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(A) Display of <t>ULBP1</t> and CD155 on CombiCells detected by mAbs and NKG2D-Fc, and DNAM-1-Fc, respectively. (B&C) KIR2DL1+ and KIR2DL1-NK-cell degranulation (CD107a upregulation) in response to ULBP1, CD155, and HLA-C*05:01 displayed on CombiCells. (C) Three types of HLA-C*05:01 were tested, all containing P2 (IIDKSGSTV); wild-type, open and dipeptide exchanged. Data from three independent experiments with NK cells from separate donors are shown.
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Transcriptomic profiling reveals upregulation of <t>ULBP1</t> and ferroptosis-related genes following Erastin treatment. (A) Volcano plots showing differentially expressed genes in KELLY and SK-N-AS neuroblastoma cell lines treated with 1 µM and 2 µM Erastin for 24 hours, respectively, compared to DMSO control. Non-significant genes are shown in gray; significantly upregulated and downregulated genes are shown in red and blue, respectively. (B) KEGG pathway enrichment analysis of DEGs in KELLY and SK-N-AS cells, showing significantly enriched pathways including ferroptosis and amino acid metabolism. (C) Gene Ontology (GO) enrichment network highlighting clusters associated with oxidative stress response, amino acid metabolic processes, and signaling receptor binding, with key genes indicated.
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Transcriptomic profiling reveals upregulation of <t>ULBP1</t> and ferroptosis-related genes following Erastin treatment. (A) Volcano plots showing differentially expressed genes in KELLY and SK-N-AS neuroblastoma cell lines treated with 1 µM and 2 µM Erastin for 24 hours, respectively, compared to DMSO control. Non-significant genes are shown in gray; significantly upregulated and downregulated genes are shown in red and blue, respectively. (B) KEGG pathway enrichment analysis of DEGs in KELLY and SK-N-AS cells, showing significantly enriched pathways including ferroptosis and amino acid metabolism. (C) Gene Ontology (GO) enrichment network highlighting clusters associated with oxidative stress response, amino acid metabolic processes, and signaling receptor binding, with key genes indicated.
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Transcriptomic profiling reveals upregulation of <t>ULBP1</t> and ferroptosis-related genes following Erastin treatment. (A) Volcano plots showing differentially expressed genes in KELLY and SK-N-AS neuroblastoma cell lines treated with 1 µM and 2 µM Erastin for 24 hours, respectively, compared to DMSO control. Non-significant genes are shown in gray; significantly upregulated and downregulated genes are shown in red and blue, respectively. (B) KEGG pathway enrichment analysis of DEGs in KELLY and SK-N-AS cells, showing significantly enriched pathways including ferroptosis and amino acid metabolism. (C) Gene Ontology (GO) enrichment network highlighting clusters associated with oxidative stress response, amino acid metabolic processes, and signaling receptor binding, with key genes indicated.
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Image Search Results


(A) Display of ULBP1 and CD155 on CombiCells detected by mAbs and NKG2D-Fc, and DNAM-1-Fc, respectively. (B&C) KIR2DL1+ and KIR2DL1-NK-cell degranulation (CD107a upregulation) in response to ULBP1, CD155, and HLA-C*05:01 displayed on CombiCells. (C) Three types of HLA-C*05:01 were tested, all containing P2 (IIDKSGSTV); wild-type, open and dipeptide exchanged. Data from three independent experiments with NK cells from separate donors are shown.

Journal: bioRxiv

Article Title: Using peptide-exchange systems to interrogate peptide-specific KIR binding to HLA Class I

doi: 10.64898/2026.03.03.708729

Figure Lengend Snippet: (A) Display of ULBP1 and CD155 on CombiCells detected by mAbs and NKG2D-Fc, and DNAM-1-Fc, respectively. (B&C) KIR2DL1+ and KIR2DL1-NK-cell degranulation (CD107a upregulation) in response to ULBP1, CD155, and HLA-C*05:01 displayed on CombiCells. (C) Three types of HLA-C*05:01 were tested, all containing P2 (IIDKSGSTV); wild-type, open and dipeptide exchanged. Data from three independent experiments with NK cells from separate donors are shown.

Article Snippet: Plasmids encoding the ectodomains of ULBP1 (pD649-HAsp-ULBP1-Fc(DAPA)-AviTag-6xHis) and CD155 (pMP71-hCD155) were obtained from Addgene. pMP71-hCD155 was a gift from Sébastien Walchli (Addgene plasmid # 118630; http://n2t.net/addgene:118630 ; RRID:Addgene_118630) [ ]. pD649-HAsp-ULBP1-Fc(DAPA)-AviTag-6xHis was a gift from Chris Garcia (Addgene plasmid # 156597; http://n2t.net/addgene:156597 ; RRID:Addgene_156597) [ ].

Techniques:

Transcriptomic profiling reveals upregulation of ULBP1 and ferroptosis-related genes following Erastin treatment. (A) Volcano plots showing differentially expressed genes in KELLY and SK-N-AS neuroblastoma cell lines treated with 1 µM and 2 µM Erastin for 24 hours, respectively, compared to DMSO control. Non-significant genes are shown in gray; significantly upregulated and downregulated genes are shown in red and blue, respectively. (B) KEGG pathway enrichment analysis of DEGs in KELLY and SK-N-AS cells, showing significantly enriched pathways including ferroptosis and amino acid metabolism. (C) Gene Ontology (GO) enrichment network highlighting clusters associated with oxidative stress response, amino acid metabolic processes, and signaling receptor binding, with key genes indicated.

Journal: Frontiers in Immunology

Article Title: Erastin-induced ferroptosis enhances natural killer cell anti-tumor activity and offers therapeutic potential in neuroblastoma

doi: 10.3389/fimmu.2026.1739503

Figure Lengend Snippet: Transcriptomic profiling reveals upregulation of ULBP1 and ferroptosis-related genes following Erastin treatment. (A) Volcano plots showing differentially expressed genes in KELLY and SK-N-AS neuroblastoma cell lines treated with 1 µM and 2 µM Erastin for 24 hours, respectively, compared to DMSO control. Non-significant genes are shown in gray; significantly upregulated and downregulated genes are shown in red and blue, respectively. (B) KEGG pathway enrichment analysis of DEGs in KELLY and SK-N-AS cells, showing significantly enriched pathways including ferroptosis and amino acid metabolism. (C) Gene Ontology (GO) enrichment network highlighting clusters associated with oxidative stress response, amino acid metabolic processes, and signaling receptor binding, with key genes indicated.

Article Snippet: Separately, NB cells (KELLY, SK-N-AS, SK-N-BE (2), and SK-N-FI) were seeded and washed with PBS, then stained for 30 minutes at 4°C with anti-ULBP1 primary antibody (1:100, clone 170818, R&D systems, #MAB-1380-500) prior to washing and 30 min incubation with secondary antibody (1:500, Invitrogen, # A55747 ).

Techniques: Control, Binding Assay

Low ULBP1 expression correlates with poor prognosis in neuroblastoma patients from the SEQC cohort. Kaplan–Meier overall survival analysis was performed using the SEQC neuroblastoma dataset (n = 498) via the R2 Genomics Analysis and Visualization Platform (A) Complete cohort; (B) MYCN -amplified subset; (C) Patients with progressive disease; (D) INSS stage 4 subset.

Journal: Frontiers in Immunology

Article Title: Erastin-induced ferroptosis enhances natural killer cell anti-tumor activity and offers therapeutic potential in neuroblastoma

doi: 10.3389/fimmu.2026.1739503

Figure Lengend Snippet: Low ULBP1 expression correlates with poor prognosis in neuroblastoma patients from the SEQC cohort. Kaplan–Meier overall survival analysis was performed using the SEQC neuroblastoma dataset (n = 498) via the R2 Genomics Analysis and Visualization Platform (A) Complete cohort; (B) MYCN -amplified subset; (C) Patients with progressive disease; (D) INSS stage 4 subset.

Article Snippet: Separately, NB cells (KELLY, SK-N-AS, SK-N-BE (2), and SK-N-FI) were seeded and washed with PBS, then stained for 30 minutes at 4°C with anti-ULBP1 primary antibody (1:100, clone 170818, R&D systems, #MAB-1380-500) prior to washing and 30 min incubation with secondary antibody (1:500, Invitrogen, # A55747 ).

Techniques: Expressing, Amplification

Erastin treatment increases ULBP1 surface expression and enhances NK cell-mediated cytotoxicity in neuroblastoma cells. (A) Surface expression of ULBP1 was measured by flow cytometry in KELLY, SK-N-AS, SK-N-BE (2), and SK-N-FI cells treated with DMSO (control) or Erastin. (B) NK cell-mediated cytotoxicity assay using NK-92 cells co-cultured with neuroblastoma cells (E:T ratio was 8:1) pre-treated with either DMSO (Control), Erastin, or Erastin in combination with Liproxstatin-1 (Lip-1). Cell lysis percentages were quantified in KELLY, SK-N-AS, and SK-N-FI cells. n = 3 biologically independent experiments. *P<0.05, **P<0.01, ***P<0.001; Paired t test.

Journal: Frontiers in Immunology

Article Title: Erastin-induced ferroptosis enhances natural killer cell anti-tumor activity and offers therapeutic potential in neuroblastoma

doi: 10.3389/fimmu.2026.1739503

Figure Lengend Snippet: Erastin treatment increases ULBP1 surface expression and enhances NK cell-mediated cytotoxicity in neuroblastoma cells. (A) Surface expression of ULBP1 was measured by flow cytometry in KELLY, SK-N-AS, SK-N-BE (2), and SK-N-FI cells treated with DMSO (control) or Erastin. (B) NK cell-mediated cytotoxicity assay using NK-92 cells co-cultured with neuroblastoma cells (E:T ratio was 8:1) pre-treated with either DMSO (Control), Erastin, or Erastin in combination with Liproxstatin-1 (Lip-1). Cell lysis percentages were quantified in KELLY, SK-N-AS, and SK-N-FI cells. n = 3 biologically independent experiments. *P<0.05, **P<0.01, ***P<0.001; Paired t test.

Article Snippet: Separately, NB cells (KELLY, SK-N-AS, SK-N-BE (2), and SK-N-FI) were seeded and washed with PBS, then stained for 30 minutes at 4°C with anti-ULBP1 primary antibody (1:100, clone 170818, R&D systems, #MAB-1380-500) prior to washing and 30 min incubation with secondary antibody (1:500, Invitrogen, # A55747 ).

Techniques: Expressing, Flow Cytometry, Control, Cytotoxicity Assay, Cell Culture, Lysis