MAP-1B CRISPR Activation Plasmid (h): sc-400981-ACT

Human MAP1B encodes microtubule-associated protein 1B (MAP-1B), a cytoskeletal regulator that binds microtubules and promotes their stabilization and dynamic remodeling during neuronal development. MAP-1B supports axon outgrowth, growth cone guidance, and neurite extension by coordinating microtubule–actin crosstalk and intracellular transport processes required for polarized cell architecture. Its activity intersects with signaling programs that modulate cytoskeletal organization, including pathways governing neuritogenesis and synaptic maturation. Altered MAP1B expression or regulation has been linked to neurodevelopmental phenotypes and neurologic disease-relevant cellular dysfunction, making it a useful target for mechanistic studies of neuronal structure and connectivity.

MAP-1B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAP1B expression without altering the underlying DNA sequence.

MAP-1B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAP1B 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 MAP1B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MAP-1B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAP1B locus and enabling the study of MAP-1B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MAP-1B pathway restoration in tumor cells with silenced or reduced MAP1B expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.