ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload
oleh: Karoline B. Rypdal, A. Olav Melleby, Emma L. Robinson, Jia Li, Sheryl Palmero, Deborah E. Seifert, Daniel Martin, Catelyn Clark, Begoña López, Kristine Andreassen, Christen P. Dahl, Ivar Sjaastad, Theis Tønnessen, Mathis K. Stokke, William E. Louch, Arantxa González, Stephane Heymans, Geir Christensen, Suneel S. Apte, Ida G. Lunde
| Format: | Article |
|---|---|
| Diterbitkan: | Nature Portfolio 2022-12-01 |
Deskripsi
The role of ADAMTSL3 in heart pathology and cardiac disease is investigated with Adamtsl3-deficient mice using CRISPR-Cas9 gene editing.