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Träfflista för sökning "WFRF:(Borén Christofer) srt2:(2004)"

Sökning: WFRF:(Borén Christofer) > (2004)

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1.
  • Flood, Christofer, 1974, et al. (författare)
  • Molecular mechanism for changes in proteoglycan binding on compositional changes of the core and the surface of low-density lipoprotein-containing human apolipoprotein B100
  • 2004
  • Ingår i: Arterioscler Thromb Vasc Biol. - 1524-4636. ; 24:3, s. 564-70
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The aim of this study was to investigate the molecular mechanism for changes in proteoglycan binding and LDL receptor affinity on two compositional changes in LDL that have been associated with atherosclerosis: cholesterol enrichment of the core and modification by secretory group IIA phospholipase A2 (sPLA2) of the surface. METHODS AND RESULTS: Transgenic mice expressing recombinant apolipoprotein (apo) B and sPLA2 were generated. Recombinant LDL were isolated and tested for their proteoglycan and LDL receptor-binding activity. The results show site A (residues 3148-3158) in apoB100 becomes functional in sPLA2-modified LDL and that site A acts cooperatively with site B (residues 3359-3369), the primary proteoglycan-binding site in native LDL, in the binding of sPLA2-modified LDL to proteoglycans. Our results also show that cholesterol enrichment of LDL is associated with increased affinity for proteoglycans and for the LDL receptor. This mechanism is likely mediated by a conformational change of site B and is independent of site A in apoB100. CONCLUSIONS: Site A in apoB100 becomes functional in sPLA2-modified LDL and acts cooperatively with site B resulting in increased proteoglycan-binding activity. The increased binding for proteoglycans of cholesterol-enriched LDL is solely dependent on site B.
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2.
  • Gustafsson, Maria, 1976, et al. (författare)
  • Retention of atherogenic lipoproteins in atherogenesis
  • 2004
  • Ingår i: Cell Mol Life Sci. - : Springer Science and Business Media LLC. - 1420-682X. ; 61:1, s. 4-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Atherosclerosis is a multifactorial disease whose pathogenesis is still unclear. Mounting evidence, however, supports the concept that subendothelial retention of apoB100-containing lipoproteins is the initiating event in atherogenesis. Subsequently, a series of biological responses to this retained material leads to specific molecular and cellular processes that promote lesion formation.
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