The CC2D1A Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CC2D1A gene in the HAP1 human cell line. This product provides a heterogeneous pool of knockout cells, offering an efficient loss-of-function model for studying CC2D1A biology. The polyclonal format ensures broad representation of editing events while maintaining the host cell??s near-haploid genomic background, enabling efficient gene targeting and genetic screening applications. Researchers can utilize these cells to investigate CC2D1A-dependent transcriptional regulation and its implications in neurodevelopmental and psychiatric disorders.
The HAP1 cell line is a near-haploid human cell line derived from a male patient with BCR-ABL-positive chronic myelogenous leukemia (CML). Its haploid karyotype simplifies knockout generation and genetic manipulation, making it a preferred model for functional genomics and drug discovery studies in cancer biology and beyond. While originating from a leukemic background, HAP1 cells retain core signaling pathways and have been used extensively to study chromatin remodeling, transcriptional control, and signal transduction. The CC2D1A knockout in this context facilitates exploration of gene function in a tractable experimental system.
CC2D1A encodes a calcium-responsive transcriptional repressor that recruits the NuRD complex (containing CHD4, HDAC1, HDAC2, MTA1, MTA2) to target gene promoters such as DRD2, repressing dopamine signaling and neuronal gene expression programs critical for cognition. Upstream regulators include calcium, NICD, and PKA, integrating GPCR and cAMP signals; CC2D1A also interfaces with NF-??B signaling. Disruption of CC2D1A abrogates NuRD-mediated silencing, enabling study of chromatin remodeling in neuronal and immune-related gene networks.
Deploying the CC2D1A knockout in HAP1 polyclonal cells harnesses the haploid genome for uniform gene disruption, reducing wild-type background and strengthening phenotypic readouts. Although HAP1 is a leukemia line, it endogenously expresses chromatin regulators and signaling components, making it suitable for probing conserved transcriptional repression mechanisms. This model reveals CC2D1A-dependent impacts on NuRD activity, histone deacetylation, and downstream transcription, yielding insights transferable to neuronal contexts via differentiation or heterologous expression.
These polyclonal knockout cells support functional genomics of chromatin remodeling, neurological disease modeling (e.g., autosomal recessive intellectual disability type 3, schizophrenia, autism spectrum disorder), and dopamine receptor regulation studies. Typical assays include RT-qPCR, Western blotting, ChIP-qPCR for NuRD-DRD2 promoter occupancy, co-immunoprecipitation of CC2D1A-NuRD complexes, luciferase reporters, immunofluorescence, and calcium imaging to probe calcium-dependent gene repression. The cells also enable screening for modulators of CC2D1A with neuropsychiatric therapeutic potential. For further information, please contact Ascent Research.
