Description

The ERG28 Knockout HeLa Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the ERG28 gene in human HeLa cells. This product provides a genetically disrupted loss-of-function model for the scaffold protein ERG28, which is essential for cholesterol biosynthesis feedback regulation. The CRISPR/Cas9-mediated gene disruption generates a stable knockout cell line that lacks functional ERG28 protein expression, enabling precise interrogation of its role in lipid metabolism and cancer biology.

He parental HeLa cell line is a well-characterized immortalized human cervical adenocarcinoma cell line containing integrated HPV-18 sequences and exhibiting a highly aneuploid karyotype. HeLa cells are widely employed as a model for cancer research, including studies on viral oncogenesis, cellular metabolism, and proliferative signaling. Their robust growth and well-documented cholesterol metabolism make them a suitable host for investigating ERG28-dependent pathways.

ERG28 encodes a scaffold protein that directly interacts with SCAP and INSIG1/2 to regulate the trafficking and proteolytic activation of SREBP-2, a master transcription factor governing cholesterol homeostasis. In response to cellular cholesterol levels, the ERG28?CSCAP?CINSIG complex controls the ER-to-Golgi transport of SREBP-2, thereby modulating the expression of downstream targets such as HMGCR and LDLR. Knockout of ERG28 disrupts this scaffold, impairing SREBP-2 processing and leading to dysregulated cholesterol synthesis and lipid metabolism. The model thus provides a defined system to study the SREBP signaling cascade and its crosstalk with the mevalonate pathway.

In the HeLa background, loss of ERG28 is expected to disturb endogenous cholesterol biosynthetic feedback, potentially altering membrane composition, raft formation, and proliferative capacity. Given the reliance of rapidly dividing cancer cells on lipid synthesis for membrane biogenesis and energy, this knockout tool offers a unique platform to dissect how ERG28-mediated cholesterol regulation impacts cancer cell growth. It also facilitates the exploration of HPV-18-driven oncogenic signaling intersecting with lipid metabolism.

Research applications for this cell line include investigating cholesterol metabolism, delineating SREBP pathway mechanisms, screening compounds for lipid disorders, and studying cancer metabolism. Experimental readouts can involve Western blotting for ERG28 and SREBP cleavage, qRT-PCR for cholesterol synthesis genes, cholesterol quantification, immunofluorescence to monitor SREBP transport, proliferation assays, and lipidomics analyses. For additional details, please contact Ascent Research.