Diep-Khanh Ho Vo

ORCID: 0000-0003-2267-8245
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About
Contact & Profiles
Research Areas
  • Endoplasmic Reticulum Stress and Disease
  • Cholesterol and Lipid Metabolism
  • Lipid metabolism and biosynthesis
  • interferon and immune responses
  • RNA and protein synthesis mechanisms
  • NF-κB Signaling Pathways
  • Pancreatic function and diabetes
  • Retinoids in leukemia and cellular processes
  • Hormonal Regulation and Hypertension
  • DNA Repair Mechanisms
  • Monoclonal and Polyclonal Antibodies Research
  • Genomics, phytochemicals, and oxidative stress
  • Biotin and Related Studies
  • Cell death mechanisms and regulation

Otto-von-Guericke University Magdeburg
2017-2021

Doshisha University
2015-2019

Life Systems (United States)
2017

The G-protein-coupled estrogen receptor (GPER) mediates rapid non-genomic effects of estrogen. Although GPER is able to induce proliferation, it down-regulated in breast, ovarian and colorectal cancer. During cancer progression, high expression levels are favorable for patients' survival. GPER-specific agonist G1 leads an inhibition cell proliferation elevated level intracellular calcium (Ca2+). purpose this study elucidate the mechanism G1-induced death by focusing on connection between...

10.3390/biom9090503 article EN cc-by Biomolecules 2019-09-18

The 24(S)-hydroxycholesterol (24S-OHC), which plays an important role in maintaining brain cholesterol homeostasis, has been shown to possess neurotoxicity. We have previously reported that 24S-OHC esterification by ACAT1 and the resulting lipid droplet (LD) formation are responsible for 24S-OHC-induced cell death. In present study, we investigate functional roles of esters LD death, identify four long-chain unsaturated fatty acids (oleic acid, linoleic arachidonic DHA) with is esterified...

10.1194/jlr.m068775 article EN cc-by Journal of Lipid Research 2016-09-20

Endoplasmic reticulum (ER) stress induced by disruption of protein folding activates the unfolded response (UPR), which while generally pro-survival in effect can also induce cell death under severe ER stress. 24(S)-hydroxycholesterol (24S-OHC), is enzymatically produced neurons, plays an important role maintaining brain cholesterol homeostasis but shows neurotoxicity when subjected to esterification acyl-CoA:cholesterol acyltransferase 1 (ACAT1) ER. In this study, we demonstrated that...

10.1038/s41420-019-0192-4 article EN cc-by Cell Death Discovery 2019-07-05

Dysregulation of c‐Jun N ‐terminal kinase (JNK) activation promoted DNA damage response bypass and tumorigenesis in our model hydrogen peroxide‐associated ulcerative colitis (UC) patients with quiescent UC (QUC), UC‐related dysplasia, carcinoma (UC‐CRC), thereby adapting to oxidative stress. In the model, we have observed features oncogenic transformation: increased proliferation, undetected damage, apoptosis resistance. Here, show that Chk1 was downregulated but activated acute chronic...

10.1155/2017/9303158 article EN cc-by Oxidative Medicine and Cellular Longevity 2017-01-01

Translation initiation comprises complex interactions of eukaryotic factor (eIF) subunits and the structural elements mRNAs. is a key process for building cell’s proteome. It not only determines total amount protein synthesized but also controls translation efficiency individual transcripts, which important cancer or ageing. Thus, understanding during one that contributes to how eIF subunit composition influences other pathways yet attributed eIFs. We applied BioID technique two rapidly...

10.3390/cancers13061293 article EN Cancers 2021-03-14
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