The AP5M1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-cell line. This product features targeted disruption of the AP5M1 gene, encoding the mu subunit of the adaptor protein complex 5 (AP-5). The polyclonal format provides a heterogeneous pool of gene-edited cells, enabling robust loss-of-function studies without clonal selection.
The Jurkat cell line is an immortalized CD4-positive T-lymphoblast line established from an acute T-cell leukemia patient. Jurkat cells are widely used to study T-cell receptor (TCR) signaling, apoptosis, and immune cell biology. Their well-characterized signaling networks and ease of manipulation make them a suitable host for investigating membrane trafficking pathways that intersect with immune function, especially in the context of endosomal sorting and lysosomal biology.
AP5M1 encodes the mu subunit of the AP-5 adaptor complex, which mediates retrograde transport of the cation-independent mannose 6-phosphate receptor (CI-MPR/IGF2R) and sortilin (SORT1) from late endosomes to the trans-Golgi network. This trafficking is essential for lysosomal enzyme delivery and autophagic cargo degradation, linking AP5M1 to lysosomal biogenesis and autophagy. The AP-5 complex interacts with the hereditary spastic paraplegia proteins SPG11 (spatacsin) and SPG15 (spastizin), retromer components VPS26, VPS29, VPS35, and clathrin. Disruption of AP5M1 impairs retrograde transport, causing mislocalization of CI-MPR and sortilin, defective lysosomal enzyme trafficking, and accumulation of autophagic substrates, ultimately leading to lysosomal dysfunction and contributing to the neurodegenerative pathology observed in SPG48.
In Jurkat T cells, AP5M1 knockout offers a model to examine how endosomal sorting defects and lysosomal dysfunction influence T-cell biology. Although AP-5 is ubiquitously expressed, its loss may intersect with T-cell-specific processes such as TCR signaling, activation-induced autophagy, or cytokine secretion. This system provides a convenient platform for studying the cellular consequences of lysosomal impairment and for screening potential therapeutic agents targeting lysosomal storage disorders or neurodegenerative conditions.
The AP5M1 Knockout Jurkat Polyclonal Cells support diverse research applications, including hereditary spastic paraplegia modeling, endosomal trafficking studies, and autophagy research. Key assays include immunofluorescence for CI-MPR and LAMP1, Lysotracker staining for lysosomal integrity, and autophagy flux measurement via LC3-II turnover. Co-immunoprecipitation can characterize AP-5 subunit interactions (AP5B1, AP5S1, AP5Z1), while flow cytometry assesses surface receptor changes. These cells are well-suited for drug discovery efforts targeting lysosomal dysfunction. For further information or to request a quotation, please contact Ascent Research.
