The EFCAB6 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human near-haploid HAP1 cell line. This product features targeted disruption of the EFCAB6 gene, which encodes a calcium-binding transcriptional corepressor. The polyclonal format provides a heterogeneous pool of edited cells, enabling loss-of-function studies without the need for clonal isolation. It serves as a knockout model for dissecting EFCAB6-dependent signaling and transcriptional regulation in a cancer-relevant cellular background.
HAP1 is a fibroblast-like, near-haploid cell line isolated from a male patient with chronic myeloid leukemia. Its haploid genome simplifies genetic manipulation, reducing gene redundancy and facilitating knockout screening and functional genomics. The line retains key cancer signaling pathways, including those controlling proliferation and apoptosis, making it a robust model for target validation. The leukemic origin provides a contextually relevant platform for studying oncogenic mechanisms and androgen receptor signaling.
EFCAB6 functions as a calcium-dependent transcriptional corepressor that interacts with the androgen receptor (AR) and DJ-1 (PARK7). Through its EF-hand domains, it binds calcium and is recruited to AR target gene promoters, where it represses transcription of androgen-responsive genes and cell proliferation genes. This corepressor activity integrates calcium and androgen signals, with upstream regulators including androgens and calcium/calmodulin. Representative downstream targets include AR?regulated genes and proliferative genes. By forming complexes with AR and DJ-1, EFCAB6 modulates critical nodes in androgen receptor signaling and calcium?mediated transcriptional control.
In the HAP1 leukemic background, EFCAB6 knockout allows dissection of AR corepressor mechanisms in a cancer model. Loss of EFCAB6 relieves repression, potentially activating AR target genes and altering cell proliferation. The near-haploid nature simplifies analysis of genetic interactions, while the DJ-1 linkage connects the model to Parkinson??s disease research. This polyclonal pool is suitable for pooled CRISPR screens and drug sensitivity profiling, facilitating identification of vulnerabilities associated with EFCAB6 loss.
Researchers can apply this knockout model in functional genomics, cancer signaling studies, drug target validation, and CRISPR screening. Key assays include western blotting and RT-qPCR for expression analysis, reporter assays for AR activity, co-immunoprecipitation for protein interactions, and calcium imaging for signaling dynamics. Proliferation, apoptosis, and drug sensitivity assays further enable phenotypic characterization. The EFCAB6 Knockout HAP1 Polyclonal Cells thus offer a versatile tool for probing the repressive role of EFCAB6 in androgen receptor signaling and its relevance to prostate cancer and neurodegenerative conditions. For further information or technical support, please contact Ascent Research.
