MYCBP CRISPR Activation Plasmid (h): sc-404476-ACT

MYCBP (MYC binding protein) is a nuclear cofactor that binds the N-terminal region of c-MYC and modulates MYC-dependent transcriptional programs controlling cell growth, metabolism, and cell cycle progression. By influencing MYC/MAX-driven regulation of RNA polymerase II target genes, MYCBP contributes to pathways governing ribosome biogenesis, proliferation, and cellular stress responses. Altered MYCBP expression or MYC–MYCBP regulatory balance has been linked to oncogenic transcriptional states, making it relevant for studies of tumor biology, transcriptional addiction, and regulatory network remodeling. Its context-dependent effects on MYC activity support investigation of how cofactor availability tunes oncogene-driven phenotypes.

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

MYCBP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYCBP 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 MYCBP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYCBP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYCBP locus and enabling the study of MYCBP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYCBP pathway restoration in tumor cells with silenced or reduced MYCBP expression.

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