KIDINS220 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by targeted disruption of the KIDINS220 gene in the Jurkat human T lymphocyte line. As a pooled loss-of-function model, this product enables the investigation of KIDINS220-dependent molecular mechanisms without the constraints of clonal selection, preserving biological heterogeneity relevant to T cell signaling studies.
Jurkat cells are derived from an acute T cell leukemia patient and serve as a widely accepted model for T cell receptor (TCR) signaling and leukemogenesis. These suspension cells recapitulate key activation events, including tyrosine phosphorylation cascades, calcium flux, and transcriptional responses, making them a robust platform for dissecting immune receptor pathways and oncogenic signaling networks.
The KIDINS220 protein, also known as ARMS, functions as a scaffold adaptor that couples activated receptors such as the neurotrophin receptors TrkA and TrkB, the ephrin receptor EphA4, and the T cell receptor to downstream signaling modules. Upon stimulation by ligands including NGF, BDNF, ephrins, or VEGF, KIDINS220 recruits signaling complexes to promote activation of the Ras?CRaf?CMEK?CERK cascade and the PI3K?CAkt pathway, leading to phosphorylation and nuclear translocation of downstream effectors like ERK1/2, Akt, NF-??B, and CREB. This scaffold also interfaces with TCR-proximal kinases and adaptors such as Lck, ZAP-70, LAT, and SLP-76, positioning KIDINS220 as a critical node in immune and neurotrophin signal integration.
In the Jurkat host cell context, disruption of KIDINS220 impairs TCR-mediated ERK activation and NF-??B signaling, resulting in attenuated T cell activation, reduced expression of activation markers like CD69, and compromised cell survival. This polyclonal knockout model therefore captures the multifactorial impact of KIDINS220 loss on proliferation, apoptosis, and differentiation programs, providing a physiologically relevant system to study both canonical T cell pathways and crosstalk with neurotrophin signaling that may contribute to leukemic progression.
Researchers can apply this polyclonal KIDINS220 knockout product to a range of experimental designs, including functional genomics screens, drug target validation, and mechanistic studies of T cell leukemia and neurotrophin signaling in immune cells. Typical downstream assays include western blotting of phospho-ERK and total ERK, RT-qPCR profiling of target genes, flow cytometry for CD69 surface expression, apoptosis and proliferation assays, luciferase reporter assays for NF-??B or AP-1 activity, and transcriptomic analysis by RNA-seq. For detailed technical support or ordering information, please contact Ascent Research.
