Gene Knock-in

Knock-in is introduction of specific mutations or exogenous genes, such as point mutations (mimicking human genetic disease models) at the location of the target gene or reporter genes (e.g., EGFP, RFP, mCherry, YFP, LacZ, Luciferase etc.) or functional cDNAs (such as Cre, Dre etc.) into a specific site of the target gene through homologous recombination, thereby allowing the reporter gene or other cDNA to be consistently expressed with the target gene. The replacement of a murine endogenous gene by a reporter gene or cDNA indicates the simultaneous occurrence of knockout and knock-in. A humanized mice model can be customized by replacing the murine endogenous gene with a human gene or by inserting a human cDNA at the ATG site of the murine endogenous gene.

Generating knock-in mouse models can simulate the human genetic mechanism, explore the pathogenic mechanism, and simplify the process of drug development.

  • Simulate human genetic mechanism, and explore pathogenic mechanism

  • Gene expression tracking

  • Genetic lineage tracing defines cell origin 

  • Create humanized mouse model to accelerate drug research and development

  • Introduce the tools of molecular genetics into mouse models

Knock-in models include:

It usually takes 6-9 months to generate a conditional gene knock-in mouse model by CRISPR gene editing technology.

It usually takes 9-12 months to generate a conditional gene knock-in mouse model by ES cell targeting technology.

Shanghai Model Organisms Center (SMOC) has more than 900 research-ready GEM models and one of them may contain the strain that you are interested in. Click here to search the SMOC Research-Ready Models Repository.

Alternatively, you may contact our technical consultants to design and customize your gene knock-in mouse model.

Conventional gene knock-in

Co-expression of exogenous genes:


Replacement of murine endogenous genes with exogenous genes (i.e. knock-in and knockout simultaneously):


Point mutation

Introduction of point mutations (human pathogenic point mutation candidates) into the corresponding positions of murine homologous genes.




Conditional point mutation

Tissue-specific point mutations can be achieved by combining point mutations (human pathogenic point mutation candidates) to the Cre-LoxP system and introducing them into the corresponding positions of mouse homologous genes.


 Conditional point mutations can be achieved by inserting  two loxp sites and the exon with mutations.




The mouse endogenous gene was replaced with a human homologous gene to generate a humanized genetically engineered mouse model for disease, immunity, physiological research, and antibody drug screening and drug efficacy evaluation.

Complete replacement:


Direct insertion of human cDNA:


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