Yen-Yin Tsai

Fu Jen Catholic University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Yi-Huei Huang

Chung Shan Medical University

Shan-Wen Tan

National Taiwan Ocean University

Han‐Min Chen

Soochow University

Cheng-Yuh Tsai

National Taiwan Ocean University

Li‐Te Chin

National Defense Medical Center

Kuang-Yu Hu

Chung Hua University

Chi‐Shun Tu

Fu Jen Catholic University

Shiu-Huey Chou

Fu Jen Catholic University

Ai‐Ling Hour

Fu Jen Catholic University

Yeong-Der Yao

Institute of Physics, Academia Sinica

Cooperative Institutions

Fu Jen Catholic University

National Taiwan Ocean University

National Defense Medical Center

National Chiayi University

National Research Institute of Chinese Medicine

National Yang Ming Chiao Tung University

Weatherford College

Tunghai University

National Chung Cheng University

National Taiwan University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Identification of the Nanogold Particle-Induced Endoplasmic Reticulum Stress by Omic Techniques and Systems Biology Analysis

ACS Nano (2011)

Yen-Yin Tsai Yi-Huei Huang Ya-Li Chao Kuang-Yu Hu Li‐Te Chin

Growth inhibition and apoptotic/necrotic phenotype was observed in nanogold particle (AuNP)-treated human chronic myelogenous leukemia cells. To elucidate the underlying cellular mechanisms, proteomic techniques including two-dimensional electrophoresis/mass spectrometry and protein microarrays were utilized to study the differentially expressed proteome and phosphoproteome, respectively. Systems biology analysis of the proteomic data revealed that unfolded protein-associated endoplasmic reticulum (ER) stress response was the predominant event. Concomitant with transcriptomic analysis using mRNA expression, microarrays show ER stress response in the AuNP-treated cells. The ER stress protein markers' expression assay unveiled AuNPs as an efficient cellular ER stress elicitor. Upon ER stress, cellular responses, including reactive oxygen species increase, mitochondrial cytochrome c release, and mitochondria damage, chronologically occurred in the AuNP-treated cells. Conclusively, this study demonstrates that AuNPs cause cell death through induction of unmanageable ER stress.

Proteome

10.1021/nn2027775

Cite

Citations (111)