Jian Ying Chuang


Affiliation: Taipei Medical University
Country: Taiwan


  1. Wu C, Lee P, Kao T, Chou S, Su R, Lee Y, et al. Upregulation of Znf179 acetylation by SAHA protects cells against oxidative stress. Redox Biol. 2018;19:74-80 pubmed publisher
    ..Additionally, HDAC inhibitors may have therapeutic potential for induction of Znf179 acetylation, strengthening the Znf179 protective functions against neurodegenerative processes. ..
  2. Su T, Lin S, Lee P, Yeh S, Hsieh T, Chou S, et al. The sigma-1 receptor-zinc finger protein 179 pathway protects against hydrogen peroxide-induced cell injury. Neuropharmacology. 2016;105:1-9 pubmed publisher
    ..In summary, these results reveal that Znf179 plays a novel role in neuroprotection, and Sig-1R agonists may be therapeutic candidates to prevent ROS-induced damage in neurodegenerative and neurotraumatic diseases. ..
  3. Hsu C, Chang W, Hsu T, Liu J, Yeh S, Wang J, et al. Suberoylanilide hydroxamic acid represses glioma stem-like cells. J Biomed Sci. 2016;23:81 pubmed
    ..Our results provide a perspective on targeting GSCs via SAHA treatment, and suggest that SAHA could be used as a potent agent to overcome drug resistance in GBM patients. ..
  4. Chuang J, Kao T, Lin S, Wu A, Lee P, SU T, et al. Specificity protein 1-zinc finger protein 179 pathway is involved in the attenuation of oxidative stress following brain injury. Redox Biol. 2017;11:135-143 pubmed publisher
  5. Ke Y, Huang Y, Chien W, Loh H, Chuang J, Yeh S. Mapping the naloxone binding sites on the mu-opioid receptor using cell-based photocrosslinkers. Biochim Biophys Acta Proteins Proteom. 2017;1865:336-343 pubmed publisher
    ..In conclusion, these results indicate that MOR has two naloxone binding sites and that the hydrophobic and polar/uncharged residues within these sites are important for naloxone binding. ..
  6. Chang K, Hsu T, Hsu C, Tsai S, Liu J, Chou S, et al. Specificity protein 1-modulated superoxide dismutase 2 enhances temozolomide resistance in glioblastoma, which is independent of O6-methylguanine-DNA methyltransferase. Redox Biol. 2017;13:655-664 pubmed publisher
    ..Inhibition of this pathway may represent a potential therapeutic target for restoring treatment susceptibility in GBM. ..
  7. Chang K, Huang C, Hsu T, Hsu C, Liu J, Chuang C, et al. Stress stimuli induce cancer-stemness gene expression via Sp1 activation leading to therapeutic resistance in glioblastoma. Biochem Biophys Res Commun. 2017;493:14-19 pubmed publisher
    ..Thus, Sp1 inhibition may prevent recurrence of malignant cells persisting after primary therapy. ..