The BMAL1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HeLa human cervical adenocarcinoma cell line. This product features targeted disruption of the BMAL1 (ARNTL) gene, eliminating BMAL1-dependent circadian transcriptional regulation and providing a valuable loss-of-function model. The polyclonal format offers a bulk population with heterogeneous editing, enabling robust loss-of-function studies without the confounding effects of clonal selection.
HeLa cells are a widely adopted model in cancer research, virology, and cell biology, originating from an HPV18-positive cervical adenocarcinoma. These adherent epithelial cells exhibit rapid proliferation and retain a functional circadian clock, making them suitable for investigating clock gene functions. The transformed nature of HeLa cells provides a relevant context for studying BMAL1’s roles in oncogenic processes and circadian disruption.
BMAL1 is a bHLH-PAS transcription factor that heterodimerizes with CLOCK to bind E-box elements, driving rhythmic expression of PER1/2/3 and CRY1/2. These proteins form repressor complexes that inhibit BMAL1/CLOCK activity, generating a ~24-hour feedback loop. BMAL1 is regulated by upstream signals such as SIRT1 and AMPK, and it interacts with coactivators (CBP/p300) and corepressors (HDAC3, REV-ERB??). It targets clock-controlled genes like DBP, TEF, and metabolic regulators PEPCK and G6PC, and also influences cell cycle genes (WEE1, c-MYC), integrating circadian, metabolic, and oncogenic pathways.
Introducing BMAL1 knockout in HeLa cells allows dissection of clock-dependent and clock-independent functions of this transcription factor in a cancer setting. HeLa cells, as a transformed line, may exhibit altered circadian dynamics, and BMAL1 disruption aids in revealing tumor-specific roles in proliferation and metabolism. The polyclonal population avoids artifacts from single-cell cloning and provides a more averaged representation of biological responses, suitable for population-level studies of circadian outputs and downstream gene expression changes.
These cells support a range of assays including circadian transcriptomics (RNA-seq), RT-qPCR for rhythmic genes (e.g., NR1D1, DBP), Western blotting for BMAL1 and clock proteins, luciferase reporters, flow cytometry for cell cycle, and metabolic flux analysis. Applications encompass circadian rhythm disruption, cancer chronobiology, metabolic regulation, and drug chronotherapy. For additional details or purchasing, contact Ascent Research.
