The BST1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated through targeted disruption of the human BST1 gene (also known as CD157) in Jurkat T lymphoblastoid cells. This loss-of-function model eliminates BST1 expression across a heterogeneous cell pool, providing a robust system for investigating BST1-mediated signaling and adhesion without the clonal variability associated with single-cell-derived lines. The knockout is produced using CRISPR/Cas9 technology, ensuring efficient gene disruption while maintaining the native genetic background of the host cell line.
The Jurkat host cell line is derived from a human male with acute T-cell leukemia and serves as a well-established model for T-cell signaling, activation, and leukemia cell biology. Jurkat cells are widely employed to dissect T-cell receptor-mediated pathways, cytokine signaling, and integrin-dependent adhesion and migration processes. Their suspension growth and ease of genetic manipulation make them an ideal platform for generating gene knockouts to study acute T-cell leukemia and immune cell function.
BST1/CD157 is a glycosylphosphatidylinositol (GPI)-anchored ectoenzyme that functions both as an ADP-ribosyl cyclase, catalyzing the synthesis of cyclic ADP-ribose (cADPR) from NAD+, and as an adhesion receptor. cADPR mobilizes intracellular calcium through ryanodine receptors, activating downstream effectors including CaMKII and MAPK pathways. Additionally, BST1 interacts with integrin ??4??1 to mediate cell adhesion and transendothelial migration. Upstream, BST1 expression is regulated by TNF, IL-1, IL-6, retinoic acid, and NF-??B, linking it to inflammatory and immune signaling networks. Key interacting factors include LYN kinase and lipid raft components, which facilitate BST1 signaling at the plasma membrane.
In Jurkat cells, BST1 contributes to T-cell adhesion, migration, and calcium signaling, processes that are critical for leukemic cell trafficking and immune responses. Disruption of BST1 in this leukemic background allows researchers to dissect its role in integrin-mediated adhesion to VCAM-1, calcium-dependent signaling cascades, and potential cross-talk with TNF receptor pathways. This knockout model is particularly relevant for studying how BST1 influences leukemic cell behavior, including survival, proliferation, and cytoskeletal reorganization downstream of cADPR and integrin engagement.
Researchers can apply this polyclonal knockout cell population to a range of functional studies, including calcium flux assays using Fluo-4 AM to assess cADPR-mediated calcium release, adhesion assays to recombinant VCAM-1 to evaluate integrin ??4??1-dependent binding, and transwell migration/transmigration assays to model leukocyte extravasation. The model also supports phospho-ERK and phospho-Akt analysis to investigate downstream signaling, as well as RT-qPCR and flow cytometry for BST1/CD157 expression validation. These cells are suitable for drug target validation in inflammatory diseases such as rheumatoid arthritis, immune deficiencies, and T-cell leukemia. For further details or to discuss your specific research needs, please contact Ascent Research.
