The INF2 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the Jurkat immortalized T lymphocyte line. This product features targeted disruption of the INF2 gene, generating a physiologically relevant loss-of-function model for studying inverted formin-2 biology in a human T cell context. The polyclonal pool maintains a heterogeneous genetic background, enabling functional analyses without the biases of clonal selection. These cells are suitable for mechanistic studies of actin dynamics, mitochondrial fission, and T cell signaling, providing a versatile tool for biomedical research.
The parental Jurkat cell line was originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia and serves as a classic model for T cell signaling, apoptosis, and leukemia biology. These cells express the T cell receptor (TCR) and associated signaling machinery, allowing detailed examination of activation-induced cytoskeletal rearrangements and immunological synapse formation. Jurkat cells are widely utilized in immunology and cancer research due to their robust growth, straightforward transfection, and well-characterized signaling pathways.
INF2 encodes an inverted formin protein that functions as both an actin nucleator and severing factor, directly regulating actin filament assembly and disassembly. At endoplasmic reticulum (ER)?Cmitochondria contact sites, INF2 polymerizes actin to facilitate the recruitment of the dynamin-related protein Drp1 (DNM1L), thereby promoting mitochondrial fission. This process is modulated by upstream regulators including the small GTPase RhoA, Ca2?/calmodulin, and CDC42, and downstream the mechanoenzyme myosin II and mitochondrial fission factors Mff and Fis1. INF2 also interacts with Spire1, the myelin and lymphocyte protein (MAL), CD2AP, and CaMKK2, integrating signals from calcium, Rho-family GTPases, and serum response factor to coordinate cytoskeletal dynamics, focal adhesion turnover, and organelle homeostasis.
In Jurkat T cells, INF2-mediated actin remodeling is critical for T cell activation, immune synapse maturation, and migration. Disruption of INF2 in this polyclonal knockout pool allows researchers to dissect the roles of INF2-dependent mitochondrial fission in leukemic T cell proliferation and survival, as well as in antigen receptor-proximal signaling. The model provides a unique system to investigate how INF2 bridges extracellular cues to cytoskeletal and mitochondrial responses, offering insights into INF2-related pathologies such as focal segmental glomerulosclerosis (FSGS) and Charcot-Marie-Tooth disease while probing T cell malignancy mechanisms.
This polyclonal knockout cell product empowers a wide range of experimental applications, including immunoblotting and RT-qPCR for confirming INF2 ablation, immunofluorescence co-localization of actin and mitochondria, flow cytometric assessment of proliferation and apoptosis, and Drp1 phosphorylation analysis. Functional assays such as MitoTracker-based mitochondrial morphology phenotyping, T cell activation readouts (e.g., CD69 expression), and lymphocyte migration assays can be directly applied to decipher INF2 contributions. The cells are ideal for screening small molecules targeting the INF2/Drp1 axis or for elucidating INF2??s role in immune synapse formation, focal adhesion dynamics, and calcium-mediated signaling. For further technical details and ordering information, please contact Ascent Research.
