Laboratory of Transgenic Models of Diseases

We uncover the mechanisms of human diseases using genome editing and in-deep phenotyping

+ genome editing, + mouse modes of human diseases, + craniofacial and skeleton development, + proteases, + UB-ligases

Radislav Sedláček

Group leader

radislav.sedlacek@img.cas.cz

www.phenogenomics.cz

Scientific Career – Milestones

since 2021: Chair of the Steering Committee, International Mouse Phenotyping Consortium

since 2012: Director of Research Infrastructure – Czech Centre for Phenogenomics

since 2008: Research Group Leader, IMG, Prague

2006: PD (Privatdozent), Faculty of Medicine, University of Kiel, Germany

1997: PhD (Dr. rer. nat. habil.), University of Konstanz, Germany

Prevention of spike protein binding to the viral receptor using bispecific neutralizing antibodies (CoV-X2)

We have shown that the bispecific neutralizing antibody (CoV-X2) prevents spike protein binding to the viral receptor (angiotensin-converting enzyme 2) in the mouse model of COVID-19 infection, protects the mice from disease and suppresses viral escape. [pubmed] [doi]

Enamel disorganization due to impairment of ameloblastin self-assembly

Using targeted mutations in mice and high-resolution imaging, we have shown that impairment of ameloblastin self-assembly causes enamel disorganization and that this self-assemly is crucial for the formation of properly structured enamel. [pubmed] [doi]

Development of Netherton syndrome caused by unregulated activities of KLK5 and KLK7 proteases

By studying epidermal proteases in Netherton syndrome on the background of new LEKTI-deficient mice, we have shown that unregulated activities of KLK5 and KLK7 proteases are responsible for the development of this disease. [pubmed] [doi]