
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTBP CRISPR Activation Plasmid (h) | sc-404307-ACT | 20 µg | $397.00 |
Human MTBP (MDM2 binding protein) is a nuclear factor that coordinates DNA replication origin firing and S-phase progression through its interaction with Treslin/TICRR and the CDC45–MCM–GINS helicase activation machinery. By coupling replication initiation with checkpoint control, MTBP contributes to genome stability and influences proliferation programs under replication stress. Altered MTBP expression has been linked to dysregulated cell-cycle control and chromosomal instability, contexts frequently studied in tumor biology and other disorders marked by impaired DNA replication fidelity. MTBP also interfaces with pathways governing replication timing, DNA damage responses, and transcriptional programs that shape cell growth.
MTBP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MTBP expression without altering the underlying DNA sequence.
MTBP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MTBP 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 MTBP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MTBP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MTBP locus and enabling the study of MTBP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MTBP pathway restoration in tumor cells with silenced or reduced MTBP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.