CSH1 CRISPR Activation Plasmid (h): sc-401213-ACT

CSH1 encodes chorionic somatomammotropin hormone 1, a placental glycoprotein hormone in the growth hormone/prolactin family that modulates maternal metabolic adaptation and supports fetal growth during pregnancy. CSH1 is predominantly expressed by syncytiotrophoblasts and acts through cytokine receptor–associated signaling, including JAK/STAT and related transcriptional programs that coordinate nutrient partitioning, insulin sensitivity, and lactogenic responses. Altered placental expression of CSH1 has been associated in the literature with impaired placental function and adverse pregnancy phenotypes, making it a useful molecular readout for trophoblast differentiation and endocrine placental biology. In research settings, CSH1 is commonly leveraged as a marker and functional node within pathways governing placental development, hormone secretion, and maternal–fetal communication.

CSH1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSH1 expression without altering the underlying DNA sequence.

CSH1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CSH1 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 CSH1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CSH1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CSH1 locus and enabling the study of CSH1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CSH1 pathway restoration in tumor cells with silenced or reduced CSH1 expression.

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