This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GPR137 gene in the HeLa host cell line. The polyclonal population comprises a heterogeneous mixture of edited cells, each carrying distinct gene disruptions introduced by CRISPR/Cas9-mediated genome editing, resulting in a loss-of-function model for GPR137. This knockout model enables the study of GPR137 function without the isolation of single-cell clones, providing a robust cellular system for investigating the orphan G protein-coupled receptor’s role in cellular signaling and disease.
The host cell line, HeLa, is a well-established human cervical adenocarcinoma epithelial cell line positive for human papillomavirus type 18 (HPV18). Originally derived from a cervical tumor, HeLa cells are extensively used as a model for cancer research due to their transformed phenotype and continuous proliferation capacity. Their epithelial origin and tumorigenic properties make them particularly suitable for studying oncogenic signaling, cell migration, and therapeutic responses in a cancer context.
GPR137 is an orphan G protein-coupled receptor (GPCR) that lacks a confirmed endogenous ligand but is implicated in the regulation of autophagy and cell proliferation. Its activity is modulated by upstream signals including cellular nutrient status sensed by mTOR, as well as hypoxic conditions. Downstream of GPR137, signaling cascades converge on mTORC1, ULK1, ATG13, and ERK1/2, connecting the receptor to both autophagy initiation and mitogenic pathways. GPR137 is known to interact with G??12/13 and ??-arrestin, suggesting involvement in G protein-dependent and arrestin-mediated signaling. Representative pathway components such as Beclin 1 and LC3 are central to autophagic processes, while ERK and its substrate RSK facilitate proliferative signaling. In the knockout context, disruption of GPR137 is expected to impair autophagic flux and alter ERK-dependent mitogenic signaling, although the precise mechanisms remain an active area of investigation.
In HeLa cells, which rely on robust autophagy and MAPK/ERK pathway activity for survival and proliferation, the loss of GPR137 provides a valuable model to dissect the receptor’s contributions to tumor cell biology. Because HeLa cells exhibit constitutive activation of growth pathways, the GPR137 polyclonal knockout allows researchers to examine how orphan GPCR signaling intersects with mTOR and ERK networks in a cancer-relevant setting. This model may help elucidate the role of GPR137 in processes such as nutrient sensing, hypoxia adaptation, and metastasis, thereby establishing a platform for identifying potential therapeutic vulnerabilities in cancers characterized by dysregulated autophagy and proliferation.
Typical research applications for this product include detailed investigation of orphan GPCR function in autophagy using Western blot detection of LC3-II conversion and p62 degradation, as well as autophagy flux assays with lysosomal inhibitors. Proliferation assays (MTT, BrdU) and migration/invasion assays can be employed to assess the impact of GPR137 loss on cell growth and motility. Phospho-ERK and mTOR signaling analyses via immunoblotting or phospho-specific flow cytometry enable dissection of downstream signaling alterations. Additionally, RNA-sequencing of the knockout population may reveal transcriptomic changes associated with GPR137 disruption. This polyclonal knockout model is well suited for drug target identification studies aimed at modulating autophagy or GPCR-mediated signaling in cancer and neurodegenerative disease research. For further technical information or to discuss integration into your experimental workflow, please contact Ascent Research.
