HLA-F CRISPR/Cas9 KO Plasmid (h): sc-410821

Overview

HLA-F encodes a non-classical MHC class I molecule that participates in immune surveillance by shaping interactions between antigen-presenting cells and lymphocytes through binding to inhibitory and activating receptors on NK cells and subsets of T cells. Unlike highly polymorphic classical HLA-I proteins, HLA-F displays distinctive expression dynamics, including intracellular retention and surface upregulation under cellular stress, infection, or activation states, supporting modulation of immune checkpoints and tolerance. HLA-F contributes to antigen presentation-related processes, regulation of cytotoxic responses, and immune evasion mechanisms within inflamed tissues and tumor microenvironments. Dysregulated HLA-F expression has been reported across multiple immune-mediated and oncologic contexts, making it relevant for dissecting pathways controlling immune activation, interferon responses, and cell–cell recognition.

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

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

Key Features

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

Design Variants

CRISPRs +/- HDRs

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