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Shi Yin Foo

Bio: Shi Yin Foo is an academic researcher from Harvard University. The author has contributed to research in topics: Antibody & Small hairpin RNA. The author has an hindex of 1, co-authored 1 publications receiving 1630 citations.

Papers
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Journal ArticleDOI
24 Mar 2006-Cell
TL;DR: A screen based on high-content imaging was developed to identify genes required for mitotic progression in human cancer cells and applied to an arrayed set of 5,000 unique shRNA-expressing lentiviruses that target 1,028 human genes, providing a widely applicable resource for loss-of-function screens.

1,760 citations

Journal ArticleDOI
TL;DR: In this article , the frequency of anti-DSG2 antibodies in a population of post COVID-19 patients was determined by electrochemiluminescent-based immunoassay utilizing the extracellular domain of DSG2.

10 citations


Cited by
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Journal ArticleDOI
25 May 2012-Cell
TL;DR: This paper identified the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes.

7,192 citations

Journal ArticleDOI
TL;DR: The first free, open-source system designed for flexible, high-throughput cell image analysis, CellProfiler is described, which can address a variety of biological questions quantitatively.
Abstract: Biologists can now prepare and image thousands of samples per day using automation, enabling chemical screens and functional genomics (for example, using RNA interference). Here we describe the first free, open-source system designed for flexible, high-throughput cell image analysis, CellProfiler. CellProfiler can address a variety of biological questions quantitatively, including standard assays (for example, cell count, size, per-cell protein levels) and complex morphological assays (for example, cell/organelle shape or subcellular patterns of DNA or protein staining).

4,578 citations

Journal ArticleDOI
TL;DR: Monocle is described, an unsupervised algorithm that increases the temporal resolution of transcriptome dynamics using single-cell RNA-Seq data collected at multiple time points that revealed switch-like changes in expression of key regulatory factors, sequential waves of gene regulation, and expression of regulators that were not known to act in differentiation.
Abstract: Defining the transcriptional dynamics of a temporal process such as cell differentiation is challenging owing to the high variability in gene expression between individual cells. Time-series gene expression analyses of bulk cells have difficulty distinguishing early and late phases of a transcriptional cascade or identifying rare subpopulations of cells, and single-cell proteomic methods rely on a priori knowledge of key distinguishing markers. Here we describe Monocle, an unsupervised algorithm that increases the temporal resolution of transcriptome dynamics using single-cell RNA-Seq data collected at multiple time points. Applied to the differentiation of primary human myoblasts, Monocle revealed switch-like changes in expression of key regulatory factors, sequential waves of gene regulation, and expression of regulators that were not known to act in differentiation. We validated some of these predicted regulators in a loss-of function screen. Monocle can in principle be used to recover single-cell gene expression kinetics from a wide array of cellular processes, including differentiation, proliferation and oncogenic transformation.

4,119 citations

Journal ArticleDOI
Rameen Beroukhim, Craig H. Mermel1, Craig H. Mermel2, Dale Porter3, Guo Wei1, Soumya Raychaudhuri4, Soumya Raychaudhuri1, Jerry Donovan3, Jordi Barretina2, Jordi Barretina1, Jesse S. Boehm1, Jennifer Dobson1, Jennifer Dobson2, Mitsuyoshi Urashima5, Kevin T. Mc Henry3, Reid M. Pinchback1, Azra H. Ligon4, Yoon Jae Cho6, Leila Haery1, Leila Haery2, Heidi Greulich, Michael R. Reich1, Wendy Winckler1, Michael S. Lawrence1, Barbara A. Weir1, Barbara A. Weir2, Kumiko E. Tanaka2, Kumiko E. Tanaka1, Derek Y. Chiang1, Derek Y. Chiang2, Derek Y. Chiang7, Adam J. Bass2, Adam J. Bass1, Adam J. Bass4, Alice Loo3, Carter Hoffman1, Carter Hoffman2, John R. Prensner1, John R. Prensner2, Ted Liefeld1, Qing Gao1, Derek Yecies2, Sabina Signoretti2, Sabina Signoretti4, Elizabeth A. Maher8, Frederic J. Kaye, Hidefumi Sasaki9, Joel E. Tepper7, Jonathan A. Fletcher4, Josep Tabernero10, José Baselga10, Ming-Sound Tsao11, Francesca Demichelis12, Mark A. Rubin12, Pasi A. Jänne2, Pasi A. Jänne4, Mark J. Daly1, Mark J. Daly2, Carmelo Nucera13, Ross L. Levine14, Benjamin L. Ebert2, Benjamin L. Ebert4, Benjamin L. Ebert1, Stacey Gabriel1, Anil K. Rustgi15, Cristina R. Antonescu14, Marc Ladanyi14, Anthony Letai2, Levi A. Garraway1, Levi A. Garraway2, Massimo Loda4, Massimo Loda2, David G. Beer16, Lawrence D. True17, Aikou Okamoto5, Scott L. Pomeroy6, Samuel Singer14, Todd R. Golub2, Todd R. Golub1, Todd R. Golub18, Eric S. Lander19, Eric S. Lander2, Eric S. Lander1, Gad Getz1, William R. Sellers3, Matthew Meyerson2, Matthew Meyerson1 
18 Feb 2010-Nature
TL;DR: It is demonstrated that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival, and a large majority of SCNAs identified in individual cancer types are present in several cancer types.
Abstract: A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.

3,375 citations