MYBBP1A CRISPR Activation Plasmid (m): sc-422090-ACT

Mybbp1a encodes the mouse MYBBP1A (MYB-binding protein 1A), a predominantly nucleolar transcriptional coregulator that integrates chromatin-associated signaling with ribosome biogenesis and cell-cycle control. MYBBP1A has been reported to modulate transcriptional programs linked to RNA polymerase I activity, nucleolar stress responses, and metabolic regulation, influencing cellular growth and proliferation. Through interactions with transcription factors and chromatin-modifying complexes, MYBBP1A can impact pathways governing differentiation and stress-adaptive gene expression. Altered MYBBP1A expression or function is associated with dysregulated proliferation and genome maintenance phenotypes that are relevant to cancer biology and other contexts where nucleolar function and transcriptional homeostasis are perturbed.

MYBBP1A CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Mybbp1a expression without altering the underlying DNA sequence.

MYBBP1A CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Mybbp1a 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 Mybbp1a transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYBBP1A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Mybbp1a locus and enabling the study of MYBBP1A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYBBP1A pathway restoration in tumor cells with silenced or reduced Mybbp1a expression.

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