Quyen Thu Bui

ORCID: 0000-0002-3195-9404
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About
Contact & Profiles
Research Areas
  • Ubiquitin and proteasome pathways
  • Protein Degradation and Inhibitors
  • Histone Deacetylase Inhibitors Research
  • RNA Research and Splicing
  • Cancer-related molecular mechanisms research
  • Adipokines, Inflammation, and Metabolic Diseases
  • Microtubule and mitosis dynamics
  • Adipose Tissue and Metabolism
  • Cancer Genomics and Diagnostics
  • Hippo pathway signaling and YAP/TAZ
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Streptococcal Infections and Treatments
  • Cancer Cells and Metastasis
  • Wnt/β-catenin signaling in development and cancer
  • Erythrocyte Function and Pathophysiology
  • Inflammasome and immune disorders
  • Infective Endocarditis Diagnosis and Management
  • Lipid metabolism and disorders
  • Antioxidant Activity and Oxidative Stress
  • 14-3-3 protein interactions
  • Neonatal and Maternal Infections
  • Cancer-related Molecular Pathways
  • PI3K/AKT/mTOR signaling in cancer
  • Circular RNAs in diseases
  • Sphingolipid Metabolism and Signaling

Seoul National University
2017-2024

University of Massachusetts Chan Medical School
2024

University of Ulsan
2021-2022

Asan Medical Center
2021-2022

Ulsan College
2021-2022

San Diego Biomedical Research Institute
2014-2022

Torrey Pines Institute For Molecular Studies
2014

The most common therapy for estrogen receptor-positive breast cancer is antihormone therapy, such as tamoxifen. However, acquisition of resistance to tamoxifen in one third patients presents a serious clinical problem. Polo-like kinase 1 (Plk1) key oncogenic regulator completion G2-M phase the cell cycle. We assessed Plk1 expression five chemoresistant types and found that its downstream phosphatase Cdc25c were selectively overexpressed tamoxifen-resistant MCF-7 (TAMR-MCF-7) cells. Real-time...

10.1158/1535-7163.mct-17-0545 article EN Molecular Cancer Therapeutics 2018-02-08

Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid that interacts via 5 G-protein coupled receptors, S1PR1-5, to regulate signalling pathways critical biological processes including cell growth, immune trafficking, and inflammation.We demonstrate in Type 2 diabetic (T2D) subjects, plasma S1P levels significantly increased response the anti-diabetic drug, rosiglitazone, and, correlated positively with measures of improved glucose homeostasis. In HFD-induced obese C57BL/6 J mice S1PR3...

10.1080/21623945.2021.2021700 article EN cc-by Adipocyte 2022-01-30

Failure to inhibit hepatic gluconeogenesis is a major mechanism contributing fasting hyperglycemia in type 2 diabetes and, along with steatosis, the hallmark of insulin resistance. Obesity associated chronic inflammation multiple tissues, and mechanistically linked both steatosis Here, we delineate role for coagulation signaling via tissue factor (TF) proteinase-activated receptor (PAR2) obesity-mediated inflammation, gluconeogenesis. In diet-induced obese mice, TF tail independent PAR2...

10.1016/j.ajpath.2014.10.008 article EN cc-by-nc-nd American Journal Of Pathology 2014-12-02

Estrogen receptor-α (ERα) is a 66 kDa (ERα66) nuclear receptor transcription factor and it functionally plays crucial role in various processes associated with human breast cancer.36 novel variant of ERα66 has been identified cloned, named as ERα36.As reported previously, we observed downregulation expression an elevation ERα36 levels tamoxifen-resistant cancer (TAMR-MCF-7) compared to the parental MCF-7 cells.We investigated functional roles their potential mechanisms regulating...

10.58502/dtt.23.0020 article EN cc-by-nc Drug Targets and Therapeutics 2024-03-27

Purpose: Most breast cancers are hormone-receptor-positive, and thus the first-line therapy for them is an anti-estrogen medication such as tamoxifen. If metastasis occurs or resistance to tamoxifen develops, 5-year survival rates cancer patients significantly decrease. Hence, a better understanding of molecular mechanisms that contribute aggressiveness great importance. ERα36 estrogen receptor variant known be upregulated in receiving treatment triple-negative cells. However, specific...

10.3389/fphar.2022.1057276 article EN cc-by Frontiers in Pharmacology 2022-12-02
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