The KLC4 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Jurkat T lymphoblastoid cells, providing a loss-of-function model for the KLC4 gene. This polyclonal pool enables robust investigation of kinesin-1 cargo adaptor functions without clonal biases.
Jurkat cells are an immortalized CD4+ T lymphoblastoid line from an acute lymphoblastic leukemia patient, widely used to study T-cell receptor signaling, apoptosis, and cytokine secretion, making them an ideal host for dissecting gene function in immune-related pathways.
KLC4 encodes a kinesin light chain subunit that serves as a cargo recognition and binding adaptor for the kinesin-1 motor complex, enabling microtubule-based intracellular transport. It directly interacts with kinesin heavy chains KIF5B and KIF5C and with JNK-interacting proteins (JIPs) to mediate the trafficking of JNK/MAPK signaling modules. This transport process is tightly regulated by upstream MAP kinases, particularly JNK, which phosphorylates KLC4 to modulate cargo adaptor availability and complex assembly. Consequently, KLC4 controls the subcellular localization of JNK activity, influencing downstream events such as the delivery of signaling complexes to specific destinations, mitochondrial distribution, and modulation of transcriptional responses. Key pathway components include the MAP kinase cascade members JNK, MKK7, and MLK, all of which are linked to KLC4-dependent transport.
Within Jurkat T lymphoblastoid cells, KLC4-mediated trafficking is critical for the spatial and temporal regulation of JNK signaling, a pathway implicated in activation-induced cell death and cytokine secretion. By controlling the microtubule-dependent delivery of JNK signaling complexes, KLC4 influences apoptotic thresholds and immune effector functions. Disruption of KLC4 in this knockout model may alter the dynamics of JNK pathway activation, providing a powerful tool to investigate how kinesin-dependent transport mechanisms contribute to T-cell biology and pathology, including T-cell acute lymphoblastic leukemia progression.
This KLC4 knockout polyclonal population is suited for a wide range of research applications, including the study of intracellular trafficking in T-cell signaling, elucidation of kinesin-mediated apoptosis mechanisms, and validation of drug targets for leukemia. Representative experimental approaches include Western blotting and RT-qPCR to confirm KLC4 ablation, flow cytometry with Annexin V staining to assess apoptosis, immunofluorescence microscopy to visualize mislocalization of kinesin cargoes, co-immunoprecipitation to analyze kinesin complex integrity, phospho-JNK western analysis to monitor signaling changes, and cell migration assays to evaluate functional outcomes. For technical inquiries and ordering information, please contact Ascent Research.
