The ARL13B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte line. This product harbors a targeted disruption of the ARL13B gene, creating a loss-of-function model for investigating ARL13B-dependent cellular processes. The polyclonal format ensures a heterogeneous pool of gene-edited cells, enabling robust functional analysis while minimizing clonal bias. These cells offer a versatile system for exploring ARL13B functions in Hedgehog signaling and ciliary protein trafficking.
The parental Jurkat cell line is an immortalized human T lymphocyte line isolated from a patient with acute T cell leukemia. Jurkat cells are a cornerstone model in immunology and cancer biology, extensively used to study T cell receptor signaling, apoptosis, and leukemogenesis. Their well-defined signaling networks, rapid growth as a suspension culture, and amenability to genetic manipulation make them an ideal host for functional genomic studies in a hematopoietic context.
ARL13B encodes a cilia-specific small GTPase indispensable for primary cilium structure and function. It serves as a master regulator of ciliary membrane protein trafficking and Hedgehog pathway signal transduction, controlling the localization and activity of key components including the receptor PTCH1, the transducer SMO, and the transcription factors GLI1, GLI2, and GLI3. Upstream regulators such as RFX family transcription factors and serum starvation modulate ARL13B expression, while direct interactions with IFT46, IFT52, PDE6D, and INPP5E facilitate its ciliary trafficking functions. Disruption of ARL13B abolishes proper protein delivery to the cilium and blocks Sonic Hedgehog-induced GLI activation, resulting in diminished downstream target gene expression.
In the Jurkat T cell leukemia background, the ARL13B knockout provides a unique platform to examine the intersection of Hedgehog signaling and T cell biology. Although Jurkat cells lack primary cilia, they retain expression of Hedgehog pathway components, and ARL13B may influence T cell activation, proliferation, or transformation through cilia-independent mechanisms. By disrupting ARL13B, researchers can investigate its potential roles in hematopoietic cell signaling and the contribution of Hedgehog pathway dysregulation to T cell malignancies, thereby extending understanding of ARL13B beyond ciliogenesis.
These polyclonal knockout cells are well-suited for a range of assays, including RT-qPCR and Western blotting for gene and protein expression analysis, GLI luciferase reporter assays to quantify Hedgehog pathway activity, flow cytometry for cell surface marker profiling, and immunofluorescence for subcellular localization studies. They also facilitate ciliogenesis assays in appropriate cell systems and serve as a tool for drug target validation in ciliopathies such as Joubert syndrome. For additional information or technical assistance, please contact Ascent Research.
