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.
Tctex1 CRISPR Activation Plasmid (h): sc-402886-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tctex1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Tctex1 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 Tctex1 CRISPR Activation Plasmid (h) and Tctex1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DYNLT1 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: Tctex1 Antibody (H-11): sc-365567
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tctex1 CRISPR Activation Plasmid (h) | sc-402886-ACT | 20 µg | $397.00 | |||
Tctex1 CRISPR Activation Plasmid (h2) | sc-402886-ACT-2 | 20 µg | $397.00 |
Human DYNLT1 encodes Tctex1, a dynein light chain that assembles with cytoplasmic dynein to support microtubule-based transport, organelle positioning, and intracellular trafficking. Through interactions within the dynein–dynactin motor complex, Tctex1 contributes to processes such as mitotic spindle organization, centrosome function, and cargo movement that shape cell polarity and division. DYNLT1-dependent transport has been linked to neuronal and ciliary biology via regulation of protein localization and signaling compartmentalization. Dysregulation of dynein-associated transport pathways is frequently studied in the context of neurodegenerative mechanisms and altered proliferative states, making DYNLT1 a useful node for investigating cytoskeletal dynamics and signaling outcomes.
Tctex1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DYNLT1 expression without altering the underlying DNA sequence.
Tctex1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DYNLT1 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 DYNLT1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Tctex1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DYNLT1 locus and enabling the study of Tctex1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Tctex1 pathway restoration in tumor cells with silenced or reduced DYNLT1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.