APLP2 Knockout Jurkat Polyclonal Cells are a population of Jurkat cells edited with CRISPR/Cas9 to disrupt the APLP2 gene. As a polyclonal pool, this product provides a heterogeneous cell population for loss-of-function studies, without isolating single-cell clones. The knockout is achieved via CRISPR/Cas9-mediated gene disruption, resulting in abrogation of APLP2 protein expression. This product enables investigation of APLP2’s role in cellular processes, particularly in the context of T lymphocyte biology.
The Jurkat cell line, derived from a human acute T cell leukemia, is a widely used model for T cell receptor signaling, apoptosis, and leukemia. Jurkat cells exhibit characteristics of mature T lymphocytes and are extensively employed to dissect signaling pathways governing T cell activation, proliferation, and survival. Their genetic tractability and well-characterized signaling networks make them suitable hosts for CRISPR-based gene editing, enabling functional studies of genes implicated in T cell biology and disease.
APLP2 is a type I transmembrane protein belonging to the APP family. It undergoes proteolytic cleavage by ADAM10 or BACE1, followed by ??-secretase processing involving PSEN1, releasing the intracellular domain AICD. The AICD translocates to the nucleus, where it interacts with adaptor Fe65 (APBB1) to influence gene transcription. APLP2 participates in integrin-mediated adhesion by binding ITGB1 and regulates migration via FAK phosphorylation and Rho family GTPases. It is embedded in pathways intersecting with APP processing and Notch signaling, featuring interactions with PTPN11 and APBA1, and responding to upstream signals from integrin receptors and growth factors.
In Jurkat T cells, APLP2 knockout allows dissection of adhesion-TCR signaling crosstalk. Disruption of APLP2 may impair integrin-dependent attachment to fibronectin, altering FAK and PTPN11 signaling and cytoskeletal reorganization essential for immune synapse formation and T cell activation. Loss of AICD-mediated transcription could affect genes controlling cell cycle and apoptosis, relevant to leukemia. Thus, this model helps elucidate how adhesion signals modulate T lymphocyte function and malignant phenotypes.
Applications include Western blotting for APP fragments, co-IP of Fe65, adhesion assays, transwell migration, flow cytometry for integrins, and luciferase reporter assays for AICD activity. The cells are useful for APP processing modulator screening, Alzheimer’s pathway studies in lymphocytes, and investigation of APLP2 in T cell leukemia. Contact Ascent Research for assistance.
