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.
Sar1a CRISPR Activation Plasmid (h): sc-404190-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sar1a CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Sar1a 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 Sar1a CRISPR Activation Plasmid (h) and Sar1a CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SAR1A 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: Sar1a Antibody (K-44): sc-130463
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sar1a CRISPR Activation Plasmid (h) | sc-404190-ACT | 20 µg | $397.00 |
Human SAR1A encodes Sar1a, a small COPII-associated GTPase that initiates budding of transport vesicles from the endoplasmic reticulum and supports ER-to-Golgi trafficking. By cycling between GDP- and GTP-bound states, Sar1a recruits Sec23/24 and Sec13/31 coat components to regulate cargo selection, vesicle curvature, and secretory flux. SAR1A-dependent trafficking intersects with proteostasis pathways including ER stress signaling and the unfolded protein response, influencing the cellular handling of membrane and secreted proteins. Dysregulated secretory pathway dynamics and ER homeostasis are commonly implicated in disease-relevant phenotypes such as altered extracellular matrix deposition, aberrant receptor trafficking, and stress-adaptive signaling in transformed cells.
Sar1a CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SAR1A expression without altering the underlying DNA sequence.
Sar1a CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SAR1A 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 SAR1A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Sar1a expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SAR1A locus and enabling the study of Sar1a-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Sar1a pathway restoration in tumor cells with silenced or reduced SAR1A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.