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Science
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Publications
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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)
- 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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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 reendothelialization in the injured vessels.
- ETPs can be useful therapeutic agents repairing vascular injuries such as those caused by stenting.
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