TAL2 CRISPR Activation Plasmid (m): sc-423262-ACT

Mouse Tal2 encodes the basic helix-loop-helix transcription factor TAL2, a DNA-binding regulator that influences lineage specification and differentiation programs through transcriptional networks. TAL2 activity intersects with core developmental gene regulatory circuitry, where bHLH factors coordinate chromatin accessibility and cell state transitions. In hematopoietic and neural contexts, dysregulated TAL2 expression has been linked to aberrant transcriptional control and oncogenic gene expression signatures, supporting its use as a mechanistic entry point for studying transformation-associated pathways. As a nuclear transcription factor, TAL2 provides a tractable model for probing upstream regulators, downstream targets, and context-dependent gene network rewiring.

TAL2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Tal2 expression without altering the underlying DNA sequence.

TAL2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Tal2 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 Tal2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TAL2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Tal2 locus and enabling the study of TAL2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TAL2 pathway restoration in tumor cells with silenced or reduced Tal2 expression.

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