Tak1 Lentiviral Activation Particles (m2): sc-424044-LAC-2

Mouse Map3k7 encodes TAK1 (TGF-β–activated kinase 1), a MAP3K that integrates signals from TGF-β/BMP receptors, TNF receptor superfamily members, Toll-like receptors, and IL-1 receptor complexes to activate downstream NF-κB and MAPK cascades (JNK, p38, and ERK). Through phosphorylation of MAP2Ks and the IKK complex via TAB adaptors, TAK1 regulates inflammatory and innate immune signaling, stress responses, apoptosis/survival decisions, and tissue homeostasis in multiple cell types. Dysregulated TAK1 signaling is linked to aberrant cytokine production, impaired barrier integrity, and pathological remodeling in models of inflammatory disease, autoimmunity, and cancer-associated signaling networks. Map3k7-targeted gene editing supports mechanistic dissection of receptor-proximal signaling, pathway crosstalk, and cell-type–specific phenotypes using knockout/knockin, epitope tagging, or kinase-domain perturbation in mouse cells and in vivo systems.

Tak1 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 Map3k7 upregulation across a broader range of human cell types.

Tak1 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 Map3k7 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Tak1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Map3k7 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.