The ITPRIP Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HT29 human colorectal adenocarcinoma line. This product features targeted disruption of the ITPRIP gene, encoding a protein that sensitizes IP3 receptors to enhance endoplasmic reticulum calcium release. The polyclonal knockout pool, generated via CRISPR/Cas9-mediated gene disruption, provides a heterogeneous model free from clonal artifacts, suitable for robust study of ITPRIP-dependent signaling in a cancer-relevant epithelial context.
The HT29 parental line is a widely used model of human colon adenocarcinoma, exhibiting epithelial morphology and retaining intestinal cell characteristics. It is routinely applied in colorectal cancer research, calcium signaling studies, and apoptosis investigations. The adherent HT29 cells facilitate gene editing, live-cell imaging, and biochemical assays. The colorectal origin is particularly pertinent given the frequent dysregulation of calcium homeostasis and apoptotic pathways in colon cancer.
ITPRIP positively modulates IP3 receptor activity by directly binding ITPR1, ITPR2, and ITPR3. This interaction sensitizes the receptors to IP3, amplifying calcium release from the ER. Subsequent elevation of intracellular calcium activates calmodulin, the NFAT signaling cascade, and caspases, thereby regulating gene expression and apoptosis. ITPRIP thus serves as a critical amplifier linking IP3 production to calcium-dependent cell fate decisions. Knockout of ITPRIP disrupts this sensitization, attenuating calcium mobilization and permitting dissection of its specific contributions.
Within HT29 colorectal adenocarcinoma cells, ITPRIP loss may unveil how altered ER calcium release impacts cancer cell survival. Colorectal tumors often exhibit aberrant apoptosis and calcium flux, and ITPRIP??s role in tuning IP3 receptor sensitivity positions it as a potential determinant of these processes. The knockout model enables investigation of impaired agonist-induced calcium spikes and reduced apoptotic responsiveness, providing a physiologically relevant system to study tumor-associated calcium signaling defects.
Key experimental applications include calcium imaging with fluorescent dyes, western blotting for protein expression analysis, Annexin V apoptosis assays, and flow cytometric assessment of calcium flux or caspase cleavage. These techniques allow rigorous interrogation of ITPRIP??s role in calcium dynamics and cell death. The ITPRIP Knockout HT29 Polyclonal Cells therefore offer a valuable resource for colorectal cancer and calcium signaling research. For inquiries, please contact Ascent Research.
