
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CEP192 Lentiviral Activation Particles (h2) | sc-406971-LAC-2 | 200 µl | $455.00 |
Human CEP192 encodes a centrosomal scaffold protein essential for centrosome maturation and microtubule-organizing center (MTOC) activity, coordinating recruitment of pericentriolar material and promoting proper bipolar spindle assembly during mitosis. CEP192 functions within core centrosome duplication and cell-cycle control pathways, interfacing with regulators such as PLK1 and AURKA to support microtubule nucleation and mitotic progression. Dysregulation or mutation of CEP192 has been associated with chromosomal instability and aberrant centrosome number, features linked to developmental disorders and cancer-related proliferative phenotypes. Gene editing of CEP192 enables mechanistic studies of centrosome biology, spindle checkpoint integrity, and genome stability using cellular models, including live-cell imaging and proteomic mapping of centrosomal complexes.
CEP192 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient CEP192 upregulation across a broader range of human cell types.
CEP192 Lentiviral Activation Particles (h2) 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 CEP192 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CEP192 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CEP192 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.