RMA.Trh4 Kb KO cells

This cell line overexpresses the ER-resident ceramide synthase Trh4 (transduced by CRISPR) and lacks the H2-Kb gene.

Contributors

Inventor Institute
Thorbald Van Hall Leiden University and Leiden University Medical Center; Stichting Oncode Institute
Cat. #: 157678
Tool sub type: Primary
Unit size: 1×10^6 cells / vial
Cancer types: Blood cancer
Research Fields: Cancer
Organism: Mouse
Tissue: Lymphatic Tissue
Model: Knock-Out
Cancer Types In Detail: Mouse Leukemia
Product description: This cell line overexpresses the ER-resident ceramide synthase Trh4 (transduced by CRISPR) and lacks the H2-Kb gene. It serves as a control in helping to understanding T-cell recognition of the Trh4-derived peptide presented by the MHC class I molecule H2-Db. This peptide-epitope is a prototypic example of a neo-antigen selectively presented by cells with processing defects in the classical MHC class I (MHC-I) pathway. RMA cells have an intact processing pathway and a functional TAP peptide transporter, but overexpress the Trh4 protein and therefore can present the Trh4 peptide. Clear T cell recognition can be observed since the irrelevant MHC class I H2-Kb was knocked out.This population acts as a clear control. CRISPR edited RMA cells.
Production details: Retroviral transduction of the mouse Trh4 gene in an IRES-GFP construct and CRISPR/Cas9 technology
Additional notes: CRISPR edited RMA cells. Cancer Research Technology Limited (trading research tools as Ximbio) has been granted a non-exclusive license to the CRISPR-Cas9 technology by ERS Genomics Ltd under the patent rights listed here. This license from ERS Genomics Ltd allows Ximbio to develop and commercialise CRISPR-Cas9 modified cell lines for research use only. Ximbio can provide…
Cellosaurus ID: CVCL_J385
Parental cell line: RMA
disease: Cancer
Format: Frozen
Storage conditions: Liquid Nitrogen
Shipping conditions: Dry ice
Growth medium: Suspension cells in DMEM+8% FCS
Recommended controls: RMA.Trh4 Db KO cells
Mycoplasma free: Yes
Biosafety level: 1
References:

Doorduijn et al. 2018. Oncoimmunology. 7(3):e1382793. PMID: 29399388.

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