The ABCB10 Knouckout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the ABCB10 gene. Generated via CRISPR/Cas9-mediated gene disruption, this product provides a heterogeneous pool of HT29 cells with targeted elimination of functional ABCB10 protein expression. The polyclonal format avoids single-cell cloning artifacts, preserving genetic diversity and enabling robust population-level analyses of mitochondrial transporter function. This knockout model is an essential tool for researchers investigating heme biosynthesis, oxidative stress signaling, and mitochondrial biology in a human epithelial cancer context.
The host cell line HT29 is a well-characterized epithelial model derived from a primary colorectal adenocarcinoma of a 44-year-old female. Retaining key features of intestinal epithelial biology, HT29 cells are extensively employed in studies of intestinal absorption, barrier function, and colorectal cancer pathogenesis. This adherent cell line responds to diverse culture conditions that induce differentiation, making it particularly suitable for examining metabolic and stress pathways. Its tumorigenic background provides a relevant setting for exploring how mitochondrial dysfunctions, such as impaired heme trafficking, influence cancer cell phenotypes and therapeutic responses.
ABCB10 encodes a mitochondrial inner membrane ATP-binding cassette transporter essential for heme biosynthesis and antioxidant defense. The protein is transcriptionally regulated by GATA1 and NFE2L2 (NRF2) and is induced by hemin and oxidative stress. ABCB10 interacts with ferrochelatase (FECH), mitoferrin-1 (SLC25A37), and the related transporter ABCB7 to mediate the import of heme synthesis intermediates. Downstream, it promotes heme and hemoglobin production, supports mitochondrial respiration, and contributes to reactive oxygen species (ROS) detoxification. The broader pathway includes ALAS2, FECH, SLC25A37, ABCB7, and HMOX1, integrating iron metabolism and redox homeostasis.
Disruption of ABCB10 in HT29 cells establishes a powerful model for studying mitochondrial iron handling and heme biology in colorectal adenocarcinoma. Loss of ABCB10 function impairs heme synthesis, elevates oxidative stress, and compromises mitochondrial integrity??processes that are particularly relevant in cancer, where altered metabolism and redox balance drive proliferation and drug resistance. This model facilitates investigation of how heme deficiency affects tumor cell survival and the adaptive responses to oxidative damage, shedding light on potential vulnerabilities in heme-dependent cancers. The combination of a cancer epithelial host and a critical mitochondrial gene knockout makes this system highly relevant for translational research.
This polyclonal knockout product supports a wide range of experimental applications, including heme quantification via biochemical assays, ROS measurement with fluorescent indicators, cell viability tests under oxidative stress conditions, and mitochondrial membrane potential analysis. Further approaches encompass western blotting for heme biosynthesis enzymes such as ALAS2 and HMOX1, RT-qPCR profiling of pathway genes, and flow cytometry for mitochondrial mass using MitoTracker dyes. These assays enable detailed dissection of ABCB10’s role in mitochondrial transport, heme regulation, and oxidative stress, with implications for cancer biology and drug resistance. For more information or to inquire about this product, please contact Ascent Research.
