DNMBP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Homo sapiens Jurkat T lymphocyte line, featuring targeted disruption of the DNMBP gene. This polyclonal format yields a heterogeneous pool of edited cells suitable for bulk functional studies without single-cell cloning, enabling robust assessment of loss-of-function phenotypes while minimizing clone-specific artifacts.
The Jurkat host cell line, originally isolated from an acute T cell leukemia patient, is a widely utilized model for T-cell receptor (TCR) signaling, apoptosis, and adaptive immune responses. Its suspension growth, rapid proliferation, and genetic tractability facilitate investigations of actin dynamics, endocytosis, and immune synapse formation, while its leukemic origin provides a relevant context for oncogenic signaling and migration studies.
The DNMBP gene encodes a scaffold protein that couples the GTPase CDC42 to dynamin and the actin cytoskeleton, serving as a pivotal node in CDC42 signaling. DNMBP is activated by upstream regulators including CDC42, Rac1, RhoA, SRC kinases, EGFR, and TCR engagement. It interacts with CDC42, Rac1, dynamin, cortactin, WASL/WASP, and actin to regulate downstream effectors such as dynamin (DNM1/2), cortactin, and tight junction components (claudins, occludin). Mechanistically, DNMBP coordinates membrane invagination during endocytosis and stabilizes tight junctions by scaffolding actin filaments to intercellular junctions.
In Jurkat T cells, loss of DNMBP is predicted to impair actin-dependent processes essential for immune function, including immune synapse organization, receptor internalization, and cell migration. As CDC42 signaling is central to T-cell activation and leukemic transformation, this knockout model offers a powerful tool for dissecting mechanisms underlying T-cell leukemia, aberrant adaptation responses, and potential contributions to cancer metastasis. The polyclonal configuration allows population-level interrogation of these dynamic cellular behaviors.
Key research applications include elucidating DNMBP??s role in T-cell actin dynamics and endocytosis, characterizing immune synapse architecture, screening for leukemia-associated migration defects, and identifying novel interacting partners in TCR signaling pathways. Compatible assays include Western blotting, immunofluorescence and phalloidin staining for F-actin, flow cytometry for cell cycle and apoptosis, Transwell migration assays, transferrin endocytosis assays, co-immunoprecipitation for CDC42/dynamin complexes, and RT-qPCR for target gene expression. For additional technical details or custom cell services, please contact Ascent Research.
