Date published: 2026-7-2

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Hemoglobin α1 CRISPR/Cas9 KO Plasmid (m): sc-420800

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Hemoglobin α1 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 Hemoglobin α1 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Hemoglobin α1 CRISPR/Cas9 KO Plasmid (m)

    sc-420800
    20 µg
    $397.00

    Overview

    Hba-a1 encodes the mouse hemoglobin α1 subunit, a core component of the adult hemoglobin tetramer that binds heme and supports reversible oxygen transport in erythrocytes. Its expression is tightly coordinated during erythropoiesis with β-globin genes and heme biosynthetic enzymes, linking Hba-a1 to globin gene regulation, iron handling, and red blood cell maturation. Disruption of α-globin dosage perturbs hemoglobin assembly and redox balance, promoting ineffective erythropoiesis and hemolytic stress phenotypes that model features of α-thalassemia and related anemia biology. As a highly expressed, lineage-restricted gene, Hba-a1 is commonly used to interrogate regulatory architecture at the α-globin locus and mechanisms governing erythroid differentiation.

    Hemoglobin α1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Hba-a1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Hba-a1 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 Hba-a1 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 Hemoglobin α1 protein expression.

    This CRISPR knockout system enables efficient generation of Hba-a1-deficient cell models for investigation of Hemoglobin α1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Hba-a1 exon(s) critical for Hemoglobin α1 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 Hba-a1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Hemoglobin α1 CRISPR/Cas9 KO Plasmid (m) and Hemoglobin α1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Hba-a1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Hemoglobin α1 HDR Plasmid (m) and Hemoglobin α1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Hba-a1 homology arms to support homology-directed repair at defined Hba-a1 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.