
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLAIN2 CRISPR Activation Plasmid (m) | sc-429242-ACT | 20 µg | $397.00 |
Slain2 encodes SLAIN2, a microtubule plus-end–tracking adaptor that cooperates with EB proteins and the ch-TOG/XMAP215 complex to promote persistent microtubule growth and coordinate cytoskeletal organization. By regulating microtubule dynamics, SLAIN2 influences intracellular transport, cell polarity, and mitotic spindle function, processes central to neuronal morphogenesis and proliferative control. Perturbation of microtubule regulatory networks can disrupt axon outgrowth and synaptic connectivity and can also impact chromosomal stability through altered spindle assembly. For mouse biomedical research, Slain2 provides a tractable entry point to study how microtubule plus-end regulation interfaces with cell-cycle progression and differentiation programs.
SLAIN2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Slain2 expression without altering the underlying DNA sequence.
SLAIN2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Slain2 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 Slain2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLAIN2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Slain2 locus and enabling the study of SLAIN2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLAIN2 pathway restoration in tumor cells with silenced or reduced Slain2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.