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polyclonal antibody  (Proteintech)


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    Structured Review

    Proteintech polyclonal antibody
    Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ulbp1/ULBP1+Antibody/pmc12823515-28-1-9
    Average 93 stars, based on 11 article reviews
    polyclonal antibody - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Western Blot:

    Article Title: TAK-981 potentiates doxorubicin immunocide in triple-negative breast cancer by IFN I-dependent NK cell stimulation.
    Article Snippet: Protein bands were visualized using enhanced chemiluminescence (ECL) reagents (Meilun Biotechnology, Dalian, China). .. The antibodies employed in this Western blot analysis included GAPDH (dilution 1:1000, #60004-1- Ig, Proteintech, Wuhan, China), SUMO1 (dilution 1:1000, #ab5316, Abcam, Cambridge, England), JAK1 (dilution 1:1000, #3332,Cell Signaling Technology, Boston, USA), p-JAK1 (dilution 1:1000, #74129,Cell Signaling Technology, Boston, USA), STAT1(dilution 1:1000, #82016-1- RR, Proteintech, Wuhan, China), p-STAT1(dilution 1:800, #AF6300, affinity biosciences, Affinity Biosciences, Ohio, USA), NF-κB(dilution 1:1000, #10745-1-AP, Proteintech, Wuhan, China), p- nf-κB(dilution 1:500, #80379-2-RR, Proteintech, Wuhan, China), IFNβ (dilution 1:200, #27506- 1-AP, Proteintech, Wuhan, China), ULBP1 (dilution 1:1000, #17715-1-AP, Proteintech, Wuhan, China), ULBP2 (dilution 1:1000, #13133-1-AP, Proteintech, Wuhan, China), ULBP3 (dilution 1:1000, #30058-1-AP, Proteintech, Wuhan, China), NKG2A (dilution 1:1000, #10935-1- AP, Proteintech, Wuhan, China), NKG2D (dilution 1:1000, #ab96606, Abcam, Cambridge, England), MIC A + MIC B (dilution 1:1000, #ab224702, Abcam, Cambridge, England), anti-Goat Anti-Rabbit IgG (H + L) HRP (dilution 1:5000, #S0001, Affinity Biosciences, Ohio, USA), and anti-Goat Anti-Mouse IgG (H + L) HRP (dilution 1:5000, #S0002, Affinity Biosciences, Ohio, USA). ..

    Article Title: TAK-981 potentiates doxorubicin immunocide in triple-negative breast cancer by IFN I-dependent NK cell stimulation
    Article Snippet: Protein bands were visualized using enhanced chemiluminescence (ECL) reagents (Meilun Biotechnology, Dalian, China). .. The antibodies employed in this Western blot analysis included GAPDH (dilution 1:1000, #60004-1-Ig, Proteintech, Wuhan, China), SUMO1 (dilution 1:1000, #ab5316, Abcam, Cambridge, England), JAK1 (dilution 1:1000, #3332,Cell Signaling Technology, Boston, USA), p-JAK1 (dilution 1:1000, #74129,Cell Signaling Technology, Boston, USA), STAT1(dilution 1:1000, #82016-1-RR, Proteintech, Wuhan, China), p-STAT1(dilution 1:800, #AF6300, affinity biosciences, Affinity Biosciences, Ohio, USA), NF-κB(dilution 1:1000, #10745-1-AP, Proteintech, Wuhan, China), p- nf-κB(dilution 1:500, #80379-2-RR, Proteintech, Wuhan, China), IFNβ (dilution 1:200, #27506-1-AP, Proteintech, Wuhan, China), ULBP1 (dilution 1:1000, #17715-1-AP, Proteintech, Wuhan, China), ULBP2 (dilution 1:1000, #13133-1-AP, Proteintech, Wuhan, China), ULBP3 (dilution 1:1000, #30058-1-AP, Proteintech, Wuhan, China), NKG2A (dilution 1:1000, #10935-1-AP, Proteintech, Wuhan, China), NKG2D (dilution 1:1000, #ab96606, Abcam, Cambridge, England), MIC A + MIC B (dilution 1:1000, #ab224702, Abcam, Cambridge, England), anti-Goat Anti-Rabbit IgG (H + L) HRP (dilution 1:5000, #S0001, Affinity Biosciences, Ohio, USA), and anti-Goat Anti-Mouse IgG (H + L) HRP (dilution 1:5000, #S0002, Affinity Biosciences, Ohio, USA). .. Total RNA was isolated from cellular samples using Trizol reagent (TaKaRa, Shiga, Japan).



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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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    R&D Systems anti ulbp1 primary antibody
    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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    Proteintech polyclonal antibody
    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