In Stock Cell Lines
Homo sapiens (Human)
Ovary
Adherent
The B2M Knockout SK-OV-3 Cell Line is a CRISPR/Cas9-edited ovarian adenocarcinoma model with targeted disruption of the B2M gene, encoding beta-2-microglobulin. Loss of this MHC class I light chain abrogates HLA class I surface expression, impairing CD8+ T cell recognition while potentially sensitizing tumors to NK cell killing. This cell line enables immune evasion studies, immunotherapy testing, and MHC class I regulation research driven by interferons and CIITA. Interacting factors such as calreticulin and TAP1/TAP2 are disrupted, and applications include co-culture cytotoxicity assays, flow cytometry, and drug screening.
NEFH Knockout A2780 Polyclonal Cells
Cat. No. ARG19136
FAM111A Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17685
MS4A7 Knockout NCI-H1703 Polyclonal Cells
Cat. No. ARG12571
LRFN3 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7143
DFFA Knockout HEK293T Polyclonal Cells
Cat. No. ARG3817
DCUN1D3 Knockout AGS Polyclonal Cells
Cat. No. ARG2167
The B2M Knockout SK-OV-3 Cell Line is a CRISPR/Cas9-edited cell model featuring targeted disruption of the B2M gene in the SK-OV-3 ovarian adenocarcinoma background. This ready-to-use knockout cell line provides constitutive loss of beta-2-microglobulin, ensuring stable MHC class I deficiency for immunological studies without reliance on transient gene silencing or antibody blockade. It is suitable for in vitro functional assays and co-culture systems requiring long-term B2M ablation.
The host SK-OV-3 cell line is a well-characterized human ovarian adenocarcinoma epithelial line originally isolated from malignant ascites. Exhibiting adherent epithelial morphology, SK-OV-3 cells are extensively used in ovarian cancer research, including studies of cell signaling, drug resistance, and tumor microenvironment interactions. Its derivation from a metastatic site makes it particularly relevant for investigating immune escape mechanisms within the peritoneal cavity.
The B2M gene encodes beta-2-microglobulin, a small extracellular protein that non-covalently associates with the heavy chains of HLA class I molecules (HLA-A, HLA-B, HLA-C) to form peptide-presenting complexes on the cell surface. Beta-2-microglobulin is essential for stabilizing the peptide-loading complex, which includes the chaperones calreticulin, tapasin, and ERp57, as well as the TAP1/TAP2 peptide transporters. Transcription of B2M is induced by interferons (IFN-??, IFN-??) through the transcription factors NF-??B, IRF1, and CIITA, thereby linking inflammation to antigen presentation. As the obligate light chain, B2M enables display of antigen peptides to CD8+ T cell receptors and influences NK cell recognition via missing-self.
Disruption of B2M in SK-OV-3 cells abrogates surface MHC class I expression, rendering them invisible to CD8+ T cell-mediated killing while potentially increasing susceptibility to NK cell cytotoxicity due to reduced engagement of inhibitory KIRs. This dual immune phenotype provides a powerful tool to dissect adaptive and innate immune surveillance mechanisms in the context of ovarian cancer. The model is particularly valuable for evaluating therapeutic strategies designed to exploit missing-self recognition or to restore MHC class I-independent antitumor immunity.
Researchers can utilize this knockout cell line in a variety of assays, including co-cultures with antigen-specific CD8+ T cells or ex vivo?Cexpanded NK cells to measure tumor cell lysis by flow cytometry or ELISA-based IFN-?? detection. It is suited for mechanistic studies on MHC class I transcriptional regulation by interferons and CIITA, and for drug screening campaigns seeking compounds that upregulate alternative antigen presentation pathways. Additional applications include vaccine development, allograft rejection modeling, and investigation of beta-2-microglobulin-associated amyloidosis. For additional technical information or support, please contact Ascent Research.
