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

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...

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Main Authors: Janik Boehnke, Salim Atakhanov, Marcelo A.S. Toledo, Herdit M. Schüler, Stephanie Sontag, Nicolas Chatain, Steffen Koschmieder, Tim H. Brümmendorf, Rafael Kramann, Martin Zenke
Format: Article
Language:English
Published: Elsevier 2021-08-01
Series:Stem Cell Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S1873506121003378
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author Janik Boehnke
Salim Atakhanov
Marcelo A.S. Toledo
Herdit M. Schüler
Stephanie Sontag
Nicolas Chatain
Steffen Koschmieder
Tim H. Brümmendorf
Rafael Kramann
Martin Zenke
author_facet Janik Boehnke
Salim Atakhanov
Marcelo A.S. Toledo
Herdit M. Schüler
Stephanie Sontag
Nicolas Chatain
Steffen Koschmieder
Tim H. Brümmendorf
Rafael Kramann
Martin Zenke
author_sort Janik Boehnke
collection DOAJ
description 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.
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spelling doaj.art-d5201e98c76548fb80312315e5bbd47d2022-12-21T23:31:13ZengElsevierStem Cell Research1873-50612021-08-0155102490CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutationJanik Boehnke0Salim Atakhanov1Marcelo A.S. Toledo2Herdit M. Schüler3Stephanie Sontag4Nicolas Chatain5Steffen Koschmieder6Tim H. Brümmendorf7Rafael Kramann8Martin Zenke9Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, GermanyInstitute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, GermanyInstitute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany; Department of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, RWTH Aachen University Hospital, Aachen, Germany; Center for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD), Aachen, GermanyInstitute for Human Genetics, RWTH Aachen University Hospital, Aachen, GermanyInstitute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, GermanyDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, RWTH Aachen University Hospital, Aachen, Germany; Center for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD), Aachen, GermanyDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, RWTH Aachen University Hospital, Aachen, Germany; Center for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD), Aachen, GermanyDepartment of Hematology, Oncology, Hemostaseology and Stem Cell Transplantation, RWTH Aachen University Hospital, Aachen, Germany; Center for Integrated Oncology Aachen Bonn Cologne Düsseldorf (CIO ABCD), Aachen, GermanyInstitute of Experimental Medicine and Systems Biology, RWTH Aachen University Medical School, Aachen, GermanyInstitute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Medical School, Aachen, Germany; Helmholtz Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany; Corresponding author at: Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Hospital, Pauwelsstrasse 30, Aachen 52074, Germany.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.http://www.sciencedirect.com/science/article/pii/S1873506121003378Induced pluripotent stem celliPS cellsHematopoiesisCXCL4PF4JAK2 V617F
spellingShingle Janik Boehnke
Salim Atakhanov
Marcelo A.S. Toledo
Herdit M. Schüler
Stephanie Sontag
Nicolas Chatain
Steffen Koschmieder
Tim H. Brümmendorf
Rafael Kramann
Martin Zenke
CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
Stem Cell Research
Induced pluripotent stem cell
iPS cells
Hematopoiesis
CXCL4
PF4
JAK2 V617F
title CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
title_full CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
title_fullStr CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
title_full_unstemmed CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
title_short CRISPR/Cas9 mediated CXCL4 knockout in human iPS cells of polycythemia vera patient with JAK2 V617F mutation
title_sort crispr cas9 mediated cxcl4 knockout in human ips cells of polycythemia vera patient with jak2 v617f mutation
topic Induced pluripotent stem cell
iPS cells
Hematopoiesis
CXCL4
PF4
JAK2 V617F
url http://www.sciencedirect.com/science/article/pii/S1873506121003378
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