Science

홈ScienceSciences

Published journal

Nature (2005)

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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Molecular Cell (2011)

Molecular Cell (2011)

  • PrxII specifically prevents the oxidative inactivation of VEGFR2 in ECs.
  • VEGFR2 oxidation involves the formation of cysteine disulfide in 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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Circulation (2013)

Circulation (2013)

  • Inactivation of PrxII by hyperoxidation is involved in SMC hyperplasia of injured vessel.
  • The ETP class of fungal metabolites was discovered as novel small molecules that exhibit the 2-Cys Prx-like activity.
  • ETPs inhibit PDGFRβ signaling in SMCs but promote VEGFR2 signaling in ECs.
  • ETPs inhibit Neointimal SMC hyperplasia and induce reendothelialization in the injured vessels.
  • ETPs can be useful therapeutic agents to repair vascular injury like stenting.
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