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- Inventor Info
|Antigen/Gene or Protein Targets||Androgen Receptor variants|
|Disease Keywords||Prostate Cancer|
Resistance to androgen receptor (AR)-targeted therapies in prostate cancer (PC) is a major clinical problem. A key mechanism of treatment resistance in advanced PC is the generation of alternatively spliced forms of the AR termed AR variants (AR-Vs) that are refractory to targeted agents and drive tumour progression. Our understanding of how AR-Vs function is limited due to difficulties in distinguishing their discriminate activities from full-length AR (FL-AR).
The CWR22Rv1-AR-EK (Androgen Receptor-Exon Knockout) cell line is a prostate cancer cell line which is knockout for FL-AR but retains expression of all endogenous AR-Vs making it a valuable model for the study of receptor splice variants. This new derivative is dependent upon AR-Vs for growth and is refractory to all FL-AR-targeting agents.
|Production Details||CRISPR-derived cell line that has lost expression of full length androgen receptor (FL-AR), but retains all endogenous androgen receptor variants (AR-Vs). Two gRNAs were designed to target distinct loci within exon 5 of the AR gene. To knock-in a stop codon into exon 5 of the AR locus, a 180 bp ssODN template was designed containing a central TAA sequence and flanked by 75 bp 5′ and 3′ termini 100% complementary to the AR gene sequence.|
|Research Area||Cancer, Drug Discovery & Development|
|Recommended Growing Conditions||RPMI 1640 media supplemented with 10% foetal calf serum (FCS) and 5% L-glutamine at 37°C|
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Dr Luke Gaughan