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.
Titin CRISPR Activation Plasmid (h): sc-402827-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Titin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Titin 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 Titin CRISPR Activation Plasmid (h) and Titin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TTN 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: Titin Antibody (E-2): sc-271946
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Titin CRISPR Activation Plasmid (h) | sc-402827-ACT | 20 µg | $397.00 | |||
Titin CRISPR Activation Plasmid (h2) | sc-402827-ACT-2 | 20 µg | $397.00 |
Human TTN encodes titin, a giant sarcomeric protein that spans from the Z-disc to the M-line and functions as a molecular scaffold and spring to maintain myofibril integrity, passive elasticity, and force transmission in striated muscle. Titin coordinates sarcomere assembly through interactions with actin, myosin, and Z-disc/M-line complexes, and contributes to mechanosensing processes that couple stretch to remodeling of the contractile apparatus. TTN activity is integrated with muscle structural homeostasis pathways, including cytoskeletal organization, protein quality control, and stress-responsive signaling that shapes cardiomyocyte and skeletal myofiber function. Genetic variation and dysregulation of TTN are strongly associated with muscle disease phenotypes, making it a central locus for studying sarcomere biology and genotype–function relationships in human models.
Titin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TTN expression without altering the underlying DNA sequence.
Titin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TTN 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 TTN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Titin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TTN locus and enabling the study of Titin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Titin pathway restoration in tumor cells with silenced or reduced TTN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.