B-Myb CRISPR Activation Plasmid (h): sc-401318-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- B-Myb CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- B-Myb CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by B-Myb CRISPR Activation Plasmid (h) and B-Myb CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the MYBL2 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: B-Myb Antibody (C-5): sc-390198
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
B-Myb CRISPR Activation Plasmid (h) | sc-401318-ACT | 20 µg | $397.00 | |||
B-Myb CRISPR Activation Plasmid (h2) | sc-401318-ACT-2 | 20 µg | $397.00 |
MYBL2 encodes the human B-Myb transcription factor, a Myb family regulator required for cell-cycle progression and proliferative gene expression programs. B-Myb supports S-phase entry and mitotic progression by coordinating transcriptional networks that intersect with CDK activity, E2F-dependent signaling, and DNA replication and repair processes. Dysregulated MYBL2 expression has been associated with genomic instability and altered checkpoint control, and it is frequently linked to proliferative phenotypes across diverse cancer-relevant contexts. As a nuclear transcriptional regulator, B-Myb is commonly studied for its role in lineage expansion, stress responses, and transcriptional control of G2/M gene modules.
B-Myb CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYBL2 expression without altering the underlying DNA sequence.
B-Myb CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYBL2 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 MYBL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous B-Myb expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYBL2 locus and enabling the study of B-Myb-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of B-Myb pathway restoration in tumor cells with silenced or reduced MYBL2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.