CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation

Stem Cell Research

Tim H. Brümmendorf¹  Steffen Koschmieder²  Salim Atakhanov³  Herdit M. Schüler³  Nicolas Chatain³  Martin Zenke⁴  Marcelo A.S. Toledo⁴  Janik Boehnke⁴  Stephanie Sontag⁴  Rafael Kramann⁵ 

[1] Center for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD), Aachen, Germany;Department of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, RWTH Aachen University Hospital, Aachen, Germany;Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany;Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany;Institute for Human Genetics, RWTH Aachen University Hospital, Aachen, Germany;

关键词: Induced pluripotent stem cell;    iPS cells;    Hematopoiesis;    CXCL4;    PF4;    JAK2 V617F;   

DOI  :  

来源: DOAJ

【 摘 要 】

The chemokine CXCL4/platelet factor 4 (PF4) gene, a key player in myelofibrosis, was knocked out by CRISPR/Cas9 in induced pluripotent stem cells (iPS cells) of a polycythemia vera (PV) patient with JAK2 V617F mutation. Two CXCL4KO iPS cell lines with and without JAK2 V617F mutation (UKAi002-B-1 and UKAi002-A-1, respectively) were generated. CXCL4KO iPS cells showed deletion of exon 1 and complete loss of CXCL4 protein. Pluripotency of iPS cells was confirmed by expression of pluripotency markers and trilineage differentiation. CXCL4KO iPS cells are expected to provide a valuable tool for investigating the role of CXCL4 in human diseases.

【 授权许可】

Unknown