The AGTRAP Knockout Jurkat Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-cell line, engineered for targeted disruption of the AGTRAP gene. This pooled knockout model enables loss-of-function studies of the angiotensin II type 1 receptor-associated protein (AGTRAP) within a consistent T-cell genetic background, avoiding clonal selection artifacts. The polyclonal format preserves representative genotypic heterogeneity while ensuring efficient gene disruption across the population, making it suitable for pooled phenotypic assays and screening applications.
Jurkat cells are an immortalized human T-lymphocyte line originally isolated from an acute lymphoblastic leukemia patient. These suspension cells retain many characteristics of mature T cells and are widely employed in immunological research, including studies of T-cell activation, signal transduction, and cytokine production. The Jurkat model provides a physiologically relevant platform for examining the role of AGTRAP in adaptive immune cells, where components of the renin-angiotensin system are increasingly recognized as modulators of T-cell function.
AGTRAP functions as a negative regulator of AT1R signaling. It constitutively associates with the C-terminal tail of AT1R, facilitating receptor internalization through clathrin-coated pits via interactions with the AP-2 adaptor complex and ??-arrestin, and subsequently targets AT1R for degradation. This mechanism dampens angiotensin II-induced downstream cascades, including G??q/11?CPLC??-mediated calcium mobilization, ERK1/2 phosphorylation, and NF-??B activation. Consequently, AGTRAP attenuates cellular responses to angiotensin II and is positioned upstream of key signaling hubs influenced by reactive oxygen species and inflammatory mediators.
In Jurkat T cells, AT1R expression allows angiotensin II to modulate immune functions such as migration, adhesion, and cytokine secretion. AGTRAP knockout in this context is expected to sensitize cells to angiotensin II stimulation, leading to enhanced and prolonged activation of ERK1/2 and NF-??B pathways. This model thus enables dissection of AGTRAP??s role in regulating T-cell responses under conditions mimicking inflammatory or hypertensive microenvironments, bridging cardiovascular and immunological research.
Applications include investigating AGTRAP-dependent modulation of T-cell signaling, analyzing the crosstalk between the renin-angiotensin system and adaptive immunity, and screening compounds that target AT1R trafficking or downstream effectors. Representative assays with these polyclonal knockout cells include angiotensin II-induced phospho-ERK western blotting, calcium mobilization measurements, AT1R internalization assays, co-immunoprecipitation of AGTRAP?CAT1R complexes, and flow cytometric analysis of surface AT1R. Migration assays can further reveal functional consequences of AGTRAP loss. For additional details or customization options, please contact Ascent Research.
