hnRNP A3 CRISPR/Cas9 KO Plasmid (h): sc-418346
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- hnRNP A3 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 hnRNP A3 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
hnRNP A3 CRISPR/Cas9 KO Plasmid (h) | sc-418346 | 20 µg | $397.00 |
Overview
HNRNPA3 encodes heterogeneous nuclear ribonucleoprotein A3 (hnRNP A3), an RNA-binding protein that associates with pre-mRNAs and mature transcripts to regulate alternative splicing, mRNA stability, and nucleocytoplasmic transport. hnRNP A3 participates in ribonucleoprotein complex assembly and helps coordinate gene expression programs linked to RNA processing and translation. Dysregulation of hnRNP family members is frequently connected to altered RNA metabolism, stress granule dynamics, and proteostasis pathways. These processes are relevant to disease biology where aberrant post-transcriptional regulation and aggregation-prone RNA-binding proteins contribute to cellular dysfunction.
hnRNP A3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the HNRNPA3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the HNRNPA3 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 HNRNPA3 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 hnRNP A3 protein expression.
This CRISPR knockout system enables efficient generation of HNRNPA3-deficient cell models for investigation of hnRNP A3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting HNRNPA3 exon(s) critical for hnRNP A3 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 HNRNPA3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by hnRNP A3 CRISPR/Cas9 KO Plasmid (h) and hnRNP A3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the HNRNPA3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by hnRNP A3 HDR Plasmid (h) and hnRNP A3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by HNRNPA3 homology arms to support homology-directed repair at defined HNRNPA3 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.