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.
α1a Tubulin CRISPR Activation Plasmid (h): sc-400022-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1a Tubulin CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- α1a Tubulin CRISPR Activation Plasmid (h) 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 α1a Tubulin CRISPR Activation Plasmid (h) and α1a Tubulin CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TUBA1A 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: α1a Tubulin Antibody (7-RY28): sc-134237
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α1a Tubulin CRISPR Activation Plasmid (h) | sc-400022-ACT | 20 µg | $397.00 | |||
α1a Tubulin CRISPR Activation Plasmid (h2) | sc-400022-ACT-2 | 20 µg | $397.00 |
TUBA1A encodes human α1a tubulin, a core component of α/β-tubulin heterodimers that polymerize into microtubules to support cytoskeletal architecture, intracellular transport, and mitotic spindle formation. Microtubule dynamics driven by α1a tubulin contribute to cell polarity, axonal growth, and neuronal migration, integrating with pathways controlling cytoskeleton remodeling, cell cycle progression, and motor protein–mediated trafficking. Dysregulated TUBA1A function is associated with neurodevelopmental phenotypes linked to impaired microtubule assembly and altered neuronal connectivity, making it a useful marker for studying cytoskeletal integrity in neural systems. As a broadly expressed structural protein, α1a tubulin is frequently leveraged in assays interrogating microtubule stability, organelle positioning, and differentiation-associated changes in the cytoskeleton.
α1a Tubulin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TUBA1A expression without altering the underlying DNA sequence.
α1a Tubulin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TUBA1A 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 TUBA1A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α1a Tubulin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TUBA1A locus and enabling the study of α1a Tubulin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α1a Tubulin pathway restoration in tumor cells with silenced or reduced TUBA1A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.