PEBP2β CRISPR Activation Plasmid (h): sc-401983-ACT

CBFB encodes core-binding factor subunit beta (PEBP2β), a non–DNA-binding partner that heterodimerizes with RUNX family transcription factors to enhance DNA binding and stabilize transcriptional complexes. This RUNX/CBFβ axis regulates lineage-specific gene expression programs central to hematopoiesis, immune differentiation, osteogenesis, and cell-cycle control. CBFB-dependent transcription influences pathways governing myeloid and lymphoid development, cytokine signaling outputs, and maturation of skeletal and stromal lineages. Dysregulation of CBFB, including chromosomal rearrangements and altered RUNX interactions, is implicated in hematologic malignancy biology and developmental phenotypes, making it a useful node for mechanistic studies of transcriptional control.

PEBP2β CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CBFB expression without altering the underlying DNA sequence.

PEBP2β CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CBFB locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the CBFB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PEBP2β expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CBFB locus and enabling the study of PEBP2β-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PEBP2β pathway restoration in tumor cells with silenced or reduced CBFB expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.