The CASZ1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in the HAP1 near-haploid human cell line, designed to eliminate functional CASZ1 expression. This product provides a robust loss-of-function model for investigating the biological roles of the CASZ1 zinc finger transcription factor. The polyclonal format ensures a heterogeneous pool of edited cells, capturing a range of knockout genotypes without requiring single-cell cloning, and is generated through a well-established gene disruption workflow that avoids introducing defined mutations. Researchers can confidently use these cells to study gene function in a physiologically relevant context without assuming clonal uniformity.
Derived from the KBM-7 chronic myeloid leukemia (CML) cell line, HAP1 cells possess a near-haploid karyotype (25 chromosomes) in a male genetic background, which simplifies genome editing and genetic analysis. As a myeloid progenitor model with leukemic origin, HAP1 retains key signaling pathways relevant to hematological malignancies and developmental biology. The near-haploid state reduces gene redundancy and facilitates unambiguous genotype?Cphenotype correlations, making it an ideal platform for targeted knockout studies. These characteristics allow for efficient CRISPR/Cas9-mediated gene disruption and enable downstream applications such as transcriptome-wide screening and drug response profiling.
CASZ1 encodes a zinc finger transcription factor that plays a pivotal role in cardiac development and tumor suppression by modulating chromatin remodeling and transcriptional programs. It is regulated by upstream signals including TGF-??, its downstream mediators SMAD2 and SMAD3, and the transcriptional repressor REST/NRSF. CASZ1 directly targets genes such as NKX2-5, TIMP3, CDKN1A, and BAX, while interacting with the NuRD complex through components like HDAC1, HDAC2, and MTA2. Through these interactions, CASZ1 orchestrates cell cycle arrest, apoptosis, and differentiation, and its disruption is implicated in congenital heart defects and neuroblastoma. In this knockout model, ablation of CASZ1 protein abolishes its transcriptional regulatory functions, allowing dissection of these signaling axes.
In the HAP1 myeloid progenitor context, CASZ1 knockout uniquely enables the study of tumor suppression mechanisms within a leukemia-relevant background. The loss of CASZ1 function in this near-haploid cell line permits clear assessment of its impact on cell proliferation, apoptosis, and TGF-??-dependent responses, which are often dysregulated in CML and other cancers. Furthermore, the model can be leveraged to explore CASZ1??s role in RhoA and Wnt/??-catenin signaling pathways that converge on cell cycle control and chromatin remodeling. By combining this knockout with the simplified genetic landscape of HAP1, researchers can directly link molecular perturbations to cellular phenotypes, such as altered drug sensitivity or migration.
Typical research applications include functional genomics, disease modeling for dilated cardiomyopathy and neuroblastoma, and drug target validation. The cells are compatible with an array of representative assays: Western blotting and immunofluorescence for CASZ1 protein detection, RT-qPCR and RNA-seq for transcriptional profiling of downstream targets like NKX2-5 and TIMP3, ChIP-qPCR for CASZ1 binding-site analysis, and functional assays for proliferation, apoptosis, migration, and drug sensitivity. These tools support signal transduction studies and tumor suppressor research. For further information or to place an order, please contact Ascent Research.
