Julie Chen
Novartis
4 Papers
Julie Chen is an academic researcher from Novartis. The author has contributed to research in topics: Induced pluripotent stem cell & CRISPR. The author has an hindex of 2, co-authored 2 publications.
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Papers
p53 inhibits CRISPR–Cas9 engineering in human pluripotent stem cells
Robert J. Ihry,Kathleen A. Worringer,Max R. Salick,Elizabeth Frias,Daniel J. Ho,Kraig M. Theriault,Sravya Kommineni,Julie Chen,Marie Sondey,Chaoyang Ye,Ranjit Randhawa,Tripti Kulkarni,Zinger Yang,Gregory McAllister,Carsten Russ,John S. Reece-Hoyes,William C. Forrester,Gregory R. Hoffman,Ricardo E. Dolmetsch,Ajamete Kaykas +19 more
TL;DR: The results indicate that Cas9 toxicity creates an obstacle to the high-throughput use of CRISPR/Cas9 for genome engineering and screening in hPSCs, and as h PSCs can acquire P53 mutations14, cell replacement therapies using CRISpr/cas9-enginereed hPSCS should proceed with caution, and such engineered hPSPs should be monitored for P53 function.
Genome-wide tiled detection of circulating Mycobacterium tuberculosis cell-free DNA using Cas13
Sri Gowtham Thakku,Kanagavel Murugesan,Julie Chen,Grant Theron,Niaz Banaei,Paul C. Blainey,James T. Gomez,Sharon Y. Wong,Deborah T. Hung +8 more
TL;DR: WATSON as mentioned in this paper is a method to detect low amounts of pathogen cfDNA that couples pooled amplification of genomic targets tiled across the genome with pooled CRISPR/Cas13-based detection of these targets.
P53 toxicity is a hurdle to CRISPR/CAS9 screening and engineering in human pluripotent stem cells
Robert J. Ihry,Kathleen A. Worringer,Max R. Salick,Elizabeth Frias,Daniel J. Ho,Kraig M. Theriault,Sravya Kommineni,Julie Chen,Marie Sondey,Chaoyang Ye,Ranjit Randhawa,Tripti Kulkarni,Zinger Yang,Gregory McAllister,Carsten Russ,John S. Reece-Hoyes,William C. Forrester,Gregory R. Hoffman,Ricardo E. Dolmetsch,Ajamete Kaykas +19 more
TL;DR: It is demonstrated the toxic response is tp53-dependent and the toxic effect of t p53 severely reduces the efficiency of precise genome-engineering in hPSCs, highlighting that CRISPR-based therapies derived from h PSCs should proceed with caution.
Expressed barcoding enables high resolution tracking of the evolution of drug tolerance.
Jennifer L. Cotton,Javier Estrada Diez,Vivek Sagar,Julie Chen,Michelle Piquet,John Alford,Youngchul Song,Xiaoyan Li,Markus Riester,Matthew T DiMare,Katja Schumacher,Gaylor Boulay,Kathleen Sprouffske,Lin Fan,Tyler Burks,Leandra Mansur,Joel Wagner,Hyo-eun C. Bhang,O. Iartchouk,John S. Reece-Hoyes,Erick J. Morris,Peter S. Hammerman,David A. Ruddy,Joshua M. Korn,Jeffrey A. Engelman,Matthew J. Niederst +25 more
TL;DR: Drug tolerant cells had higher expression of key survival pathways such as YAP and EMT at baseline and could also differentially adapt their gene expression following EGFRi treatment compared to sensitive cells, and drug combinations targeting common downstream components (MAPK) or orthogonal factors (chemotherapy) showed greater efficacy.
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