The DNTTIP1 Knockout Huh-7 Polyclonal Cells are a genetically modified cell population in which the DNTTIP1 gene has been disrupted via CRISPR/Cas9-mediated gene editing. This product is offered as a polyclonal knockout pool, ensuring a diverse representation of loss-of-function alleles without clonal selection. The mixed genetic background provides a robust in vitro model for studying DNTTIP1-dependent processes while avoiding clone-specific artifacts. This knockout tool is particularly suited for loss-of-function studies in liver cancer research, enabling the dissection of DNTTIP1-mediated pathways in a hepatocellular carcinoma context.
Huh-7 is a well-differentiated human hepatocellular carcinoma cell line established from a male Japanese patient in 1982. Widely employed in liver cancer and hepatitis C virus replication studies, Huh-7 cells retain epithelial characteristics and key oncogenic signaling networks relevant to hepatocarcinogenesis. Their well-characterized biology and genetic tractability make them an excellent host for CRISPR/Cas9-edited knockout models, facilitating detailed investigation of gene function in a liver cancer background.
DNTTIP1 encodes a nucleolar protein that binds terminal deoxynucleotidyltransferase (TdT) and enhances its activity during V(D)J recombination. In non-lymphoid cells, DNTTIP1 localizes to the nucleolus, where it interacts with nucleolar proteins such as nucleolin and fibrillarin to participate in ribosomal RNA (rRNA) transcription and processing. Transcriptionally regulated by MYC and responsive to nucleolar stress signals, DNTTIP1 sits at the nexus of ribosome biogenesis and the DNA damage response. Downstream, DNTTIP1 influences the maturation of pre-ribosomal RNA and the production of ribosomal proteins, thereby modulating translational capacity and cell growth.
In the Huh-7 hepatocellular carcinoma context, DNTTIP1 disruption is particularly relevant for exploring the dysregulation of ribosome biogenesis that frequently underlies uncontrolled proliferation in liver cancer. As MYC is a central oncogenic driver in HCC, this knockout model enables investigation of how DNTTIP1 mediates MYC-driven translational control and nucleolar stress responses. The resulting loss-of-function phenotype can reveal vulnerabilities in cancer cell ribosome homeostasis, making DNTTIP1 a candidate for therapeutic target validation in hepatocellular carcinoma.
This DNTTIP1 knockout polyclonal cell population is suitable for a variety of functional assays, including cell viability and colony formation to assess proliferation defects, RNA-sequencing to analyze rRNA processing intermediates, nucleolar marker immunofluorescence to evaluate nucleolar integrity, and Western blotting for ribosomal protein levels. These applications support research into the molecular mechanisms of liver cancer and the preclinical evaluation of DNTTIP1 as a drug target. For further technical inquiries, please contact Ascent Research.
