
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAM98A CRISPR Activation Plasmid (h) | sc-411841-ACT | 20 µg | $397.00 | |||
FAM98A CRISPR Activation Plasmid (h2) | sc-411841-ACT-2 | 20 µg | $397.00 |
FAM98A encodes a conserved RNA-binding protein that localizes predominantly to the cytoplasm and participates in post-transcriptional gene regulation. It has been linked to RNA processing and translation-related protein complexes, supporting cellular proteostasis and growth-associated programs. Altered FAM98A expression has been reported across multiple tumor types and is frequently explored in the context of proliferation, stress-adaptation, and metastasis-associated phenotypes. These attributes make FAM98A a useful target for studying how RNA metabolism interfaces with oncogenic signaling and cellular homeostasis in human model systems.
FAM98A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FAM98A expression without altering the underlying DNA sequence.
FAM98A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FAM98A 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 FAM98A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FAM98A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FAM98A locus and enabling the study of FAM98A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FAM98A pathway restoration in tumor cells with silenced or reduced FAM98A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.