Tung Chao

ORCID: 0000-0003-3641-4996
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About
Contact & Profiles
Research Areas
  • Immune cells in cancer
  • Mitochondrial Function and Pathology
  • Immune Cell Function and Interaction
  • DNA Repair Mechanisms
  • Autophagy in Disease and Therapy
  • Genomic variations and chromosomal abnormalities
  • Immune Response and Inflammation
  • Ubiquitin and proteasome pathways
  • Genomics, phytochemicals, and oxidative stress
  • PARP inhibition in cancer therapy
  • Retinoids in leukemia and cellular processes
  • T-cell and B-cell Immunology
  • Congenital heart defects research
  • Epigenetics and DNA Methylation
  • Cyclopropane Reaction Mechanisms
  • Reproductive Biology and Fertility
  • Chromosomal and Genetic Variations
  • Genetics and Neurodevelopmental Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Catalytic C–H Functionalization Methods
  • Ovarian cancer diagnosis and treatment
  • Mechanisms of cancer metastasis
  • Catalytic Cross-Coupling Reactions

National Taiwan University
2021-2024

University of Lausanne
2017-2020

National Sun Yat-sen University
2020

Ludwig Cancer Research
2017

Tzu Chi University
2014

National Yang Ming Chiao Tung University
2013

High-grade serous ovarian carcinoma (HGSOC) originates mainly from the fallopian tube (FT) epithelium and always carries early TP53 mutations. We previously reported that tumors initiate in FT fimbria because of apoptotic failure expansion cells with DNA double-strand breaks (DSB) caused by bathing epithelial reactive oxygen species (ROSs) hemoglobin-rich follicular fluid (FF) after ovulation. Because ovulation is frequent HGSOC rare, we hypothesized luteal-phase progesterone (P4) could...

10.1016/j.celrep.2017.02.049 article EN cc-by Cell Reports 2017-03-01

Abstract NME3 is a member of the nucleoside diphosphate kinase (NDPK) family localized on mitochondrial outer membrane (MOM). Here, we report role in hypoxia-induced mitophagy dependent its active site phosphohistidine but not NDPK function. Mice carrying knock-in mutation Nme3 gene disrupting histidine phosphorylation are vulnerable to ischemia/reperfusion-induced infarction and develop abnormalities cerebellar Our mechanistic analysis reveals that phosphatidic acid (PA) mitochondria...

10.1038/s41467-024-46385-7 article EN cc-by Nature Communications 2024-03-13

Genotoxic insult causes nuclear and mitochondrial DNA damages with macroautophagy/autophagy induction. The role of (mtDNA) damage in the requirement autophagy for (nDNA) stability is unclear. Using site-specific approaches, we show that specific nDNA alone does not require repair unless presence mtDNA damage. We provide evidence after IR exposure-induced damages, suppression non-apoptotic permeability, by which ENDOG (endonuclease G) released translocated to nuclei sustain a TET (tet...

10.1080/15548627.2021.1874209 article EN Autophagy 2021-01-19

Abstract This study used DNA methyltransferase 3b (DNMT3b) knockout cells and the functional loss of DNMT3b mutation in immunodeficiency-centromeric instability-facial anomalies syndrome (ICF) to understand how dysfunction causes genome instability. We demonstrated that R-loops contribute damages ICF cells. More prominent damage signal was due expression acquirement p53 mutation. Genome-wide ChIP-sequencing mapped sites at satellite repetitive sequences including (peri-)centromere regions....

10.1038/s41419-022-04989-1 article EN cc-by Cell Death and Disease 2022-06-11

A facile and efficient synthetic methodology for preparing dibenzosuberones via a C–H bond activation strategy is presented. The ortho-aroylated 3,5-diarylisoxazole was employed as the starting substrate to undergo palladium-catalyzed intramolecular C–H/C–Br cross-coupling produce variety of bearing an isoxazole group in 24 >99% 1H NMR yields. dibenzosuberone structure further confirmed by X-ray crystallography. developed exhibits very good functional tolerance. In addition, rational...

10.1021/acs.joc.0c00346 article EN The Journal of Organic Chemistry 2020-03-26
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