Date published: 2026-7-23

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GATA-1 CRISPR/Cas9 KO Plasmid (h): sc-400396

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • GATA-1 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 GATA-1 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: GATA-1 Antibody (N6): sc-265
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    GATA-1 CRISPR/Cas9 KO Plasmid (h)

    sc-400396
    20 µg
    $397.00

    Overview

    GATA1 encodes GATA-1, a zinc finger transcription factor that binds WGATAR motifs to control lineage-specific gene expression during hematopoiesis. It is essential for erythroid maturation and megakaryocyte differentiation, coordinating programs that govern hemoglobinization, cell-cycle exit, and terminal differentiation through partnerships with cofactors such as FOG1 (ZFPM1) and modulation of chromatin remodeling. GATA-1 activity integrates with erythropoietin/JAK–STAT signaling and broader transcriptional networks to shape erythroid and platelet gene expression. Dysregulation or mutation of GATA1 has strong relevance to disorders of blood cell development and differentiation, including congenital cytopenias and myeloid leukemias characterized by altered erythroid/megakaryocytic programs.

    GATA-1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GATA1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GATA1 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 GATA1 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 GATA-1 protein expression.

    This CRISPR knockout system enables efficient generation of GATA1-deficient cell models for investigation of GATA-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting GATA1 exon(s) critical for GATA-1 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 GATA1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by GATA-1 CRISPR/Cas9 KO Plasmid (h) and GATA-1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GATA1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by GATA-1 HDR Plasmid (h) and GATA-1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GATA1 homology arms to support homology-directed repair at defined GATA1 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.