The ATRN Knouckout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the expression of the human ATRN gene in the Jurkat T lymphocyte line. This loss-of-function model enables investigation of attractin-mediated accessory regulation of melanocortin receptor signaling without assumptions of clonal homogeneity, providing a heterogenous population suitable for pooled functional studies. The product is intended for advanced biomedical research applications focused on immune regulation and melanocortin signaling.
Jurkat cells are an immortalized human T lymphocyte line derived from a 14-year-old male with acute T cell leukemia. These cells are a well-established model for studying T cell receptor (TCR) signaling, T cell activation, and leukemia biology. Their robust, reproducible growth characteristics and sensitivity to signaling perturbations make them an ideal host for gene-editing studies aiming to dissect immunomodulatory pathways.
ATRN encodes attractin, a single-pass transmembrane protein that functions as an accessory receptor for melanocortin receptors such as MC1R and MC4R. In T cells, attractin is known to modulate cAMP/PKA and MAPK/ERK signaling downstream of melanocortin stimulation. Upon ligand binding (e.g., by ??-MSH) or TCR/CD28 co-stimulation, ATRN interacts with G??s and ??-arrestin to regulate adenylate cyclase activity, leading to cAMP production and PKA activation. This cascade subsequently influences the phosphorylation of transcription factors like CREB and ERK1/2, ultimately affecting the expression of cytokines including IL-2 and IFN-??. Thus, ATRN sits at the intersection of endocrine and immune signaling, integrating cues from upstream regulators such as ??-MSH, AgRP, and IL-2 to coordinate T cell responses.
Disruption of ATRN in Jurkat polyclonal cells yields a powerful model to dissect the precise role of attractin in T lymphocyte biology. The knockout is expected to impair melanocortin receptor-driven cAMP/PKA and MAPK pathway activation, leading to altered T cell activation dynamics, diminished cytokine production, and modified immune response regulation. Given the importance of these pathways in immune deficiency, inflammatory disorders, and metabolic syndrome, this model provides a physiologically relevant platform for exploring how melanocortin signaling interfaces with T cell function. Notably, the polyclonal nature of the knockout population allows researchers to assess functional variability and avoids clonal selection artifacts.
Typical research applications include studying melanocortin signaling in T cells, investigating immune regulation and inflammation, and performing T cell activation assays under conditions of ATRN deficiency. The knockout cells are suited for a range of downstream assays, such as Western blotting to confirm ATRN protein loss, flow cytometry for T cell activation markers (CD69, CD25), ELISA for IL-2 and IFN-?? secretion, cAMP accumulation assays, RT-qPCR for target gene expression, co-immunoprecipitation of ATRN-MC1R complexes, and CREB reporter assays. Additionally, they serve as a valuable tool for drug screening of melanocortin receptor modulators. For further details or to discuss customized applications, please contact Ascent Research.
