A C57BL/6J Fancg-KO Mouse Model Generated by CRISPR/Cas9 Partially Captures the Human Phenotype

Fanconi anemia (FA) develops due to a mutation in one of the FANC genes that are involved in the repair of interstrand crosslinks (ICLs). FANCG, a member of the FA core complex, is essential for ICL repair. Previous FANCG-deficient mouse models were generated with drug-based selection cassettes in m...

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Veröffentlicht in:	International journal of molecular sciences Jg. 24; H. 13; S. 11129
Hauptverfasser:	Shah, Ronak, van den Berk, Paul C. M., Pritchard, Colin E. J., Song, Ji-Ying, Kreft, Maaike, Pilzecker, Bas, Jacobs, Heinz
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Switzerland MDPI AG 01.07.2023 MDPI
Schlagworte:	Ablation Analysis Anemia Animals Bone marrow Cisplatin - metabolism CRISPR CRISPR-Cas Systems Crosslinked polymers DNA-Binding Proteins - metabolism Fanconi Anemia - genetics Fanconi Anemia - metabolism Fanconi Anemia Complementation Group G Protein - genetics Fanconi's anemia Fibroblasts Fibroblasts - metabolism Genetic aspects Genotype & phenotype Humans Immunotherapy Infertility Life expectancy Metabolism Mice Mice, Inbred C57BL Mitomycin Phenotype Proteins Stem cells Thymus gland Netherlands Germany fanconi anemia (FA) cisplatin (CsPt) hematopoiesis Mitomycin C (MMC) CRISPR/Cas9 DNA damage response interstrand crosslink (ICL) genetically engineered mouse model (GEMM) FANCG
ISSN:	1422-0067, 1661-6596, 1422-0067
Online-Zugang:	Volltext
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