The ADIPOR1 Knockout Jurkat Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting ADIPOR1 in the Jurkat human T lymphocyte line. This heterogeneous pool of gene-disrupted cells enables loss-of-function analysis of adiponectin receptor 1 (ADIPOR1) without single-cell cloning. Utilizing advanced CRISPR/Cas9-mediated gene disruption, these polyclonal knockout cells provide a robust model for investigating ADIPOR1-dependent signaling in an immune context.
Jurkat cells are an immortalized T lymphocyte line originally derived from a T cell leukemia patient. Extensively used in immunology and cancer research, they provide a well-characterized platform for examining T cell signaling, activation, and metabolism. Employing this cell line for ADIPOR1 knockout allows researchers to study adiponectin signaling specifically within T cells, exploring its impact on immune cell metabolic regulation.
ADIPOR1 functions as a receptor for the adipokine adiponectin (ADIPOQ). Ligand engagement promotes APPL1 recruitment, activating AMPK and PPAR-alpha pathways. These pathways regulate downstream effectors such as PGC-1alpha, CPT1, and GLUT4 to enhance fatty acid oxidation and glucose uptake. ADIPOR1 signaling also interfaces with p38 MAPK and eNOS, and is modulated by upstream regulators like PPAR-gamma and insulin. Through these interactions, ADIPOR1 integrates hormonal and metabolic signals to maintain cellular energy balance.
Targeted disruption of ADIPOR1 in Jurkat T cells creates a critical tool for elucidating adiponectin-mediated metabolic control in lymphocytes. T cell activation and differentiation involve metabolic reprogramming, and ADIPOR1 may couple adipokine signals to these processes. The polyclonal knockout population permits evaluation of ADIPOR1-dependent effects on AMPK phosphorylation, PPAR-alpha transcriptional activity, and metabolic flux in an immune setting. This model is especially relevant for investigating immune-metabolic crosstalk in obesity, insulin resistance, and associated disorders.
Key research applications include Western blotting for phosphorylated AMPK, flow cytometry-based glucose uptake assays, RT-qPCR of PPAR-alpha target genes, and metabolic profiling with Seahorse analyzers. Co-immunoprecipitation can confirm ADIPOR1-APPL1 interactions. These cells support studies on adiponectin signaling in T cell metabolism, inflammation, and the pathogenesis of metabolic diseases. For further information or technical assistance, please contact Ascent Research.
