The KPTN Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function studies of the KPTN gene. Generated via CRISPR/Cas9-mediated gene disruption in Jurkat T lymphoblasts, this heterogeneous knockout pool serves as a robust functional genomics tool. It enables investigation of KPTN??s role in actin cytoskeleton organization without requiring clonal isolation. The product is designed for academic and pharmaceutical researchers studying T cell biology and actin-related signaling.
The host Jurkat cell line is an immortalized T lymphoblast line derived from a 14-year-old male with acute T cell leukemia. Jurkat cells express CD3, T cell receptor (TCR), CD4, and IL-2 receptor, recapitulating key features of T cell signaling. They are widely used for mechanistic studies on T cell activation, apoptosis, and leukemogenesis. This well-characterized line enables controlled perturbation of actin regulators while preserving the signaling capacity of a T cell model.
KPTN is an actin-binding protein that integrates signals from Rho family GTPases (RhoA, RAC1, CDC42) to regulate actin dynamics. It is transcriptionally controlled by SRF and directly interacts with F-actin, cortactin, and cofilin to promote actin polymerization, filopodia extension, and adhesion. KPTN operates within pathways involving ROCK, LIMK, FAK, Src, and PI3K-Akt, linking upstream cues to cytoskeletal reorganization. This network positions KPTN as a key node in actin-dependent processes.
In Jurkat cells, KPTN is essential for actin-dependent events such as immunological synapse formation, T cell activation, and migration. KPTN knockout impairs actin organization and TCR signaling, as measured by CD69 and CD25 expression and cytokine output. This model is therefore ideal for studying how actin dynamics influence T cell effector functions and leukemic cell adhesion.
Applications include investigating actin-dependent T cell processes, immunological synapse dissection, and identification of KPTN binding partners. This model supports drug screening for actin dynamics disorders such as MRT41. Verification uses Western blot and phalloidin staining, while functional studies employ transwell migration, flow cytometry, and cytokine secretion assays. For technical details, validation data, or custom inquiries, please contact Ascent Research.
