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.
Sar1B CRISPR Activation Plasmid (m): sc-425994-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sar1B CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Sar1B CRISPR Activation Plasmid (m) 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 Sar1B CRISPR Activation Plasmid (m) and Sar1B CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Sar1b 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: Sar1B Antibody (AT1C7): sc-517425
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sar1B CRISPR Activation Plasmid (m) | sc-425994-ACT | 20 µg | $397.00 | |||
Sar1B CRISPR Activation Plasmid (m2) | sc-425994-ACT-2 | 20 µg | $397.00 |
Sar1b encodes the small GTPase SAR1B, a core regulator of COPII-coated vesicle biogenesis at endoplasmic reticulum exit sites. By cycling between GDP- and GTP-bound states, SAR1B initiates membrane curvature and recruits COPII components to control ER-to-Golgi trafficking of secretory and membrane proteins, including lipoprotein-associated cargos. Sar1b-dependent transport integrates with ER proteostasis, lipid handling, and the unfolded protein response, making it relevant to studies of intestinal lipid absorption, hepatocyte secretion, and metabolic homeostasis. Disruption of SAR1B function is linked to defects in chylomicron export and systemic lipid distribution, supporting its use as a mechanistic node in models of dyslipidemia and organelle stress.
Sar1B CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Sar1b expression without altering the underlying DNA sequence.
Sar1B CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Sar1b 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 Sar1b transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Sar1B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Sar1b locus and enabling the study of Sar1B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Sar1B pathway restoration in tumor cells with silenced or reduced Sar1b expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.