The BLOC1S4 Knockout Jurkat Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted BLOC1S4 gene in the Jurkat T-cell line. This polyclonal pool provides a heterogeneous loss-of-function model for studying the BLOC-1 complex in intracellular trafficking. The cells are suitable for diverse experimental workflows requiring BLOC1S4-deficient T cells without clonal isolation.
The Jurkat cell line, derived from acute T cell leukemia, is a well-established model for T lymphocyte biology. These immortalized cells exhibit mature T-cell characteristics and are used to study adaptive immunity, signal transduction, and cell-mediated responses. They are instrumental in dissecting T-cell receptor signaling, cytokine production, and immune synapse formation. Their rapid growth and genetic manipulability make them ideal for knockout studies of T-cell function.
BLOC1S4 encodes cno, a subunit of the biogenesis of lysosome-related organelles complex-1 (BLOC-1), which includes BLOC1S1, BLOC1S2, BLOC1S3, pallidin, muted, cappuccino, and dysbindin. BLOC-1 facilitates cargo sorting from early endosomes to lysosome-related organelles, acting downstream of Rab7 and Rab9 and regulated by phosphatidylinositol-3-kinase. It cooperates with the AP-3 complex to direct proteins such as LAMP1 and tyrosinase to melanosomes, platelet dense granules, and cytotoxic granules. BLOC1S4 knockout disrupts BLOC-1 assembly and cargo delivery, potentially impacting lysosomal composition, exocytosis, and receptor trafficking. In T cells, this may alter cytokine secretion and immune synapse formation.
In Jurkat T cells, BLOC1S4 loss enables dissection of lysosome-related organelle contributions to adaptive immunity. BLOC-1-dependent trafficking is critical for lytic granule biogenesis and polarized secretion during cell-mediated immune responses. Knocking out BLOC1S4 allows investigation of how defective organelle formation affects T-cell activation, surface receptor turnover, and cytokine release. This model also facilitates study of Hermansky-Pudlak syndrome, a disorder involving hypopigmentation and bleeding due to mutations in BLOC-1 subunits, recapitulating disease features in a hematopoietic line for mechanistic and drug discovery studies.
Applications include endosomal trafficking analysis in T lymphocytes, BLOC-1 complex assembly studies, and Hermansky-Pudlak syndrome immune dysfunction modeling. Compatible assays include Western blotting for BLOC-1 subunits, immunofluorescence for LAMP1/LAMP2, flow cytometry of surface receptor trafficking, cytokine ELISA, co-immunoprecipitation of BLOC-1 partners, and RNA-seq for trafficking gene expression. This polyclonal knockout model is also suited for compound screening to rescue lysosome-related organelle defects. For further information, contact Ascent Research.
