Abstract
Inactivation of the tumor suppressor gene RB1 is causal for development of retinoblastoma, a tumor of the neural retina arising in children under the age of five. In addition, secondary RB1 mutations are found in many other tumor types. To investigate retinoblastoma formation in vitro, stem cells with inactivated RB1 can be differentiated into neural retina. To enable such studies, two sublines of hESC line H9 carrying mutations in RB1 exon 3 in heterozygous or homozygous state were generated and characterized. Homozygous mutation led to loss of RB1 protein expression.Resource tableUnlabelled TableUnique stem cell lines identifierWAe009-A-12WAe009-A-13Alternative names of stem cell linesC7 (homozygous deletion, WAe009-A-12)G12LS (heterozygous deletion, WAe009-A-13)InstitutionUniversity Hospital Essen, University Duisburg-Essen, Essen, GermanyContact information of distributorDr. Laura Steenpass, laura.steenpass@uni-due.deDr. Deniz Kanber, deniz.kanber@uni-due.deType of cell linesESCOriginHumanCell SourceHuman ESC line H9 purchased from WiCellClonalityClonalMethod of reprogrammingN/AMultiline rationaleclones selected for deletion in heterozygous and homozygous stateGene modificationYESType of modificationIndels in RB1 exon 3Associated diseaseRetinoblastomaGene/locusRB1, chromosome 13q14.2Method of modificationCRISPR/Cas9 nucleaseName of transgene or resistanceN/AInducible/constitutive systemN/ADate archived/stock dateC7 12.05.2018G12LS 12.05.2018Cell line repository/bankN/AEthical approvalApproval obtained from the Robert-Koch Institute, Berlin, Germany (Az.3.04.02/0101) and from the local Ethical Review Board University Duisburg-Essen (16–7215-BO)
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