GPRC5C Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the GPRC5C gene in the Jurkat T-lymphocyte model. This product enables loss-of-function studies of the orphan G protein-coupled receptor GPRC5C, providing a versatile tool for investigating its roles in T-cell signaling and leukemia biology. The polyclonal format preserves population-level heterogeneity, allowing robust analysis of gene function without clonal selection artifacts.
Jurkat cells are an immortalized human T lymphocyte line originally derived from the peripheral blood of a 14-year-old male with acute T cell leukemia. These cells serve as an extensively validated model system for T cell receptor (TCR) signaling, leukemia progression, and apoptotic mechanisms. Their rapid growth and well-characterized signaling networks make them particularly suitable for dissecting GPCR-mediated pathways in a leukemic context.
GPRC5C is an orphan receptor implicated in retinoic acid signaling and cellular homeostasis. Mechanistically, GPRC5C is activated by retinoic acid and engages G protein subunits such as G??i and G??s, leading to modulation of adenylyl cyclase, cAMP levels, and calcium flux. Downstream, it regulates the MAPK/ERK pathway by phosphorylating ERK1/2, and the PI3K/AKT axis, promoting expression of target genes like CCND1 and MYC. The receptor also interacts with ??-arrestin and putative adaptor proteins, and operates within a network that includes retinoic acid receptors (RAR, RXR) and cytokines such as IL-2, integrating signals from TCR engagement.
Knockout of GPRC5C in Jurkat cells allows precise examination of its function in T-cell leukemia, where retinoic acid signaling influences differentiation, proliferation, and survival. This model is relevant for exploring how GPRC5C intersects with oncogenic pathways, potentially affecting tumor suppression or metabolic regulation. Its disruption helps clarify the receptor’s role in leukemic cell growth and response to retinoid-based therapies.
Typical research applications include Western blotting and RT-qPCR for gene expression analysis, flow cytometry to assess apoptosis and cell cycle changes, and phospho-ERK/AKT profiling to map signaling events. Proliferation assays and calcium flux experiments further characterize downstream effects, while reporter gene assays with retinoic acid response elements quantify transcriptional activity. These cells are valuable for studying GPCR signaling in T-cell leukemia, retinoic acid responses, and the molecular basis of cancer cell proliferation and survival. For additional information, please contact Ascent Research.
