ICA1L Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ICA1L gene in the HeLa human cervical adenocarcinoma epithelial cell line. This product provides a heterogeneous pool of ICA1L-disrupted cells generated through CRISPR/Cas9-mediated gene disruption, enabling loss-of-function studies without clonal selection. The polyclonal format ensures a diverse range of editing events across the target locus, facilitating robust comparisons between knockout and wild-type backgrounds in a widely used cancer cell model.
HeLa cells, derived from a patient with cervical adenocarcinoma, are an immortalized epithelial line characterized by aneuploidy and rapid proliferation. Extensively employed in cancer biology and cell biology research, HeLa cells offer a well-characterized model with high transfection efficiency and stable growth, making them suitable for gene editing and functional assays. Their robust proliferative capacity and epithelial nature provide a consistent platform for investigating intracellular trafficking, cytoskeletal dynamics, and oncogenic signaling.
ICA1L (islet cell autoantigen 1-like) encodes a GTPase-activating protein (GAP) that specifically accelerates GTP hydrolysis on ARF1 and ARF6 small GTPases, thereby inactivating them and negatively regulating membrane trafficking, endocytosis, and actin polymerization. Through direct interaction with ALS2/alsin and ELMO family proteins (including ELMO1 and ELMO2), ICA1L participates in membrane remodeling events essential for intracellular transport and signal transduction. The protein functions downstream of ARF-GEF activation cues and modulates coatomer complex assembly, clathrin-dependent endocytosis, and the actin cytoskeleton machinery. Key molecular components of its network include ARF1, ARF6, ALS2, ELMO, DOCK180, Rac1, and coatomer subunits, linking ICA1L to the ARF GTPase cycle, ALS2-related signaling pathways, and insulin secretion mechanisms.
In HeLa cells, a premier model for studying trafficking and cytoskeletal processes, disruption of ICA1L alters the balance of ARF GTPase activity, providing a powerful tool to dissect ARF-dependent membrane dynamics, endosomal sorting, and actin reorganization. Given the epithelial origin and cancerous phenotype of HeLa cells, this knockout model is particularly relevant for probing ICA1L??s role in cancer cell migration, invasion, and aberrant endocytic trafficking associated with tumor progression. Moreover, because ICA1L interacts with ALS2??a protein linked to amyotrophic lateral sclerosis??the knockout cells offer a tractable system to investigate motor neuron disease-relevant molecular interactions. The polyclonal nature of the population captures a spectrum of gene-disruption severities, supporting graded phenotypic analyses and functional screening.
Typical research applications include ARF GTPase activation assays to measure GAP activity, transferrin uptake endocytosis assays to quantify clathrin-dependent internalization, co-immunoprecipitation for mapping interaction networks with ALS2 and ELMO proteins, immunofluorescence microscopy to visualize actin cytoskeleton reorganization and endosomal marker distribution, and wound-healing migration assays to assess cell motility. The ICA1L Knockout HeLa Polyclonal Cells also enable high-throughput screening for modulators of ARF signaling and insulin secretion. For detailed protocols, validation data, and technical support, please contact Ascent Research.
