
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIP60 CRISPR Activation Plasmid (h) | sc-400810-ACT | 20 µg | $397.00 |
KAT5 encodes TIP60 (KAT5), a MYST family histone acetyltransferase that acetylates histones and non-histone substrates to regulate chromatin accessibility, transcriptional programs, and genome stability. TIP60 functions in multiprotein complexes that coordinate DNA double-strand break signaling and repair, including ATM-dependent responses, and it modulates cell cycle checkpoints, apoptosis, and replication stress pathways. Through its roles in epigenetic control and DNA damage response, altered TIP60 activity has been linked to dysregulated transcription networks and genomic instability observed across multiple cancer and neurodegeneration-relevant contexts.
TIP60 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KAT5 expression without altering the underlying DNA sequence.
TIP60 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KAT5 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 KAT5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TIP60 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KAT5 locus and enabling the study of TIP60-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TIP60 pathway restoration in tumor cells with silenced or reduced KAT5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.