ERK 2 Lentiviral Activation Particles (h): sc-400043-LAC

MAPK1 encodes extracellular signal-regulated kinase 2 (ERK2), a core serine/threonine kinase within the RAS–RAF–MEK–ERK MAPK cascade that transduces growth factor and stress signals from the plasma membrane to cytoplasmic and nuclear targets. ERK2 phosphorylates diverse substrates, including transcription factors and cell-cycle regulators, to control proliferation, differentiation, survival, and motility. Through pathway cross-talk with PI3K/AKT, JNK/p38, and feedback regulators such as DUSPs, MAPK1 helps shape signal amplitude and duration across many cell types. Dysregulated ERK signaling is frequently associated with oncogenic signaling states and aberrant inflammatory and neurodevelopmental processes, making MAPK1 a widely used node for mechanistic studies of signal transduction.

ERK 2 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient MAPK1 upregulation across a broader range of human cell types.

ERK 2 Lentiviral Activation Particles (h) 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 MAPK1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ERK 2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MAPK1 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.