FOXD1 CRISPR Activation Plasmid (m): sc-420847-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FOXD1 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- FOXD1 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 FOXD1 CRISPR Activation Plasmid (m) and FOXD1 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Foxd1 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: FOXD1 Antibody (2C10): sc-293238
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FOXD1 CRISPR Activation Plasmid (m) | sc-420847-ACT | 20 µg | $397.00 |
Foxd1 encodes the forkhead box transcription factor FOXD1, a nuclear DNA-binding protein that regulates lineage specification and patterning during embryonic development. In mouse, FOXD1 is best known for roles in renal stromal progenitors and nephrogenesis, where it coordinates mesenchymal programs that influence ureteric branching, extracellular matrix remodeling, and epithelial–stromal signaling. FOXD1 activity intersects with core developmental pathways, including WNT, BMP, and TGF-β signaling, to shape organ morphogenesis and cell fate decisions. Dysregulated FOXD1-driven transcriptional networks are relevant to developmental abnormalities and are frequently leveraged to study mechanisms of differentiation, fibrosis-associated stromal activation, and context-dependent oncogenic transcriptional programs.
FOXD1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Foxd1 expression without altering the underlying DNA sequence.
FOXD1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Foxd1 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 Foxd1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FOXD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Foxd1 locus and enabling the study of FOXD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FOXD1 pathway restoration in tumor cells with silenced or reduced Foxd1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.