The JMJD7 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited cell population featuring targeted disruption of the JMJD7 gene within the HT29 human colorectal adenocarcinoma cell line. This polyclonal knockout model provides a genetically stable host for studying JMJD7-dependent cellular processes without introducing clonal artifacts inherent to single-cell-derived lines. The use of CRISPR/Cas9 ensures efficient gene disruption while maintaining the parental line??s background characteristics, enabling robust comparative analyses between wild-type and JMJD7-deficient states.
HT29 cells originate from a human female colorectal adenocarcinoma and serve as a widely utilized epithelial model for intestinal biology and colorectal cancer research. These adherent cells retain key features of transformed intestinal epithelium, including the capacity for polarization and mucin production, making them suitable for investigations of colorectal tumorigenesis and mucosal barrier function. The JMJD7 knockout in this background offers a relevant context for evaluating the gene??s contribution to malignancy-associated phenotypes.
JMJD7 encodes a protein hydroxylase that specifically modifies ribosomal protein L8 (RPL8) through hydroxylation of lysine and arginine residues, a post-translational modification implicated in regulating ribosome structure and translational fidelity. Functioning downstream of the mTORC1 signaling hub, JMJD7 links nutrient-sensing cascades to the protein synthesis machinery. Its activity influences ribosomal biogenesis and translational output, with downstream targets including hydroxylated RPL8 and peptide chain release factors. Within the mTOR pathway, JMJD7 interacts with components such as eIF4E and S6K1, placing it at the intersection of growth signaling and translational control.
In the colorectal cancer setting, dysregulated protein synthesis is a hallmark of aberrant cell growth, and JMJD7 may play a role in fine-tuning translation under oncogenic stress. The HT29 knockout model allows dissection of JMJD7??s impact on ribosome assembly, translational capacity, and tumorigenic properties in a cell line derived from a colorectal adenocarcinoma. This context is particularly valuable for examining how nutrient availability and oncogenic signals converge on ribosomal modification to drive malignancy.
Researchers can employ these polyclonal knockout cells to explore JMJD7??s role in translation regulation, ribosome biology, and cancer pathogenesis. Representative experimental approaches include Western blotting to detect hydroxylated RPL8 as a readout of JMJD7 activity, ribosome profiling to map translational changes, SUnSET assays to measure global protein synthesis, and mass spectrometry for identifying novel substrates. Functional assays such as cell proliferation and colony formation provide insights into the gene??s contribution to tumor cell growth. This model also supports drug target discovery efforts aimed at modulating protein hydroxylation pathways. For additional information or customized inquiries, please contact Ascent Research.
