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Articles by Y. Xia
Total Records ( 3 ) for Y. Xia
  T. Detchprohm , M. Zhu , Y. Li , Y. Xia , L. Liu , D. Hanser and C. Wetzel
 

We demonstrate homoepitaxial growth of GaInN/GaN-based green (500–560 nm) light emitting diodes (LEDs) on a-plane and m-plane quasi-bulk GaN prepared by hydride vapor phase epitaxy (HVPE). We find that in order to achieve an emission peak wavelength beyond 500 nm, a minimum InN-fraction of 14% is needed for both, a- and m-plane quantum wells (QWs), while 8% are enough for c-plane-oriented QWs. Besides increasing the InN-fraction in these non-polar QWs, widening the QW also proves to effectively shift the emission to longer wavelengths without loosing efficiency with the benefit of maintaining a low InN-fraction.

  H Zhu , G. J Li , L Ding , X Cui , H Berg , S. M Assmann and Y. Xia
 

Heterotrimeric GTP-binding proteins, which consist of G, Gβ, and G subunits, play important roles in transducing extracellular signals perceived by cell surface receptors into intracellular physiological responses. In addition to a single prototypical G protein (GPA1), Arabidopsis has three unique G-like proteins, known as XLG1, XLG2, and XLG3, that have been found to be localized in nuclei, although their functions and mode of action remain largely unknown. Through a transcriptomic analysis, we found that XLG2 and XLG3 were rapidly induced by infection with the bacterial pathogen Pseudomonas syringae, whereas the XLG1 transcript level was not affected by pathogen infection. A reverse genetic screen revealed that the xlg2 loss-of-function mutation causes enhanced susceptibility to P. syringae. Transcriptome profiling revealed that the xlg2 mutation affects pathogen-triggered induction of a small set of defense-related genes. However, xlg1 and xlg3 mutants showed no difference from wild-type plants in resistance to P. syringae. In addition, the xlg2 xlg3 double mutant and the xlg1 xlg2 xlg3 triple mutant were not significantly different from the xlg2 single mutant in the disease resistance phenotype, suggesting that the roles of XLG1 and XLG3 in defense, if any, are less significant than for XLG2. Constitutive overexpression of XLG2 leads to the accumulation of abnormal transcripts from multiple defense-related genes. Through co-immunoprecipitation assays, XLG2 was found to interact with AGB1, the sole Gβ subunit in Arabidopsis, which has previously been found to be a positive regulator in resistance to necrotrophic fungal pathogens. However, no significant difference was found between three xlg single mutants, the xlg2 xlg3 double mutant, the xlg triple mutant, and wild-type plants in resistance to the necrotrophic fungal pathogens Botrytis cinerea or Alternaria brassicicola. These results suggest that XLG2 and AGB1 are components of a G-protein complex different from the prototypical heterotrimeric G-protein and may have distinct functions in modulating defense responses.

  R. A Irani , Y Zhang , S. C Blackwell , C. C Zhou , S. M Ramin , R. E Kellems and Y. Xia
 

Growth-restricted fetuses are at risk for a variety of lifelong medical conditions. Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is associated with fetuses who suffer from intrauterine growth restriction (IUGR). Recently, emerging evidence indicates that preeclamptic women harbor AT1 receptor agonistic autoantibodies (AT1-AAs) that contribute to the disease features. However, the exact role of AT1-AAs in IUGR and the underlying mechanisms have not been identified. We report that these autoantibodies are present in the cord blood of women with preeclampsia and retain the ability to activate AT1 receptors. Using an autoantibody-induced animal model of preeclampsia, we show that AT1-AAs cross the mouse placenta, enter fetal circulation, and lead to small fetuses with organ growth retardation. AT1-AAs also induce apoptosis in the placentas of pregnant mice, human villous explants, and human trophoblast cells. Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide. Thus, these studies identify AT1-AA as a novel causative factor of preeclampsia-associated IUGR and offer two possible underlying mechanisms: a direct detrimental effect on fetal development by crossing the placenta and entering fetal circulation, and indirectly through AT1-AA–induced placental damage. Our findings highlight AT1-AAs as important therapeutic targets.

 
 
 
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