The ERGIC1 Knockout HeLa Cell Line is a CRISPR/Cas9-edited cell line designed to disrupt the ERGIC1 gene, providing a loss-of-function model for studying ER-to-Golgi trafficking and glycoprotein secretion. This product offers researchers a defined genetic background in which ERGIC1 expression is abrogated, enabling detailed dissection of its role in intracellular transport pathways.
HeLa cells are an epithelial cell line derived from a human cervical adenocarcinoma, immortalized through HPV18 integration leading to p53 and Rb inactivation. Widely used in cancer research and cell biology, these cells serve as a robust host for gene editing, facilitating the study of secretory pathway dynamics in a transformed cellular context. The HPV18-positive status and associated oncogene expression make HeLa cells particularly relevant for examining viral pathogenesis and tumor cell protein trafficking.
ERGIC1, also known as LMAN1-like protein, functions as a lectin-type cargo receptor that cycles between the endoplasmic reticulum (ER) and the ER-Golgi intermediate compartment (ERGIC). It selectively recognizes mannose residues on glycoproteins, mediating their packaging into COPII vesicles through direct interaction with MCFD2 and the SEC23/SEC24 coat complex. This process is critical for anterograde transport of coagulation factors V and VIII, cathepsin Z, and alpha-1-antitrypsin. ERGIC1 activity is regulated by ER stress signaling, particularly via the ATF6 and XBP1 arms of the unfolded protein response. Following cargo delivery to the ERGIC, ERGIC1 recycles back to the ER via COPI-dependent retrograde transport, thereby maintaining secretory pathway flux. Downstream consequences of ERGIC1 disruption include impaired secretion of numerous glycoproteins and potential accumulation of misfolded cargoes in the ER.
In the HeLa cell context, ERGIC1 knockout provides a powerful tool to dissect the interplay between oncogenic transformation and the secretory machinery. The combined loss of p53 and Rb function, along with HPV-driven proliferative signaling, creates a unique backdrop to study how ER-to-Golgi trafficking influences cancer cell behavior. This model is particularly valuable for investigating viral glycoprotein transport, as many enveloped viruses exploit the host secretory pathway. Moreover, the ERGIC1 knockout in HeLa cells can be used to explore the cellular basis of combined factor V and VIII deficiency, a rare bleeding disorder linked to mutations in ERGIC1 or MCFD2.
Researchers can employ the ERGIC1 Knockout HeLa Cell Line in a variety of functional studies, including glycoprotein secretion assays, immunofluorescence localization of secretory cargoes, and co-immunoprecipitation to probe protein interactions within the early secretory pathway. Representative techniques such as western blotting for coagulation factors, flow cytometric analysis of cell surface glycoproteins, and RT-qPCR for ER stress markers allow quantitative assessment of knockout phenotypes. This cell line also supports studies of autophagy and lysosomal enzyme trafficking. For further information and technical support, please contact Ascent Research.
