HSPB8 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphoblast cell line. This loss-of-function model was generated by targeted disruption of the HSPB8 gene, which encodes a small heat shock protein that functions as a molecular chaperone. The polyclonal format provides a heterogeneous pool of cells with diverse HSPB8 inactivation events, enabling robust population-level studies. This product is suitable for investigating HSPB8-dependent processes in a T-cell acute lymphoblastic leukemia background without the need for single-cell cloning.
The Jurkat cell line is a widely used human T-cell leukemia line originally established from the peripheral blood of a patient with acute lymphoblastic leukemia. These cells exhibit characteristics of T lymphoblasts and serve as a model system for studying T-cell receptor (TCR) signaling, apoptosis, and leukemia biology. Their well-characterized signaling pathways and ease of genetic manipulation make them an ideal host for CRISPR/Cas9-mediated disruption of genes involved in stress responses and cell death regulation.
HSPB8 (HSP22) is a member of the small heat shock protein family that prevents protein aggregation and promotes chaperone-assisted selective autophagy (CASA). It forms complexes with BAG3 and HSP70, recruiting STUB1/CHIP to ubiquitinate misfolded cargo for autophagic degradation via the SQSTM1/p62 receptor. HSPB8 is transcriptionally regulated by heat shock factor 1 (HSF1) and responds to upstream signals including TNF-?? and NF-??B. The protein also interacts with CRYAB (??B-crystallin) and actin, and it modulates apoptosis by influencing Bcl-2/Bax balance and AKT dephosphorylation. Consequently, HSPB8 sits at the intersection of proteostasis, autophagy, and cell death pathways.
In Jurkat cells, HSPB8 disruption is expected to impair the CASA pathway, reducing the clearance of aggregated proteins and sensitizing cells to stress-induced apoptosis. Since Jurkat cells are a model for T-cell signaling, loss of HSPB8 may also perturb TCR-mediated responses and autophagy-dependent survival mechanisms. This knockout therefore provides a relevant cellular context for dissecting how chaperone-mediated autophagy affects T-cell leukemogenesis and the response to chemotherapeutic agents. Studies using this model can reveal vulnerabilities in cancer cells that rely on HSPB8 for proteotoxic stress resistance.
This polyclonal knockout cell population is suited for a range of functional assays: western blotting for HSPB8, BAG3, and LC3-II; RT-qPCR for gene expression; autophagy flux assays based on p62 and LC3 turnover; and flow cytometric apoptosis analysis using Annexin V/propidium iodide staining. Drug sensitivity assays can explore HSPB8’s role in modulating responses to chemotherapeutics or targeted inhibitors. The cells also serve as a model for HSPB8-related neuropathies, including Charcot-Marie-Tooth disease type 2L. For further information, please contact Ascent Research.
