansion rate has been assessed by longitudinal sampling. Here, to circumvent this limitation, we developed a method to infer the expansion rate from data from a single time point. We applied this method to 5,071 people with clonal haematopoiesis. A genome-wide association study revealed that a common inherited polymorphism in the TCL1A promoter was associated with a slower expansion rate in clonal haematopoiesis overall, but the effect varied by driver gene. Those carrying this protective allele exhibited markedly reduced growth rates or prevalence of clones with driver mutations in TET2, ASXL1, SF3B1 and SRSF2, but this effect was not seen in clones with driver mutations in DNMT3A. TCL1A was not expressed in normal or DNMT3A-mutated HSCs, but the introduction of mutations in TET2 or ASXL1 led to the expression of TCL1A protein and the expansion of HSCs in vitro. The protective allele restricted TCL1A expression and expansion of mutant HSCs, as did experimental knockdown of TCL1A expression. Forced expression of TCL1A promoted the expansion of human HSCs in vitro and mouse HSCs in vivo. Our results indicate that the fitness advantage of several commonly mutated driver genes in clonal haematopoiesis may be mediated by TCL1A activation.
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3.
  • Wichert, R., et al. (författare)
  • Mucus Detachment by Host Metalloprotease Meprin beta Requires Shedding of Its Inactive Pro-form, which Is Abrogated by the Pathogenic Protease RgpB
  • 2017
  • Ingår i: Cell Reports. - : Elsevier BV. - 2211-1247. ; 21:8, s. 2090-2103
  • Tidskriftsartikel (refereegranskat)abstract
    • The host metalloprotease meprin beta is required for mucin 2 (MUC2) cleavage, which drives intestinal mucus detachment and prevents bacterial over-growth. To gain access to the cleavage site in MUC2, meprin b must be proteolytically shed from epithelial cells. Hence, regulation of meprin b shedding and activation is important for physiological and pathophysiological conditions. Here, we demonstrate that meprin b activation and shedding are mutually exclusive events. Employing ex vivo small intestinal organoid and cell culture experiments, we found that ADAM-mediated shedding is restricted to the inactive pro-form of meprin beta and is completely inhibited upon its conversion to the active form at the cell surface. This strict regulation of meprin beta activity can be overridden by pathogens, as demonstrated for the bacterial protease Arg-gingipain (RgpB). This secreted cysteine protease potently converts membrane-bound meprin beta into its active form, impairing meprin beta shedding and its function as a mucus-detaching protease.
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  • Resultat 1-3 av 3

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