The EFEMP1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte line, carrying targeted disruption of the EFEMP1 gene. This heterogeneous loss-of-function model for EFEMP1 (Fibulin-3) avoids clonal bias while providing robust knockout across the pool. The polyclonal format is optimized for functional studies requiring native T-cell signaling contexts, enabling investigation of EFEMP1-dependent processes in a biologically relevant setting.
The Jurkat host cell line originates from human acute T-cell leukemia and is well established for studying T-cell signaling, proliferation, and apoptosis. Its suspension growth and well-characterized pathways, including integrin-based adhesion machinery, make it an ideal model for examining how ECM proteins influence T-lymphocyte behavior. This leukemic background also allows probing the dual tumor-suppressor and oncogenic roles of EFEMP1 in a context-dependent manner.
EFEMP1 is an ECM glycoprotein that interacts with fibronectin, tropoelastin, and integrin ??5??1 (ITGA5/ITGB1) to modulate cell adhesion and migration. Its expression is regulated by TGFB1, DNA methylation, and the transcription factor SP1. Downstream, it influences FAK phosphorylation and MMP2/MMP9-mediated ECM remodeling, intersecting with the TGF?¨CSMAD2 and PI3K?CAkt pathways. In this knockout, disrupted fibronectin-integrin interactions are expected to reduce FAK activation and alter MMP proteolysis, impairing integrin-mediated signaling and potentially affecting T-cell adhesion and migration dynamics.
Loss of EFEMP1 in Jurkat T cells may significantly impact adhesion dynamics and motility, as lymphocytes depend on integrin-ECM interactions for tissue homing and immune surveillance. The absence of Fibulin-3 could perturb the pericellular ECM, leading to altered FAK and Akt phosphorylation and downstream transcriptional events. This is particularly relevant for leukemic cell interactions with the bone marrow or lymph node microenvironments. Given the context-dependent roles of EFEMP1 in cancer, this model facilitates dissection of its dual functions in T-cell leukemia and offers insights into ECM-driven disease progression and therapy resistance.
These knockout polyclonal cells support diverse assays: Western blotting and RT-qPCR for expression validation, ECM adhesion and Transwell migration assays for functional studies, flow cytometry for surface integrin profiling, and phospho-signaling analysis of FAK/Akt. RNA-seq can map pathway alterations. Applications include T-cell adhesion and migration research, leukemia microenvironment studies, ECM signaling in lymphocytes, and tumor suppression mechanisms. For additional technical details and custom requests, please contact Ascent Research.
