The ZNF587B Knockout A2780 Cell Line is a genetically engineered human cellular model in which the ZNF587B gene has been disrupted using CRISPR/Cas9-mediated gene editing. This product provides a stable, renewable source of ZNF587B-deficient cells derived from the A2780 ovarian carcinoma background, enabling loss-of-function studies without transient knockdown artifacts. The cell line is supplied as a validated knockout population, ready for expansion and experimental use. As a CRISPR/Cas9-edited knockout cell line, it serves as a precise tool for interrogating the specific contributions of ZNF587B to chromatin regulation and transcriptional control.
The parental A2780 cell line originates from a human ovarian endometrioid adenocarcinoma tumor of an untreated patient and has been widely adopted as a model for ovarian cancer research. This adherent epithelial line retains functional wild-type p53, a key guardian of genomic stability that mediates cell cycle arrest and apoptosis in response to DNA damage. Consequently, A2780 cells are particularly valuable for exploring the interplay between transcriptional regulators and p53-dependent processes, which are frequently altered in high-grade serous ovarian carcinomas. The well-documented genetic and phenotypic characteristics of A2780 provide a reliable baseline for genetically engineered derivatives.
ZNF587B is a member of the C2H2 zinc finger protein family, characterized by DNA-binding domains that direct transcriptional regulation. It is anticipated to function through the RNA polymerase II transcriptional apparatus, associating with general transcription factors and the mediator complex to govern downstream gene expression programs. Though its specific genomic targets remain undefined, ZNF587B loss-of-function may impair proper transcriptional initiation or elongation at critical loci, perturbing networks involved in growth control and stress adaptation.
Within the A2780 ovarian tumor context, ZNF587B knockout enables dissection of its role in oncogenic transcription. Ovarian cancers often exhibit abnormal transcriptional regulation; thus, ZNF587B loss may alter gene expression signatures linked to proliferation, apoptosis, or drug response. This line allows systematic measurement of phenotypic changes and assessment of chemosensitivity to agents like cisplatin or PARP inhibitors, particularly in the presence of wild-type p53.
This ZNF587B knockout cell line is optimized for a spectrum of downstream applications central to cancer cell biology and drug discovery. Transcriptomic analyses, such as RNA sequencing and RT-qPCR, can be employed to map ZNF587B-dependent gene networks, while western blotting verifies changes at the protein level. Functional assays for proliferation, apoptosis, and cell migration/invasion provide direct readouts of phenotypic consequences. The model is also suitable for high-throughput drug screening to evaluate how ZNF587B loss modifies sensitivity to chemotherapeutics or targeted agents. For additional information regarding product specifications, genetic validation data, or experimental protocols, please contact Ascent Research.
