The KAT6A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from human HeLa cells, with targeted disruption of the KAT6A gene. This heterogeneous knockout model avoids clonal selection biases and enables the investigation of KAT6A-dependent biological processes by averaging phenotypes across diverse editing events. The cells provide a robust loss-of-function system for studying gene function in a cancer cell context.
The host cell line, HeLa, is a widely utilized human epithelial line originating from cervical adenocarcinoma. These cells are immortalized through HPV-18 transformation, which results in the degradation of the tumor suppressor p53 by the viral E6 protein. Extensively employed in cancer research, HeLa cells offer a well-characterized platform for genetic manipulation and phenotypic analysis. Their transformed background is particularly appropriate for examining KAT6A??s contributions to oncogenic processes.
KAT6A is a histone acetyltransferase and transcriptional coactivator that acetylates histones H3 at lysines 9, 14, and 23, and H4 at lysine 16, promoting open chromatin and transcriptional activation. It assembles into multimeric complexes with BRPF1, BRPF2, ING5, and EAF6, and is recruited to target genes by transcription factors such as RUNX1, MYB, MLL (KMT2A), NOTCH1, and ??-catenin. KAT6A regulates key genes including the HOXA cluster, CDKN1A, TP53, MYC, and CCND1, thereby influencing cell cycle progression, apoptosis, and differentiation. Its association with PML nuclear bodies further links it to subnuclear organization and transformation pathways.
In the HeLa cellular context, knockout of KAT6A is predicted to disrupt histone acetylation dynamics, leading to altered expression of downstream targets such as HOXA9 and MEIS1. This dysregulation may impair cell cycle checkpoints, enhance apoptosis, or shift differentiation-associated gene expression programs. Given KAT6A’s involvement in hematopoietic stem cell maintenance and its implication in acute myeloid leukemia and Ohdo syndrome, this HeLa-based knockout model provides a versatile system to explore the epigenetic mechanisms underlying cancer and developmental disorders.
Researchers can employ this polyclonal knockout population for chromatin immunoprecipitation (ChIP) with qPCR to monitor H3K9ac and H3K14ac levels at HOXA promoters, quantitative RT-PCR to measure expression changes of KAT6A target genes, and Western blotting to assess global histone acetylation status. Functional assays including proliferation, apoptosis, and cell cycle analysis can characterize the phenotypic consequences of KAT6A loss, while RNA-sequencing enables transcriptome-wide profiling. These cells are well-suited for epigenetic regulation studies, cancer signaling research, and drug target validation. For technical inquiries or purchasing details, please contact Ascent Research.
