The HSPB1 Knockout HeLa Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human HSPB1 gene in HeLa cells. This loss-of-function model enables investigation of the molecular chaperone HSPB1 (Hsp27). The polyclonal population contains heterogeneous knockout genotypes, avoiding clonal selection artifacts and providing a representative population-level response for functional studies.
HeLa, an immortalized human cervical adenocarcinoma cell line, is HPV18-positive and broadly used in cancer biology and stress response research. Its robust growth, high transfection efficiency, and well-characterized molecular landscape make it ideal for gene disruption studies involving apoptosis, cytoskeletal dynamics, and chaperone-mediated stress protection.
HSPB1 encodes a small heat shock protein functioning as an ATP-independent molecular chaperone that inhibits protein aggregation and provides cytoprotection under stress. It is activated by phosphorylation via the p38 MAPK?CMAPKAPK2 cascade, modulating its chaperone activity and interactions with apoptotic regulators. HSPB1 inhibits apoptosis by sequestering cytochrome c and procaspase-3, preventing apoptosome formation, and by binding DAXX to block Fas-mediated death. It also interacts with Akt to promote survival. In the cytoskeleton, HSPB1 binds actin and tubulin, regulating polymerization and stability, and influences migration. It forms complexes with Hsp70 and ??B-crystallin, and its phosphorylation integrates signals from TNF-??, IL-1??, oxidative stress, and heat shock.
In HeLa cervical adenocarcinoma cells, HPV18 oncoproteins subvert apoptotic and stress pathways, highlighting the significance of HSPB1. HSPB1 is often overexpressed in cancers and contributes to drug resistance and survival under genotoxic stress. Disruption of HSPB1 allows dissection of its roles in apoptosis inhibition, actin remodeling, and stress resilience. This polyclonal knockout population provides a physiologically relevant platform to study loss-of-function effects on tumor cell behavior, including responses to chemotherapeutics, heat shock, and oxidative insults. The model is valuable for elucidating HSPB1??s function in MAPK and Akt signaling and interactions with downstream targets such as Bcl-2 proteins and eIF4E.
This knockout cell product supports diverse applications including stress response studies, apoptosis regulation, cytoskeletal dynamics, and cancer drug resistance research. Typical assays are Western blotting, RT-qPCR, immunofluorescence, actin staining, caspase activity and Annexin V apoptosis assays, and co-immunoprecipitation for interaction studies. Heat shock and oxidative stress assays are also enabled. Researchers in neurodegeneration, Charcot-Marie-Tooth disease type 2F, or ischemia-reperfusion injury may employ this model. For more information, contact Ascent Research.
