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.
Tak1L CRISPR Activation Plasmid (h): sc-406747-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tak1L CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Tak1L 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 Tak1L CRISPR Activation Plasmid (h) and Tak1L CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the MAP3K7CL 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: Tak1L Antibody (G-8): sc-515478
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tak1L CRISPR Activation Plasmid (h) | sc-406747-ACT | 20 µg | $397.00 | |||
Tak1L CRISPR Activation Plasmid (h2) | sc-406747-ACT-2 | 20 µg | $397.00 |
MAP3K7CL encodes Tak1L, a MAP kinase kinase kinase–like protein related to the TAK1/MAP3K7 signaling module that couples upstream cues to downstream kinase cascades. Proteins in this axis are commonly linked to regulation of NF-κB and MAPK pathways, shaping inflammatory signaling, stress responses, and context-dependent control of transcriptional programs. Although MAP3K7CL remains less well characterized than canonical TAK1, its similarity to MAP3K family members makes it relevant for investigating kinase-network wiring, pathway redundancy, and compensatory signaling. Dysregulation of TAK1-associated signaling is implicated in immune and inflammatory phenotypes and cancer-associated signaling states, supporting exploratory studies of MAP3K7CL function in disease-relevant cellular models.
Tak1L CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAP3K7CL expression without altering the underlying DNA sequence.
Tak1L CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAP3K7CL 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 MAP3K7CL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Tak1L expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAP3K7CL locus and enabling the study of Tak1L-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Tak1L pathway restoration in tumor cells with silenced or reduced MAP3K7CL expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.