LITAF CRISPR Activation Plasmid (h): sc-404337-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LITAF CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- LITAF 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 LITAF CRISPR Activation Plasmid (h) and LITAF CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the LITAF 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: LITAF Antibody (C-5): sc-166719
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LITAF CRISPR Activation Plasmid (h) | sc-404337-ACT | 20 µg | $397.00 | |||
LITAF CRISPR Activation Plasmid (h2) | sc-404337-ACT-2 | 20 µg | $397.00 |
LITAF (lipopolysaccharide-induced TNF factor) is a transcriptional regulator implicated in innate immune signaling and inflammatory gene expression, including modulation of TNF and other cytokine-responsive programs. The protein interfaces with stress- and pathogen-sensing pathways and contributes to endosomal/lysosomal trafficking processes that shape receptor turnover and downstream signaling outputs. Altered LITAF activity has been associated with dysregulated inflammation and cellular stress responses, and genetic perturbation has been linked to neuropathic and immune-related phenotypes. These features make LITAF a useful node for studying transcriptional control of cytokine networks, membrane trafficking–inflammation crosstalk, and context-dependent regulation of immune homeostasis.
LITAF CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LITAF expression without altering the underlying DNA sequence.
LITAF CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LITAF 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 LITAF transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LITAF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LITAF locus and enabling the study of LITAF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LITAF pathway restoration in tumor cells with silenced or reduced LITAF expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.