
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BDNF CRISPR Activation Plasmid (m) | sc-419319-ACT | 20 µg | $397.00 | |||
BDNF CRISPR Activation Plasmid (m2) | sc-419319-ACT-2 | 20 µg | $397.00 |
Mouse Bdnf encodes brain-derived neurotrophic factor (BDNF), a secreted neurotrophin that binds TRKB/NTRK2 and p75NTR to regulate neuronal survival, differentiation, synaptic plasticity, and activity-dependent circuit remodeling. BDNF signaling engages MAPK/ERK, PI3K–AKT, and PLCγ pathways to modulate transcriptional programs, dendritic spine dynamics, and neurotransmitter release. In the central nervous system, BDNF is central to learning and memory processes and contributes to experience-dependent plasticity. Altered Bdnf expression or signaling has been linked to neurodevelopmental and neuropsychiatric phenotypes and is widely studied in models of neurodegeneration, stress responsivity, and metabolic regulation.
BDNF CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Bdnf expression without altering the underlying DNA sequence.
BDNF CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Bdnf 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 Bdnf transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BDNF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Bdnf locus and enabling the study of BDNF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BDNF pathway restoration in tumor cells with silenced or reduced Bdnf expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.