Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TFIIIB'' CRISPR Activation Plasmid (m): sc-436781-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TFIIIB″ CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TFIIIB″ CRISPR Activation Plasmid (m) 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 TFIIIB″ CRISPR Activation Plasmid (m) and TFIIIB″ CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Bdp1 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: BDP1 Antibody (B-6): sc-515058
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TFIIIB'' CRISPR Activation Plasmid (m) | sc-436781-ACT | 20 µg | $397.00 |
Mouse Bdp1 encodes a core subunit of the RNA polymerase III general transcription factor TFIIIB (TFIIIB''), which cooperates with TBP and BRF proteins to assemble the preinitiation complex at Pol III promoters. Through this activity, TFIIIB'' supports transcription of small noncoding RNAs such as tRNAs and other Pol III-dependent transcripts, linking Bdp1 function to protein synthesis capacity, cell growth, and stress-adaptive programs. Pol III transcriptional control is tightly connected to nutrient- and mitogen-responsive signaling pathways and is frequently altered in contexts of dysregulated proliferation. Because Pol III output influences translational homeostasis and metabolic adaptation, perturbing Bdp1 provides a tractable entry point for studying transcriptional supply lines that can become imbalanced in disease-associated states.
TFIIIB″ CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Bdp1 expression without altering the underlying DNA sequence.
TFIIIB″ CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Bdp1 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 Bdp1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TFIIIB″ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Bdp1 locus and enabling the study of TFIIIB″-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TFIIIB″ pathway restoration in tumor cells with silenced or reduced Bdp1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.