Science

홈ScienceKey Publications

Key Publications

PrxII-mediated inhibition of PDGFRβ signaling (Nature, 2005)

PrxII-mediated inhibition of PDGFRβ signaling (Nature, 2005)

  • PrxII negatively regulates PDGFRβ auto-phosphorylation and PLCγ1phosphorylation in SMCs.
  • PrxII selectively regulates the PDGFRβ phosphorylation at tyrosine 579/581 and 857.
  • PrxII directly interacts with PDGFRβ upon PDGF stimulation.
  • Deficiency of PrxII exacerbates the neointimal growth of SMCs in the injured aortic vessels in vivo.
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PrxII-mediated preservation of VEGFR2 signaling (Molecular Cell, 2011)

PrxII-mediated preservation of VEGFR2 signaling (Molecular Cell, 2011)

  • PrxII specifically prevents the oxidative inactivation of VEGFR2 in ECs.
  • VEGFR2 oxidation involves the formation of cysteine disulfide in the C-terminal tail.
  • PrxII-dependent protection of VEGFR2 against oxidation is valid within caveolae.
  • Deficiency of PrxII retards tumor growth by inhibiting angiogenesis in vivo.
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Prx mimicry reverses neointimal hyperplasia (Circulation, 2013)

Prx mimicry reverses neointimal hyperplasia (Circulation, 2013)

  • Inactivation of PrxII by hyperoxidation is involved in SMC hyperplasia of injured vessels.
  • ETP class of fungal metabolites was discovered as novel small molecules that exhibit 2-Cys Prx-like activity.
  • ETPs inhibit PDGFRβ signaling in SMCs but promote VEGFR2 signaling in ECs.
  • ETPs inhibit neointimal SMC hyperplasia and induce re-endothelialization in the injured vessels.
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Flow-dependent regulation of PrxII and VEGFR2 complex (Cell Reports, 2023)

Flow-dependent regulation of PrxII and VEGFR2 complex (Cell Reports, 2023)

  • VEGFR2 kinase activity is reversibly regulated by oxidation-reduction cycle.
  • Disturbed flow stress induces the expression of NOX4, that leads to H2O2-mediated VEGFR2 oxidation.
  • Steady laminar flow induces the expression of eNOS that mediates the S-nitrosylation of VEGFR2.
  • Oxidation-resistant VEGFR2 mutant preserves endothelial function under disturbed flow in vivo.
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