ATF4 CRISPR/Cas9 KO Plasmid (h2): sc-400155-KO-2
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ATF4 CRISPR/Cas9 Knockout (KO) Plasmid (h2) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the ATF4 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ATF4 Antibody (B-3): sc-390063
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATF4 CRISPR/Cas9 KO Plasmid (h2) | sc-400155-KO-2 | 20 µg | $397.00 |
Overview
Activating transcription factor 4 (ATF4) is a bZIP transcription factor central to the integrated stress response, where it is preferentially translated following eIF2α phosphorylation and coordinates adaptive transcriptional programs. ATF4 regulates amino acid metabolism, redox homeostasis, autophagy, and ER stress signaling, including crosstalk with PERK–EIF2AK3, ATF3, and CHOP/DDIT3 to balance survival and apoptotic outcomes. Through control of nutrient sensing and proteostasis, ATF4 influences mitochondrial function and cellular differentiation programs, and it contributes to transcriptional rewiring during hypoxia and oxidative stress. Dysregulated ATF4 activity has been implicated in cancer cell stress adaptation, neurodegeneration-associated proteotoxic stress, and metabolic disease phenotypes, making it a key node for mechanistic studies of stress-responsive gene networks.
ATF4 CRISPR/Cas9 KO Plasmid (h2) is a pool of plasmids designed for targeted disruption of the ATF4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATF4 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the ATF4 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish ATF4 protein expression.
This CRISPR knockout system enables efficient generation of ATF4-deficient cell models for investigation of ATF4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ATF4 exon(s) critical for ATF4 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple ATF4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ATF4 CRISPR/Cas9 KO Plasmid (h) and ATF4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATF4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ATF4 HDR Plasmid (h) and ATF4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATF4 homology arms to support homology-directed repair at defined ATF4 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.