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Lei S. Qi

Researcher at Stanford University

Publications -  134
Citations -  24298

Lei S. Qi is an academic researcher from Stanford University. The author has contributed to research in topics: CRISPR & Cas9. The author has an hindex of 47, co-authored 106 publications receiving 19252 citations. Previous affiliations of Lei S. Qi include Lawrence Berkeley National Laboratory & University of California.

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Repurposing CRISPR as an RNA-guided platform for sequence-specific control of gene expression.

TL;DR: This RNA-guided DNA recognition platform provides a simple approach for selectively perturbing gene expression on a genome-wide scale and can efficiently repress expression of targeted genes in Escherichia coli, with no detectable off-target effects.
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CRISPR-Mediated Modular RNA-Guided Regulation of Transcription in Eukaryotes

TL;DR: The results establish that the CRISPR system can be used as a modular and flexible DNA-binding platform for the recruitment of proteins to a target DNA sequence, revealing the potential of CRISpri as a general tool for the precise regulation of gene expression in eukaryotic cells.
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Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation

TL;DR: This work identifies rules for specific targeting of transcriptional repressors (CRISPRi), typically achieving 90%-99% knockdown with minimal off-target effects, and activators to endogenous genes via endonuclease-deficient Cas9, which enable modulation of gene expression over a ∼1,000-fold range.
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Dynamic Imaging of Genomic Loci in Living Human Cells by an Optimized CRISPR/Cas System

TL;DR: Using an EGFP-tagged endonuclease-deficient Cas9 protein and a structurally optimized small guide (sg) RNA, robust imaging of repetitive elements in telomeres and coding genes in living cells is demonstrated by repurposing the bacterial CRISPR/Cas system.

Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation

TL;DR: In this article, the authors identify rules for specific targeting of transcriptional repressors (CRISPRi), typically achieving 90%-99% knockdown with minimal off-target effects, and activators (CRisPRa) to endogenous genes via endonuclease-deficient Cas9.