This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, in which the HOMER2 gene has been disrupted to generate a loss-of-function model for studying scaffold protein functions in a human epithelial context. The polyclonal nature of the knockout population reflects the heterogeneous editing outcomes typical of CRISPR-mediated gene disruption, providing a robust cellular background for investigating HOMER2-dependent signaling networks without the confounding effects of clonal selection. These cells are intended for use in functional assays where gene knockout is required, facilitating the dissection of HOMER2-mediated pathway dynamics in a widely employed cancer cell line.
The host HeLa cell line is an immortalized human cervical adenocarcinoma epithelial model that has been a cornerstone of biomedical research for decades. HeLa cells exhibit rapid proliferation and are amenable to a broad range of genetic manipulation and biochemical assays, making them a versatile platform for studying cellular processes such as signal transduction, gene expression, and cell cycle regulation. Their derivation from cervical cancer provides a disease-relevant context for exploring the roles of scaffolding proteins in oncogenic signaling, particularly given the dysregulation of calcium and MAPK pathways in many cancers.
HOMER2 encodes a postsynaptic scaffold protein that is best characterized for its role in neurons, where it links group I metabotropic glutamate receptors (mGluR1/5) to intracellular calcium release and downstream signaling cascades. Mechanistically, HOMER2 functions by organizing macromolecular complexes that include Shank, PSD-95, and IP3 receptors, thereby coupling receptor activation to calcium mobilization from intracellular stores. This scaffold is activated by upstream signals such as BDNF/TrkB and calcium influx itself, and it facilitates downstream activation of NFAT transcription factors and ERK1/2, which in turn regulate gene expression programs mediated by CREB. Disruption of HOMER2 is thus predicted to uncouple mGluR signaling from calcium dynamics and transcription factor activation, impacting pathways critical for synaptic plasticity and broader cellular responses.
In the HeLa cell context, HOMER2 knockout provides a unique non-neuronal system to examine scaffold-mediated signaling outside the synapse. HeLa cells express many components of the mGluR?CHomer?Ccalcium axis, albeit at lower levels than neurons, and have been used to study calcium-dependent NFAT and ERK signaling in cancer biology. Knockout of HOMER2 in this model may alter the kinetics and amplitude of calcium responses to stimuli, affect NFAT nuclear translocation, and modulate ERK-dependent proliferation or survival signals. This system enables the investigation of how a neuronal scaffolding protein influences epithelial cell signaling, potentially shedding light on its roles in cancer cell migration, invasion, or adaptation to microenvironmental cues.
This knockout model is suited for a range of experimental applications, including western blotting and RT-qPCR to confirm gene disruption and downstream target expression changes, co-immunoprecipitation to assess loss of protein interactions, and calcium imaging with fluorescent indicators to monitor real-time Ca2? dynamics. Luciferase reporter assays can quantify NFAT or CREB transcriptional activity, while immunofluorescence allows visualization of protein localization changes. The cells are valuable for pharmacological studies targeting mGluRs or downstream kinases and for comparative studies with wild-type HeLa cells to delineate HOMER2-specific functions in signal transduction and cancer-associated processes. For more information, please contact Ascent Research.
