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.
HIF1a CRISPR Activation Plasmid (m): sc-420856-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HIF1a CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- HIF1a 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 HIF1a CRISPR Activation Plasmid (m) and HIF1a CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Hif1a 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: HIF1a Antibody (28b): sc-13515
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HIF1a CRISPR Activation Plasmid (m) | sc-420856-ACT | 20 µg | $397.00 | |||
HIF1a CRISPR Activation Plasmid (m2) | sc-420856-ACT-2 | 20 µg | $397.00 |
Mouse Hif1a encodes hypoxia-inducible factor 1 alpha (HIF1a), an oxygen-sensitive transcription factor that integrates cellular responses to reduced oxygen tension. Stabilized HIF1a dimerizes with ARNT to activate hypoxia response element–containing genes that regulate glycolytic metabolism, angiogenic signaling, erythropoiesis, mitochondrial function, and cell survival, intersecting with PI3K–AKT–mTOR and MAPK pathway inputs. HIF1a also coordinates inflammatory and immune programs through crosstalk with NF-κB and redox pathways, shaping myeloid polarization and barrier adaptation. Dysregulated HIF1a signaling is widely used as a mechanistic node in studies of ischemia, chronic inflammation, fibrosis, metabolic disease, and tumor hypoxia biology in mouse model systems.
HIF1a CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Hif1a expression without altering the underlying DNA sequence.
HIF1a CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Hif1a 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 Hif1a transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HIF1a expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Hif1a locus and enabling the study of HIF1a-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HIF1a pathway restoration in tumor cells with silenced or reduced Hif1a expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.