@article{mcintosh_zhang_cowger_parks_lagudah_hoxha_2011, title={Rye-derived powdery mildew resistance gene Pm8 in wheat is suppressed by the Pm3 locus}, volume={123}, ISSN={["1432-2242"]}, DOI={10.1007/s00122-011-1589-5}, abstractNote={Genetic suppression of disease resistance is occasionally observed in hexaploid wheat or in its interspecific crosses. The phenotypic effects of genes moved to wheat from relatives with lower ploidy are often smaller than in the original sources, suggesting the presence of modifiers or partial inhibitors in wheat, especially dilution effects caused by possible variation at orthologous loci. However, there is little current understanding of the underlying genetics of suppression. The discovery of suppression in some wheat genotypes of the cereal rye chromosome 1RS-derived gene Pm8 for powdery mildew resistance offered an opportunity for analysis. A single gene for suppression was identified at or near the closely linked storage protein genes Gli-A1 and Glu-A3, which are also closely associated with the Pm3 locus on chromosome 1AS. The Pm3 locus is a complex of expressed alleles and pseudogenes embedded among Glu-A3 repeats. In the current report, we explain why earlier work indicated that the mildew suppressor was closely associated with specific Gli-A1 and Glu-A3 alleles, and predict that suppression of Pm8 involves translated gene products from the Pm3 locus.}, number={3}, journal={THEORETICAL AND APPLIED GENETICS}, author={McIntosh, Robert A. and Zhang, Peng and Cowger, Christina and Parks, Ryan and Lagudah, Evans S. and Hoxha, Sami}, year={2011}, month={Aug}, pages={359–367} }
 @article{zhang_stevie_vanfleet_neelakantan_klimov_zhou_chow_2004, title={Diffusion profiles of high dosage Cr and V ions implanted into silicon}, volume={96}, ISSN={["1089-7550"]}, DOI={10.1063/1.1756221}, abstractNote={The depth profiles of high dosage Cr+52 and V+51 ions implanted in (100) crystalline silicon after thermal anneal at temperatures between 300 °C and 1000 °C are studied by secondary ion mass spectrometry and cross-sectional transmission electron microscopy. At dosages of 1×1015 ions/cm2 and above, the surface layer of silicon substrate is amorphorized. During the subsequent thermal annealing, the depth profiles of the implanted ions are strongly coupled with the solid phase epitaxial growth of amorphous silicon. Silicide precipitate formation is important to understand the differences between Cr and V diffusion. After anneal of the 1×1015 ions/cm2 implanted samples at 900 °C and 1000 °C, most of the Cr has left the silicon, but only 10% of the V has escaped. The 1×1014 ions/cm2 Cr-implanted sample shows Cr ions exist only near the surface after 1000 °C anneal. The V-implanted sample, on the other hand, only shows a narrowing of the V profile after 1000 °C anneal.}, number={2}, journal={JOURNAL OF APPLIED PHYSICS}, author={Zhang, P and Stevie, F and Vanfleet, R and Neelakantan, R and Klimov, M and Zhou, D and Chow, L}, year={2004}, month={Jul}, pages={1053–1058} }
 @article{bonner_wang_zhang_rice_zhang_adler_choe_kagan_2001, title={Role of receptor tyrosine kinases and mitogen-activated protein kinases in metal-induced pulmonary fibrosis}, volume={120}, ISSN={["0012-3692"]}, DOI={10.1378/chest.120.1_suppl.S55}, abstractNote={The proliferation of lung fibroblasts is a key component of pulmonary fibrosis. Several cell-surface receptor tyrosine kinases, including the platelet-derived growth factor receptor (PDGF-R) and epidermal growth factor receptor (EGF-R), mediate fibroblast mitogenesis via the activation of mitogen-activated protein (MAP) kinases. We have developed a model of metal-induced oxidative stress in rats using vanadium pentoxide (V2O5) that is characterized by interstitial and peribronchiolar fibrosis, airway smooth-muscle thickening, and mucous cell metaplasia. In vivo activation of the extracellular signal-regulated kinases (ERKs [ERK-1 and ERK-2]) was demonstrated by immunohistochemistry in fibrotic lesions caused by V2O5 exposure. Moreover, V2O5 injury upregulated platelet-derived growth factor α-receptor messenger RNA (mRNA) and protein in vivo. The mechanism of PDGF-Rα upregulation by V2O5 was elucidated in vitro and involved the release of interleukin-1β by alveolar macrophages, which then activated lung fibroblasts in a paracrine manner to activate p38 MAP kinase, which caused stabilization of PDGF-Rα mRNA. V2O5 also activated ERK-1 and ERK-2 in cultured lung fibroblasts in an oxidant-dependent manner that involved upstream activation of the EGF-R, Raf-1, MAP kinase kinase signaling cascade. In another study, V2O5 exposure of human bronchial epithelial cells in vitro caused the release of mitogenic activity for human lung fibroblasts that was abolished by a neutralizing antibody against heparin-binding epidermal growth factor-like growth factor. Induction of heparin-binding epidermal growth factor-like growth factor mRNA and protein by V2O5in vitro was reduced by the MAP kinase kinase inhibitor PD98059 and the p38 MAP kinase inhibitor SB203580. Finally, the intraperitoneal administration of tyrosine kinase inhibitors specific for either the PDGF-R or the EGF-R (tyrphostins AG1296 and AG1478, respectively) significantly reduced pulmonary fibrosis in rats exposed to V2O5. Collectively, these studies have identified signaling pathways and inducible genes activated by V2O5-stimulated oxidative stress that may offer potential targets for therapeutic intervention of pulmonary fibrosis.}, number={1}, journal={CHEST}, author={Bonner, JC and Wang, YZ and Zhang, P and Rice, A and Zhang, LM and Adler, K and Choe, N and Kagan, E}, year={2001}, month={Jul}, pages={55S–56S} }