CREB3L1 CRISPR Activation Plasmid (h): sc-405316-ACT

CREB3L1 (cAMP responsive element binding protein 3-like 1) is a membrane-tethered bZIP transcription factor that becomes activated through regulated intramembrane proteolysis and translocates to the nucleus to control gene expression programs linked to endoplasmic reticulum stress and secretory pathway adaptation. It influences extracellular matrix production and differentiation-associated transcriptional networks, integrating signals that coordinate collagen biosynthesis, cellular stress responses, and proteostasis. CREB3L1 activity has been implicated in contexts of altered tissue remodeling and cell-state transitions, making it relevant for mechanistic studies of fibrosis-like transcriptional programs and tumor-associated changes in invasion, metastasis, and stress tolerance. As a transcriptional regulator, it provides a tractable node for dissecting how ER stress signaling intersects with matrix remodeling and lineage-specific gene expression.

CREB3L1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CREB3L1 expression without altering the underlying DNA sequence.

CREB3L1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CREB3L1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the CREB3L1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CREB3L1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CREB3L1 locus and enabling the study of CREB3L1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CREB3L1 pathway restoration in tumor cells with silenced or reduced CREB3L1 expression.

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