The BMAL1 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from DLD-1 colorectal adenocarcinoma cells, featuring targeted disruption of the BMAL1 gene. This heterogeneous pool enables robust loss-of-function studies while preserving genetic diversity, avoiding artifacts from clonal selection.
The DLD-1 cell line, established from a Duke’s type C colorectal adenocarcinoma, is an adherent epithelial model widely used in cancer research. Its genetic background, including mutations in APC and KRAS, makes it relevant for studying colorectal tumor biology, metastasis, and drug responses.
BMAL1 (ARNTL) is a core circadian transcription factor that heterodimerizes with CLOCK to activate transcription through E-box elements. Target genes include PER1/2, CRY1/2, REV-ERB??, DBP, and cell cycle regulators WEE1, c-MYC, and p21, as well as metabolic enzyme PEPCK. The BMAL1:CLOCK complex is inhibited by PER/CRY negative feedback and modulated by ROR?? transactivation, REV-ERB?? repression, and post-translational modifications by SIRT1 and AMPK. BMAL1 also interacts with NPAS2, HIF1??, and PGC-1??, linking circadian rhythms to hypoxic and metabolic pathways.
In DLD-1 cells, BMAL1 knockout disrupts circadian clock function, leading to constitutive dysregulation of cell cycle, DNA repair, and metabolic gene expression. This may alter proliferation, apoptosis, and chronotherapeutic drug sensitivity. By comparing wild-type and knockout populations, researchers can dissect BMAL1-dependent phenotypes in a disease-relevant context.
This polyclonal knockout pool is suitable for RT-qPCR, RNA-seq, flow cytometry, apoptosis assays, drug sensitivity testing, colony formation, and migration/invasion studies. These applications enable investigation of circadian disruption in colorectal cancer and BMAL1’s impact on tumorigenesis. For further details, please contact Ascent Research.
