Homology-independent multiallelic disruption via CRISPR/Cas9-based knock-in yields distinct functional outcomes in human cells.
Chenzi ZhangXiangjun HeYvonne K KwokFeng WangJunyi XueHui ZhaoKin Wah SuenChi Chiu WangJianwei RenGeorge G ChenPaul B S LaiJiangchao LiYin XiaAndrew M ChanWai-Yee ChanBo FengPublished in: BMC biology (2018)
Multiallelic gene disruption could be readily introduced through CRISPR/Cas9-induced homology-independent knock-in of dual fluorescence reporters followed by direct tracing and cell isolation. Robust cellular mechanisms exist to spare essential genes from loss-of-function modifications, by generating partially functional transcripts through diverse DNA and RNA processing mechanisms.
Keyphrases
- crispr cas
- genome editing
- genome wide
- single molecule
- genome wide identification
- single cell
- circulating tumor
- high glucose
- diabetic rats
- cell therapy
- nucleic acid
- copy number
- drug induced
- genome wide analysis
- stem cells
- dna methylation
- oxidative stress
- energy transfer
- transcription factor
- bioinformatics analysis
- quantum dots
- circulating tumor cells