Experience

Acepodia

• United States
• Biotechnology Research
• 1 - 100 Employee

• Principal Scientist

  • Aug 2020 - Jun 2022

  devoted to develop cell therapy technologies and products to cure immune-related diseases and cancer!! devoted to develop cell therapy technologies and products to cure immune-related diseases and cancer!!



Weill Cornell Medicine

• United States
• Hospitals and Health Care
• 700 & Above Employee

• Postdoctoral Associate

  • Sep 2014 - Jan 2018

  Mentor: Dr. John Blenis, Ph.D. The Ras-ERK and PI3K-mTOR pathways • Investigated a novel MSK1-BRD2 axis in DNA damage responses, innate immunity, and lung tumorigenesis. • Established several different types of MCF10A-based epithelial-mesenchymal transition (EMT) models and investigated the biological significance of RSK isoforms in EMT. • Evaluated the contribution of post-translational modifications on RagA/B to amino acid sensing by mTORC1 and investigated a potential… Show more Mentor: Dr. John Blenis, Ph.D. The Ras-ERK and PI3K-mTOR pathways • Investigated a novel MSK1-BRD2 axis in DNA damage responses, innate immunity, and lung tumorigenesis. • Established several different types of MCF10A-based epithelial-mesenchymal transition (EMT) models and investigated the biological significance of RSK isoforms in EMT. • Evaluated the contribution of post-translational modifications on RagA/B to amino acid sensing by mTORC1 and investigated a potential negative feedback loop from the mTORC1-Sestrin2 axis. • Targeting mTORC1-hyperactive cancer cells by modulating the RUVBL1/2-TTT complex. • Performed a genome-scale CRISPR-Cas9 knockout screening to identify genes that modulate mTORC1 signaling. Show less Mentor: Dr. John Blenis, Ph.D. The Ras-ERK and PI3K-mTOR pathways • Investigated a novel MSK1-BRD2 axis in DNA damage responses, innate immunity, and lung tumorigenesis. • Established several different types of MCF10A-based epithelial-mesenchymal transition (EMT) models and investigated the biological significance of RSK isoforms in EMT. • Evaluated the contribution of post-translational modifications on RagA/B to amino acid sensing by mTORC1 and investigated a potential… Show more Mentor: Dr. John Blenis, Ph.D. The Ras-ERK and PI3K-mTOR pathways • Investigated a novel MSK1-BRD2 axis in DNA damage responses, innate immunity, and lung tumorigenesis. • Established several different types of MCF10A-based epithelial-mesenchymal transition (EMT) models and investigated the biological significance of RSK isoforms in EMT. • Evaluated the contribution of post-translational modifications on RagA/B to amino acid sensing by mTORC1 and investigated a potential negative feedback loop from the mTORC1-Sestrin2 axis. • Targeting mTORC1-hyperactive cancer cells by modulating the RUVBL1/2-TTT complex. • Performed a genome-scale CRISPR-Cas9 knockout screening to identify genes that modulate mTORC1 signaling. Show less



Harvard Medical School

• United States
• Higher Education
• 700 & Above Employee

• Postdoctoral Fellow

  • Jan 2014 - Aug 2014

  Mentor: Dr. John Blenis, Ph.D. Lymphangioleiomyomatosis (LAM) metastasis and ERK-RSK pathway • Characterized the Estrogen-ERK-RSK regulatory arm in LAM. Mentor: Dr. John Blenis, Ph.D. Lymphangioleiomyomatosis (LAM) metastasis and ERK-RSK pathway • Characterized the Estrogen-ERK-RSK regulatory arm in LAM.



UT Southwestern Medical Center

• United States
• Hospitals and Health Care
• 700 & Above Employee

• Postdoctoral Research Scholar

  • Jun 2013 - Nov 2013

  Mentor: Michael A White Ph.D. Regulation of mTORC1 by the innate immune kinase TBK1 • Uncovered that TBK1, as well as a set of TBK1 substrates and interacting proteins, participate in amino acid-induced mTORC1 activation. Mentor: Michael A White Ph.D. Regulation of mTORC1 by the innate immune kinase TBK1 • Uncovered that TBK1, as well as a set of TBK1 substrates and interacting proteins, participate in amino acid-induced mTORC1 activation.



Academia Sinica, Taiwan

• Taiwan
• Higher Education
• 700 & Above Employee

• Research Assistant (“Reserve Duty System for Technology and Science”)

  • Oct 2001 - Apr 2006

  Mentor: Dr. Sheau-Yann Shieh, Ph.D. p53- and checkpoint proteins-mediated DNA damage responses • Discovered that BTG3 is a p53 target gene upon DNA damage, and demonstrated that BTG3 is a novel E2F1 inhibitor that regulates the expression of E2F1 targets through a mechanism distinct from that used by RB. • Uncovered a novel mechanism by which CHK1 and CHK2 control the p53 activity through their compound effects on phosphorylation as well as acetylation. • Contributed… Show more Mentor: Dr. Sheau-Yann Shieh, Ph.D. p53- and checkpoint proteins-mediated DNA damage responses • Discovered that BTG3 is a p53 target gene upon DNA damage, and demonstrated that BTG3 is a novel E2F1 inhibitor that regulates the expression of E2F1 targets through a mechanism distinct from that used by RB. • Uncovered a novel mechanism by which CHK1 and CHK2 control the p53 activity through their compound effects on phosphorylation as well as acetylation. • Contributed significantly to the findings that in response to DNA damage TTK/Mps1 directly activates CHK2 by phosphorylation of the Thr68 site to participate in DNA damage checkpoints. (Mandatory military service under the program of “Reserve Duty System for Technology and Science”) Show less Mentor: Dr. Sheau-Yann Shieh, Ph.D. p53- and checkpoint proteins-mediated DNA damage responses • Discovered that BTG3 is a p53 target gene upon DNA damage, and demonstrated that BTG3 is a novel E2F1 inhibitor that regulates the expression of E2F1 targets through a mechanism distinct from that used by RB. • Uncovered a novel mechanism by which CHK1 and CHK2 control the p53 activity through their compound effects on phosphorylation as well as acetylation. • Contributed… Show more Mentor: Dr. Sheau-Yann Shieh, Ph.D. p53- and checkpoint proteins-mediated DNA damage responses • Discovered that BTG3 is a p53 target gene upon DNA damage, and demonstrated that BTG3 is a novel E2F1 inhibitor that regulates the expression of E2F1 targets through a mechanism distinct from that used by RB. • Uncovered a novel mechanism by which CHK1 and CHK2 control the p53 activity through their compound effects on phosphorylation as well as acetylation. • Contributed significantly to the findings that in response to DNA damage TTK/Mps1 directly activates CHK2 by phosphorylation of the Thr68 site to participate in DNA damage checkpoints. (Mandatory military service under the program of “Reserve Duty System for Technology and Science”) Show less