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.
TAF II p135 CRISPR Activation Plasmid (h): sc-404230-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TAF II p135 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TAF II p135 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 TAF II p135 CRISPR Activation Plasmid (h) and TAF II p135 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TAF4 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: TAF II p135 Antibody (22): sc-136093
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TAF II p135 CRISPR Activation Plasmid (h) | sc-404230-ACT | 20 µg | $397.00 |
TAF4 encodes TAF II p135, a core subunit of the TFIID complex that coordinates RNA polymerase II transcription initiation by coupling promoter recognition to assembly of the preinitiation complex. Through interactions with TBP and other TAFs, TAF II p135 integrates activator-driven signals with basal transcription machinery to regulate genes controlling cell-cycle progression, differentiation, and stress-responsive programs. As part of general transcription control, altered TAF4 activity can remodel global transcriptional output and impact proteostasis and chromatin-associated regulatory networks. Dysregulation of TFIID components, including TAF4, has been linked to transcriptional reprogramming observed in proliferative and developmental disorders, supporting its utility as a mechanistic node in gene regulation studies.
TAF II p135 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TAF4 expression without altering the underlying DNA sequence.
TAF II p135 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TAF4 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 TAF4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TAF II p135 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TAF4 locus and enabling the study of TAF II p135-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TAF II p135 pathway restoration in tumor cells with silenced or reduced TAF4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.