HNRNPA1L2 CRISPR Activation Plasmid (h): sc-403579-ACT

HNRNPA1L2 encodes a heterogeneous nuclear ribonucleoprotein A1-like factor implicated in RNA binding and post-transcriptional gene regulation, including pre-mRNA splicing, mRNA stability, and nucleocytoplasmic transport. As part of ribonucleoprotein complexes, HNRNPA1L2 is positioned to influence transcript isoform choice and the coupling between transcription and RNA processing, shaping gene expression programs in a context-dependent manner. Altered regulation of hnRNP-family proteins has been associated with dysregulated RNA metabolism, aberrant splicing patterns, and cellular stress responses relevant to cancer biology and neurodegeneration research. These features make HNRNPA1L2 a useful target for dissecting RNA processing networks and their downstream effects on proteome diversity.

HNRNPA1L2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HNRNPA1L2 expression without altering the underlying DNA sequence.

HNRNPA1L2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HNRNPA1L2 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 HNRNPA1L2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HNRNPA1L2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HNRNPA1L2 locus and enabling the study of HNRNPA1L2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HNRNPA1L2 pathway restoration in tumor cells with silenced or reduced HNRNPA1L2 expression.

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