Xia Wang
University of British Columbia
14 Papers
45 Citations
Xia Wang is an academic researcher from University of British Columbia. The author has contributed to research in topics: Aniridia & PAX6. The author has an hindex of 8, co-authored 14 publications. Previous affiliations of Xia Wang include Laboratory of Molecular Biology & Massachusetts Eye and Ear Infirmary.
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Papers
Efficacy of Postnatal In Vivo Nonsense Suppression Therapy in a Pax6 Mouse Model of Aniridia.
Xia Wang,Kevin Gregory-Evans,Kishor M. Wasan,Olena Sivak,Xianghong Shan,Cheryl Y. Gregory-Evans +5 more
TL;DR: The remarkable capacity of malformed ocular tissue to respond postnatally to Pax6 dosage in vivo demonstrates that the use of nonsense suppression could be a valuable therapeutic approach for blinding diseases caused by nonsense mutations.
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Ascorbic acid reverses valproic acid-induced inhibition of Hoxa2 and maintains glutathione homeostasis in mouse embryos in culture.
TL;DR: The results suggest VPA may, in part, exert its teratogenicity through alteration of the embryonic antioxidant status and inhibition of Hoxa2 gene expression and that ascorbic acid can protect embryos from VPA-induced oxidative stress.
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Kynurenic acid downregulates IL-17/1L-23 axis in vitro.
Sanam Salimi Elizei,Malihe-Sadat Poormasjedi-Meibod,Xia Wang,Maryam Kheirandish,Aziz Ghahary +4 more
TL;DR: It is concluded that KynA plays an important role in modulating the expression of IL-23 and IL-17 in DCs and Th17 cells through inhibiting GPCR35 and downregulation of both AC and cAMP.
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A mouse model of aniridia reveals the in vivo downstream targets of Pax6 driving iris and ciliary body development in the eye.
TL;DR: In this paper, the authors focused on identification of the downstream targets for Pax6 in the developing iris and ciliary body, where they used laser capture microdissection in mouse eyes from E12.5-E16.5, followed by chromatin immunoprecipitation, and immunohistochemistry.
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Nonsense suppression therapies in ocular genetic diseases.
Xia Wang,Cheryl Y. Gregory-Evans +1 more
TL;DR: The mechanisms that are involved in discriminating normal translation termination from premature termination codons are highlighted; the current understanding of nonsense-mediated mRNA decay models (NMD); the association and crosstalk between PTC and the underlying dynamic NMD process; and the suppression therapies that have been employed in nonsense-medicated ocular disease models are highlighted.
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