The AHSA1 Knockout SVG p12 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SV40-immortalized human fetal astrocyte line SVG p12, in which the AHSA1 gene has been disrupted to enable loss-of-function analysis. This polyclonal product comprises a heterogeneous pool of edited cells, avoiding clonal selection bias and providing a robust model for studying gene function in a glial context. The population-level knockout is well-suited for applications such as pooled genetic screens, drug sensitivity testing, and functional genomics, allowing researchers to assess overall impacts of AHSA1 disruption without the constraints of single-cell clones.
The host SVG p12 cell line originates from human fetal glial cells immortalized with SV40 large T antigen, retaining key astrocytic features including blood-brain barrier support, neuroinflammatory response capability, and permissiveness to certain viral infections. These cells are widely used as a CNS model due to their consistent growth, scalability, and physiologically relevant glial background, making them ideal for investigating astrocyte-specific chaperone functions, cellular stress responses, and protein homeostasis mechanisms in a well-characterized in vitro setting.
AHSA1 encodes a co-chaperone that directly binds to Hsp90 and stimulates its ATPase activity, accelerating the chaperone cycle to promote folding and stabilization of diverse client proteins. Key clients include kinases (AKT, RAF, CDK4, SRC), steroid hormone receptors (AR, GR, ER), mutant p53, and telomerase. AHSA1 expression is induced by stress-activated transcription factor HSF1 under conditions such as heat shock, oxidative stress, or ER stress, and it cooperates with co-chaperones p23 and CDC37, while interacting with Hsp70 and Hop within the Hsp90 machinery. This activity supports cell survival, facilitates oncogenic signaling, and participates in protein quality control networks.
In the SVG p12 astrocyte model, AHSA1 disruption enables precise dissection of Hsp90 regulation in glial homeostasis, which is critical for understanding neurodegeneration and stress adaptation. As AHSA1 is often upregulated in cancers to stabilize oncogenic clients, this non-transformed glial system provides a comparative platform for evaluating Hsp90 inhibitor toxicity and selectivity. Additionally, the model supports studies of astrocyte-mediated neuroinflammation, synaptic support, and viral replication, given the host cell’s permissiveness to viruses such as JC polyomavirus, relevant to progressive multifocal leukoencephalopathy research.
Typical applications include Western blotting for AHSA1 and client proteins, co-immunoprecipitation to assess AHSA1-Hsp90 interactions, and Hsp90 ATPase activity assays. Functional studies encompass cell viability and stress response assays (e.g., heat shock, proteasome inhibition), drug sensitivity screening with Hsp90 inhibitors like geldanamycin analogs, and immunofluorescence to monitor Hsp90 localization. Researchers can also employ RNA-seq and proteomic profiling to map global proteostasis changes upon AHSA1 loss. This polyclonal knockout cell population supports target validation, chaperone biology, and drug development. For further product information and technical support, please contact Ascent Research.
