CTDSPL2 Lentiviral Activation Particles (m2): sc-435953-LAC-2

Mouse Ctdspl2 encodes CTDSPL2, a nuclear haloacid dehalogenase (HAD) family phosphatase implicated in transcriptional regulation through dephosphorylation of serine residues within the RNA polymerase II C-terminal domain, thereby influencing gene expression programs linked to cell-cycle control and differentiation. CTDSPL2 is positioned within phosphatase-mediated signaling networks that coordinate chromatin-associated processes, RNA processing, and developmental pathway outputs in mammalian cells. Dysregulation of CTD-directed phosphatase activity is broadly relevant to models of proliferative stress and altered lineage commitment, making Ctdspl2 a useful target for studying phospho-dependent transcriptional control mechanisms. Gene editing of Ctdspl2 in mouse systems supports functional interrogation of nuclear phosphatase activity, mapping downstream transcriptional consequences by RNA-seq/ChIP-based assays, and dissecting pathway interactions in engineered cell lines or in vivo genetic models.

CTDSPL2 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Ctdspl2 upregulation across a broader range of human cell types.

CTDSPL2 Lentiviral Activation Particles (m2) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Ctdspl2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CTDSPL2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ctdspl2 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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