The ITPR1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ITPR1 gene in a colorectal adenocarcinoma background. This product results from CRISPR/Cas9-mediated gene disruption, generating a heterogeneous pool of cells with abolished ITPR1 expression. The polyclonal format maintains genetic diversity suitable for robust loss-of-function studies; users should validate knockout efficiency experimentally.
The HT29 cell line, derived from a colorectal adenocarcinoma of a 44-year-old female, is a widely used epithelial model for intestinal biology, cancer research, and drug transport studies. These adherent cells form polarized monolayers and express intestinal markers, making them relevant for investigating calcium signaling pathways in colon cancer.
ITPR1 encodes the type 1 inositol 1,4,5-trisphosphate receptor, a tetrameric ligand-gated calcium channel that releases Ca2? from the endoplasmic reticulum upon IP3 binding. Upstream activation occurs through Gq/11-coupled GPCRs or receptor tyrosine kinases stimulating phospholipase C, while channel activity is modulated by interacting partners including FKBP12, calmodulin, and Homer proteins, and by phosphorylation via PKA and PKC. The resulting calcium signal drives downstream effectors such as calmodulin, CaMKII, calcineurin, and NFAT transcription factors, ultimately regulating proliferation, apoptosis, and secretion.
In HT29 colorectal cancer cells, ITPR1 knockout enables dissection of ER calcium homeostasis in tumor biology, where dysregulated signaling promotes survival and proliferation. Loss of ITPR1 allows direct assessment of its impact on cancer cell phenotypes including migration, cell cycle progression, and drug response, and also facilitates study of intestinal epithelial barrier function and drug absorption.
Applications include Fluo-4 AM calcium imaging, Western blotting for ITPR1 and phospho-CaMKII, RT-qPCR, and flow cytometry for calcium flux. Phenotypic assays such as Annexin V apoptosis, MTT proliferation, and wound healing migration can characterize knockout effects. The model supports disease research on spinocerebellar ataxia 15/16 and Gillespie syndrome, drug screening for ER calcium modulators, and investigations of ER stress and the unfolded protein response. For further information, contact Ascent Research.
