The DNTTIP1 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss?of?function studies of DNTTIP1 in a human ovarian cancer background. This product comprises a heterogeneous pool of MES?OV cells harboring targeted gene disruption at the DNTTIP1 locus, generated via CRISPR/Cas9?mediated genome editing. The polyclonal nature allows immediate assessment of gene function without clonal selection, facilitating robust and reproducible functional investigations in an epithelial ovarian cancer context.
The parental line, MES?OV, is a well?characterized human ovarian serous adenocarcinoma cell line that retains key features of high?grade serous ovarian cancer, including epithelial morphology and tumorigenic properties. This line is widely employed as a model system for studying ovarian cancer biology, drug response, and mechanisms of malignant progression. Its use as a host for gene knockout provides a disease?relevant platform for exploring the roles of chromatin regulators and DNA repair factors in ovarian tumorigenesis.
DNTTIP1 is a subunit of the NuA4/TIP60 histone acetyltransferase complex, which acetylates histones H2A and H4 to regulate chromatin structure and gene expression. DNTTIP1 physically interacts with TIP60 (KAT5), EPC1, ING3, and other complex components, and its expression is controlled by DNA damage signals and E2F transcription factors. Functionally, DNTTIP1 promotes DNA double?strand break repair by facilitating ATM kinase activation and p53 acetylation, thereby modulating downstream effectors such as p21 and apoptosis regulators. This positions DNTTIP1 at a critical node linking chromatin remodeling to genome maintenance and cell cycle control.
In ovarian cancer, aberrant histone acetylation and DNA repair are hallmarks that drive genomic instability and drug resistance. Knockout of DNTTIP1 in MES?OV cells allows interrogation of how loss of this chromatin regulator impacts epithelial ovarian cancer cell proliferation, DNA damage signaling, and therapeutic vulnerability. The polyclonal nature avoids clonal bias and better reflects the genetic heterogeneity of tumor populations.
This model supports diverse assays: western blotting for DNTTIP1 and acetylated histones, ChIP?qPCR for histone H4 acetylation at target genes, RNA?seq for transcriptomic profiling, and immunofluorescence for ??H2AX foci to assess DNA damage. Flow cytometry enables cell cycle and apoptosis analysis, while proliferation assays and comet assays further characterize functional outcomes. Applications span chromatin biology, DNA repair research, ovarian cancer functional genomics, and epigenetic drug target validation. For additional details, please contact Ascent Research.
