- ENG
- KOR
Science
ScienceKey Publications
Key Publications
-
-
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.
-
-
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.
-
-
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.
-
-
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.
TOP