The HDAC3 Knockout HAP1 Polyclonal Cells represent a genetically engineered human cell population in which the HDAC3 gene has been disrupted using CRISPR/Cas9 technology. This product provides a polyclonal knockout model derived from the near-haploid HAP1 cell line, enabling loss-of-function studies of histone deacetylase 3 (HDAC3). The polyclonal nature ensures a heterogeneous collection of HDAC3-edited cells, suitable for pooled functional screenings and robust phenotypic assays without clonal bias. This product is designed for advanced applications in epigenetics, cancer biology, and drug target validation.
The HAP1 cell line is a near-haploid human line derived from a male chronic myelogenous leukemia patient, exhibiting fibroblastoid morphology. Its haploid karyotype (except for a diploid region of chromosome 15) simplifies genetic analyses by eliminating confounding from a second allele. Widely used in functional genomics, haploid genetic screens, and drug sensitivity profiling, HAP1 cells provide a clean genetic background for studying HDAC3 loss-of-function.
HDAC3 is a class I histone deacetylase that deacetylates histones H3 and H4 to promote chromatin compaction and transcriptional repression. It acts predominantly within the N-CoR/SMRT corepressor complexes (NCOR1/NCOR2), along with GPS2, TBL1, and TBLR1. Recruitment occurs via nuclear receptors (RAR, PPAR??, LXR) and transcription factors such as STAT3 and NF-??B. HDAC3 activity is regulated by phosphorylation (PKA, CK2, ERK) and sumoylation. Key downstream targets include p21/CDKN1A, cyclins (e.g., CCND1), MYC, p53, and NF-??B gene sets, linking HDAC3 to cell cycle progression, apoptosis, and inflammation. Additionally, HDAC3 interacts with circadian clock proteins (CLOCK-BMAL1) to modulate circadian rhythm, and participates in metabolic and DNA damage response pathways.
The near-haploid HAP1 cells enable clear HDAC3 loss-of-function phenotypes without a second allele interfering, allowing precise genotype-phenotype correlations. Its CML origin makes it particularly suitable for leukemia studies and HDAC inhibitor sensitivity assays. The polyclonal population supports dose-response studies and identification of downstream pathway dependencies. The system is ideal for functional genomics screens and synthetic lethality analyses in the context of epigenetic regulation.
Typical applications include western blotting for HDAC3 and acetylated substrates, RT-qPCR/RNA-seq for transcriptomic profiling, ChIP-qPCR for histone acetylation, and HDAC activity assays. Cell proliferation, apoptosis, flow cytometry, and metabolic profiling elucidate functional outcomes. Drug sensitivity screening with HDAC inhibitors (e.g., vorinostat, entinostat) is highly relevant, as are circadian rhythm and NF-??B/STAT3 signaling studies. This polyclonal knockout model is a powerful tool for target validation and epigenetic drug development. For further inquiries, please contact Ascent Research.
