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Gu, Bin

Cell & Molecular Biology Program and the Department of Obstetrics, Gynecology, & Reproductive Biology

Address:
3319 Bioengineering Building 
775 Woodlot Dr.  
East Lansing,  MI  48824

Office: 517-353-2544
Lab:  517-353-2543
 gubin1@msu.edu

Research in Bin Gu’s Lab:

With the tremendous advancement of genome editing technology, humans first time face the possibilities of treating human disease by targeted correcting any disease-causing mutations through precision medicine strategies.  To realize these potentials, we need to dissect the disease-causing mechanisms and testing potential correction strategies of any mutation of interest in preclinical models such as mouse models. In Gu’s Lab, we take a technology-driven approach to address these challenges in precision medicine.  We develop cutting-edge genome engineering technologies to re-create challenging human genetic defects in mouse models.  We leverage state of the art live imaging, genomics and proteomics technologies to investigate the causing mechanisms of these genetic defects.  We explore new therapeutic strategies of human disease using these mouse models.  We believe the knowledge gained from these researches will one day translate into new treatments for people with genetic diseases. Currently, we focus on two types of genetic defects in human diseases:

Genomic duplication:

Devastating genetic disease including MECP2 Duplication syndrome, Charcot Marie Tooth Diseases, Autism spectrum diseases, Congenital heart diseases, and fertility defects can all be caused or strongly associated with genomic duplications-typically a tandem duplication of a large segment of chromosome (~100 kilo base pairs to mega base pairs size).  Because the duplicated segment typically contains multiple genes and regulatory elements, it is challenging to establish specific causal gene elements by human population study. Further more because of their large size, genomic duplication is challenging to model in mouse models. We have developed a general genome editing technology to engineer genomic duplication mouse models.  We have generated the first true Xq28 MECP2 duplication syndrome mouse model which recapitulate both the neurological and immunological phenotypes of human patients.  We are now focusing on investigating the contribution of the two genes in the minimum duplication segment-IRAK1 and MECP2 to the phenotypes of MECP2 duplication syndrome and their respective mechanisms. In addition, we are developing duplication removal gene therapy using this mouse model for future translation. In the future, we will leverage this technology system to understand and resolve more human genomic duplication diseases.

Chromosome translocation:

Chromosome translocation and the subsequent formation of fusion genes such as BCR-ABL, EWS-FLI, and BRD4-Nut are the driving mutations of many types of human cancers.  A clear understanding of the evolving process during the formation of these cancers can guide the treatment development. However, due to practical reasons, it is challenging to pinpoint the cell/stem cell of origin of these cancers and follow their whole development process.  By developing a combined translocation induction, live imaging, and lineage tracing system, we are working to identify the initiating cells and follow the full developmental process of translocation cancer.  We are investigating the cell-type specific cancer-driving mechanisms of chromosome translocations.  With the knowledge, we plan to develop precision therapies for some devastating translocation cancers in the future.

Recently, due to the emergence of SARS-CoV2 pandemics, we started new projects to create novel humanization models to study human tropic virus diseases such as COVID-19 and Ebola Virus Disease. By collaborating and sharing these mouse models with the international research community, we hope to help the global efforts to defend human beings from emergent infectious diseases.