CBFB Knockout HeLa Polyclonal Cells is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human CBFB gene in HeLa cells. It provides a loss-of-function model for studying CBFB-dependent transcriptional regulation. The polyclonal nature ensures representation of diverse editing events across the population, suitable for robust functional genomics studies.
HeLa cells are a widely used human cell line derived from HPV18-positive cervical adenocarcinoma epithelial cells. They offer a well-characterized background for studying cancer biology, signal transduction, and host-pathogen interactions. Their robust growth and ease of manipulation make them ideal for CRISPR-based knockout studies. The CBFB knockout in this context allows investigation of CBFB function in an epithelial cancer model, complementing studies in hematopoietic systems.
CBFB encodes Core-binding factor beta, an obligatory partner for RUNX transcription factors (RUNX1, RUNX2, RUNX3). CBFB heterodimerizes with RUNX proteins to enhance their DNA-binding affinity and stability, thereby regulating expression of downstream targets such as CDKN1A (p21), BCL2L11 (BIM), osteocalcin (BGLAP), and myeloperoxidase (MPO). This complex functions downstream of TGF-beta and BMP signaling, interacting with corepressors like HDAC1, HDAC3, and SIN3A. CBFB knockout abolishes CBFB-RUNX heterodimer formation, impairing RUNX-mediated transcriptional programs controlling cell cycle, apoptosis, and differentiation.
In HeLa cells, disrupting CBFB expression provides insight into RUNX-dependent transcriptional networks outside the hematopoietic lineage. Although CBFB is best known for its essential roles in hematopoiesis and osteogenesis, its dysfunction is linked to acute myeloid leukemia via the CBFB-MYH11 fusion and to breast cancer pathogenesis. The HeLa knockout model facilitates examination of CBFB??s role in epithelial cell proliferation, apoptosis resistance, and response to TGF-beta signaling, bridging gaps between hematopoietic and solid tumor research.
This product is suited for diverse experimental applications, including western blotting for RUNX targets such as CDKN1A, RT-qPCR analysis of BCL2L11 expression, ChIP-qPCR to assess RUNX binding site occupancy, and reporter assays with RUNX-responsive elements. Additionally, colony forming assays and flow cytometry for differentiation markers can evaluate functional consequences of CBFB loss. Researchers can employ these cells to model leukemia-associated gene fusions, validate drug targets, or dissect TGF-beta/BMP pathway crosstalk. For further technical details or custom inquiries, please contact Ascent Research.
