The AKAP13 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the AKAP13 gene in a human T lymphocyte background. Derived from Jurkat cells, they carry a targeted disruption that ablates AKAP13 scaffold protein expression, interrupting signal integration. This polyclonal pool offers a heterogeneous population that minimizes clonal selection bias, enabling robust analysis of AKAP13-dependent pathways in T cell biology.
Jurkat is an immortalized human T lymphocyte line originating from peripheral blood of a 14-year-old male with acute T cell leukemia, widely used to study T cell receptor (TCR) signaling, apoptosis, and leukemogenesis. Its well-characterized signaling networks and genetic tractability make it a preferred host for investigating molecular mechanisms in T cells, and the AKAP13 knockout derivative retains responsiveness to TCR engagement and cAMP stimuli for focused functional dissection.
AKAP13 serves as a dual-function scaffold that anchors PKA via regulatory subunits (RII??/RII??) and acts as a RhoA-specific guanine nucleotide exchange factor (RhoGEF). Upon cAMP binding, it recruits PKA for phosphorylation events while activating RhoA-GTP, which in turn stimulates ROCK, leading to actin polymerization and SRF-dependent transcription through MRTF cofactors. This integrates cAMP/PKA and Rho GTPase signaling. Key interacting factors include ER??, 14-3-3 proteins, PKC, IQGAP1, and DLG1, with upstream regulation by cAMP, estrogen, GPCRs, and PKA phosphorylation.
In Jurkat T lymphocytes, AKAP13 links TCR and GPCR signals to cytoskeletal reorganization and transcriptional programs controlling activation, adhesion, and migration. Knockout enables precise dissection of its role in immune synapse dynamics, T cell motility, and gene expression, offering insight into how AKAP13 dysregulation contributes to diseases such as acute lymphoblastic leukemia (via its LBC oncogene activity), cardiac arrhythmias, and breast cancer.
Research applications include probing AKAP13-dependent TCR signaling, cAMP-Rho crosstalk, gene regulation, and leukemic transformation. Representative assays are Western blotting, Rho GTPase activation and cAMP ELISA, Transwell migration, phalloidin F-actin staining, SRF luciferase reporter, RNA-seq, CD69 flow cytometry, and Annexin V apoptosis tests. The polyclonal population also supports drug screening targeting AKAP13 pathways. For additional information or technical support, please contact Ascent Research.
