The AKAP12 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from Jurkat T lymphocytes, targeting the AKAP12 gene for functional loss-of-function studies. This product provides a model to investigate the scaffold protein AKAP12, a tumor suppressor involved in cAMP-PKA and PKC signaling. The polyclonal format ensures broad genetic disruption without clonal bias, suitable for population-based assays.
The Jurkat cell line is an immortalized human T lymphocyte line established from a 14-year-old patient with acute T-cell leukemia. Widely used to study T-cell activation and T-ALL, Jurkat cells offer a well-characterized signaling environment for exploring gene function in lymphoid malignancy. Their rapid proliferation and defined kinase networks make them a preferred host for cancer cell biology and signal transduction research.
AKAP12 is a scaffold protein that anchors PKA and PKC at the plasma membrane and cytoskeleton, integrating cAMP-PKA and PKC signaling to regulate cell adhesion and migration. It interacts with the PKA RII subunit, PKC??, F-actin, and integrin ??1, and its activity is modulated by upstream factors including p53, DNA methylation, and prostaglandin E2. AKAP12 controls the phosphorylation of downstream targets such as FAK and RhoA, influencing ??-catenin stability and CREB-mediated transcription. Through these interactions, AKAP12 couples GPCR-adenylyl cyclase cascades with Rho GTPase and integrin pathways to orchestrate cytoskeletal dynamics and cell cycle regulation.
In Jurkat cells, AKAP12 loss??commonly due to epigenetic silencing??abrogates its tumor-suppressive scaffolding, leading to unchecked PKA/PKC signaling and cytoskeletal dysregulation. This knockout recapitulates aspects of T-ALL pathobiology, allowing dissection of AKAP12-dependent adhesion and migration defects. The model is particularly valuable for studying crosstalk between cAMP and integrin pathways in leukemia, and for identifying therapeutic targets that reverse AKAP12 loss.
Applications include analyzing AKAP12-mediated adhesion and migration via transwell and immunofluorescence, probing signaling networks with Western blotting and co-immunoprecipitation, and examining gene expression by RT-qPCR. The cells are also suited for compound screening to restore AKAP12 expression or function, and for flow cytometry-based phospho-signaling studies. Apoptosis assays further enable investigation of cell death pathways. For technical inquiries, please reach out to Ascent Research.
