The ATP13A1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T-lymphoblastoid cell line, providing a heterogeneous loss-of-function model for the ATP13A1 gene. This polyclonal format ensures representation of diverse gene disruptions, suitable for robust functional studies without clonal selection bias.
Jurkat cells are an immortalized human T-cell line established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. These suspension cells express CD3, CD4, and IL-2 receptor, and serve as a pivotal model for T-cell signaling, activation, and leukemogenesis, enabling investigation of ATP13A1 in immune cell contexts.
ATP13A1 encodes an endoplasmic reticulum (ER)-resident P5-ATPase involved in manganese transport, mitochondrial integrity, and autophagy regulation. It is transcriptionally regulated by ER stress sensors (IRE1??, PERK, ATF6) and effectors (ATF4, XBP1). Loss of ATP13A1 function disrupts mitochondrial membrane potential, autophagy flux (manifested as altered LC3-II and p62 levels), reactive oxygen species accumulation, and apoptosis signaling (cleaved caspase-3). The protein interacts with ER chaperones HSPA5 (BiP) and PDIA6, and likely associates with coatomer complexes for ER retrieval. Representative pathway components affected include CHOP, Parkin, and PINK1, linking ATP13A1 to proteostasis and mitochondrial quality control.
In Jurkat T-leukemia cells, ATP13A1 knockout provides a powerful system to study ER-mitochondria communication and autophagy within an immune cell setting. The model is particularly relevant for exploring manganese-dependent cytotoxicity, UPR activation, and the contribution of ER stress to leukemia cell survival and drug resistance, thereby offering translational insights for both cancer biology and metabolic disorders.
Researchers can apply this model to functional genomics of ATP13A1 in T-cell leukemia, ER stress and autophagy signaling, and manganese toxicity assays. Standard readouts include flow cytometry for apoptosis, mitochondrial potential (JC-1), and ROS; Western blotting for LC3B, p62, cleaved caspase-3, and UPR markers; RT-qPCR; and viability assays (MTS, CellTiter-Glo). Immunofluorescence detection of ER-Tracker and LC3 puncta enables spatial analysis of autophagic processes. This polyclonal knockout cell population facilitates drug screening and mechanistic interrogation of ATP13A1-dependent pathways. For further information, contact Ascent Research.
