The BRSK2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the BRSK2 gene has been disrupted. This loss-of-function model eliminates endogenous BRSK2 expression, providing a controlled background for investigating kinase-dependent signaling. The heterogeneous polyclonal pool is suitable for population-level biochemical and functional assays.
HEK293T cells are a human embryonic kidney epithelial cell line stably expressing SV40 large T antigen, facilitating high-level transient protein production and lentiviral packaging. Derived from HEK293, they offer robust growth and transfectability, making them an ideal host for studying exogenously introduced genes and signaling pathway reconstitution.
BRSK2 is a serine/threonine kinase that functions downstream of the LKB1-STRAD-MO25 complex. Upon activation by LKB1-mediated phosphorylation, BRSK2 phosphorylates substrates such as MARK2 and tau, which are central to neuronal polarization and synapse formation. BRSK2 also interacts with Raptor to modulate mTORC1 signaling, impacting protein synthesis and metabolism. Additional regulatory inputs include CaMKK2 and 14-3-3 protein interactions, while downstream targets extend to RIMS1 in insulin secretion pathways.
In the HEK293T background, the BRSK2 knockout model distills core signaling mechanisms without the complexity of neuronal differentiation. This enables focused dissection of the LKB1-BRSK2-MARK2/tau axis and mTOR cross-regulation, and it supports high-throughput screening for modulators of these pathways??offering a tractable surrogate for neuronal polarity and metabolic studies.
Typical applications include western blotting for BRSK2 and phospho-MARK2/tau, RT-qPCR validation, phospho-signaling analysis, and mTOR activity reporter assays, addressing research areas such as neurodevelopmental disorders, autism, intellectual disability, and diabetes. This product is well-suited for drug target validation and functional genomics. For additional details, please contact Ascent Research.
