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.
PKD2 Lentiviral Activation Particles (m2): sc-430381-LAC-2
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- PKD2 Lentiviral Activation Particles (m2) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- PKD2 Lentiviral Activation Particles (m2) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the 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 PKD2 Lentiviral Activation Plasmid (m2) and PKD2 Lentiviral Activation Plasmid (m22) target distinct regulatory regions of the Prkd2 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: PKD2 Antibody (F-2): sc-374344
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PKD2 Lentiviral Activation Particles (m2) | sc-430381-LAC-2 | 200 µl | $455.00 |
Mouse Prkd2 encodes protein kinase D2 (PKD2), a serine/threonine kinase of the PKD family that transduces signals downstream of diacylglycerol and novel PKC isoforms to coordinate phosphorylation programs controlling gene expression, vesicle trafficking, cytoskeletal dynamics, and cell survival. PKD2 activity is frequently linked to Golgi and membrane-associated signaling, integrating inputs from GPCR and receptor tyrosine kinase pathways to regulate MAPK- and NF-κB-associated responses and stimulus-dependent cellular remodeling. Dysregulation of PRKD2/PKD2 signaling has been associated with aberrant proliferation, inflammatory signaling, and metastatic traits in cancer biology, as well as broader roles in stress and immune-related processes. Gene editing of Prkd2 in mouse models supports mechanistic studies of kinase-domain function, pathway cross-talk, and phosphorylation-dependent phenotypes using proteomics, live-cell imaging, and in vivo disease-relevant paradigms.
PKD2 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 Prkd2 upregulation across a broader range of human cell types.
PKD2 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 Prkd2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PKD2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Prkd2 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.