EZ-HRex™ New Technique

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In the process of constructing point mutation or knock in cells, the main difficulty is that the HDR repair efficiency required is insufficient. The genotypes of most of the obtained clones during production are the indels caused by NHEJ repair mode. One of the main reasons is the cell cycle dependence of HDR repair: NHEJ can occur at almost any cell cycle stage, while HDR usually occurs only in S phase and G2 phase, that is, the phase of DNA replication. This makes the opportunity window of HDR much smaller than that of NHEJ, limiting its efficiency.

After years of R&D of Ubigene, based on the original CRISPR-U™ gene-editing technique, Ubigene has upgraded it to EZ-HRex™ New Technique, by innovatively adding U⁺ Molecule.

Effectively regular cell cycles, promoting more post-transfection cells into S/G2 phases.

Reduce the NHEJ pathway activity, reducing the proportion of indel genotype to improve the HDR efficiency.

Reduce the NHEJ pathway activity, reducing the proportion of indel genotype to improve the HDR efficiency. After upgrade, the HDR efficiency for gene mutation and fragment KI in cells has been comprehensively improved, and the HDR genotype proportion at the post-transfection cell pool level accounts for up to 84%.

Case For HDR Efficiency - By EZ-HRex™ New Technique

Target Cell Line: HEK293

Target Gene: FOXP1

Target Mutation: TCG>GAT

Using EZ-HRex™, the HEK293 cells with point mutation of FOXP1 gene were constructed. Cell pool was collected after 48h of electroporation, and genomic DNA was extracted, amplified and sequenced. EZ-editor™ Genotype Analysis System was used to analyze the sequencing results, and the results showed that the HDR efficiency of the point mutation cell pool was 84%.

EZ-HRex™ Knock-in & Point Mutation Cell Service

300+ Success Cell Lines

4 Solutions Including RNP

Turnaround Time Fast As 6 wk

Inquire Now

EZ-HRex™ Knock-in & Point Mutation Cell Service

300+ Success Cell Lines

4 Solutions Including RNP

Turnaround Time Fast As 6 wk

Inquire Now

More Success Cases From Publications By Clients

IF=20.8

Lung Cancer - A549 Cells, MYC gene

DOI：https://doi.org/10.1038/s42255-024-01037-4

This study used the MYC p.K148R mutation A549 cells and MYC p.K148Q mutation A549 cells, constructed by Ubigene, to simulate the acetylated and non-acetylated c-Myc state, and study the effects of these changes on the behavior of tumor cells.

IF=5

Human Papilloma Thyroid Carcinoma -
TPC-1 Cells, TERT gene

DOI：https://doi.org/10.1210/clinem/dgae327

This study used the point mutant cells constructed by Ubigene, with C228T mutation converted back to wild-type in TPC-1 cells.

Service Work Flow and QC

Promotion period: 2024.11.07-2025.01.10

Promotion for academics only.

Note: Ubigene reserves the right to the ultimate interpretation.

Note: The selection and classification of popular cell lines in this event are based on relevant public information and project experience, for reference only. Ubigene reserves the right to the ultimate interpretation.