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rabbit anti human igfbp2 polyclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti human igfbp2 polyclonal antibody
    Rabbit Anti Human Igfbp2 Polyclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+human+igfbp2+polyclonal+antibody/pm41039587-82-14-20?v=Cell+Signaling+Technology+Inc
    Average 86 stars, based on 1 article reviews
    rabbit anti human igfbp2 polyclonal antibody - by Bioz Stars, 2026-08
    86/100 stars

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    Cell Signaling Technology Inc rabbit anti human igfbp2 polyclonal antibody
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    FIGURE 7 (A) WB for <t>IGFBP2</t> in 3 pairs patients from Nantong cohort. (B) Represented IHC for IGFBP2 in three parents with different WHO stage from Nantong cohort. (C) Boxplot of IHC for IGFBP2 in six pairs parents from Nantong cohort. (D) The expression level of IGFBP2 in glioma sample and the control normal sample. (E) Kaplan-Meier survival curve showing survival probability of high- or low-expression IGFBP2. (F) The 1-year, 2-year, 3-year, 4-year, and 5-year survival ROC curves are predicted by the expression of IGFBP2. (G) The heat map shows the correlation between IGFBP2 and eight immune checkpoints in TCGA. (H) GSEA maps of cancer and immune-related signaling pathways positively modulated by IGFBP2. ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001.
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    Santa Cruz Biotechnology rabbit polyclonal anti human igfbp2 antibody
    Figure 4. <t>IGFBP2</t> is a specific target gene of miR-592 in glioma. (a) Putative binding sites of miR-592 within the 3′-UTR region of IGFBP2 mRNA, and the sequences of wild-type and mutant-type were shown. (b) The relative luciferase activity was determined in the U87 cells cotransfected with wild-type/mutant-type IGFBP2 3′-UTR vector and miR-592/miR-NC. Firefly luciferase activity was normalized to Renilla luciferase. (c and d) IGFBP2 expression on mRNA and protein levels was determined in U87 cells after being transfected with miR-592 mimic or miR-NC. GAPDH was used as loading control. (e) IGFBP2 mRNA level was determined in glioma tissues (glioma) and their matched adjacent normal tissues. GAPDH was used as loading control. (f) The reverse relationship between IGFBP2 and miR-592 expression was explored by Spearman’s correlation in glioma tissues (n = 44; *p < 0.05 and **p < 0.01).
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    FIGURE 7 (A) WB for IGFBP2 in 3 pairs patients from Nantong cohort. (B) Represented IHC for IGFBP2 in three parents with different WHO stage from Nantong cohort. (C) Boxplot of IHC for IGFBP2 in six pairs parents from Nantong cohort. (D) The expression level of IGFBP2 in glioma sample and the control normal sample. (E) Kaplan-Meier survival curve showing survival probability of high- or low-expression IGFBP2. (F) The 1-year, 2-year, 3-year, 4-year, and 5-year survival ROC curves are predicted by the expression of IGFBP2. (G) The heat map shows the correlation between IGFBP2 and eight immune checkpoints in TCGA. (H) GSEA maps of cancer and immune-related signaling pathways positively modulated by IGFBP2. ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001.

    Journal: Frontiers in immunology

    Article Title: The cuproptosis-related signature associated with the tumor environment and prognosis of patients with glioma.

    doi: 10.3389/fimmu.2022.998236

    Figure Lengend Snippet: FIGURE 7 (A) WB for IGFBP2 in 3 pairs patients from Nantong cohort. (B) Represented IHC for IGFBP2 in three parents with different WHO stage from Nantong cohort. (C) Boxplot of IHC for IGFBP2 in six pairs parents from Nantong cohort. (D) The expression level of IGFBP2 in glioma sample and the control normal sample. (E) Kaplan-Meier survival curve showing survival probability of high- or low-expression IGFBP2. (F) The 1-year, 2-year, 3-year, 4-year, and 5-year survival ROC curves are predicted by the expression of IGFBP2. (G) The heat map shows the correlation between IGFBP2 and eight immune checkpoints in TCGA. (H) GSEA maps of cancer and immune-related signaling pathways positively modulated by IGFBP2. ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001.

    Article Snippet: The tissue sections through deparaffinization and dehydration were incubated with polyclonal rabbit anti-human IGFBP2 antibodies (1:50, Proteintech, 11065-3-AP) overnight at 4°C after epitope retrieval, H2O2 treatment, and non-specific antigens blocking.

    Techniques: Expressing, Control, Protein-Protein interactions

    Figure 4. IGFBP2 is a specific target gene of miR-592 in glioma. (a) Putative binding sites of miR-592 within the 3′-UTR region of IGFBP2 mRNA, and the sequences of wild-type and mutant-type were shown. (b) The relative luciferase activity was determined in the U87 cells cotransfected with wild-type/mutant-type IGFBP2 3′-UTR vector and miR-592/miR-NC. Firefly luciferase activity was normalized to Renilla luciferase. (c and d) IGFBP2 expression on mRNA and protein levels was determined in U87 cells after being transfected with miR-592 mimic or miR-NC. GAPDH was used as loading control. (e) IGFBP2 mRNA level was determined in glioma tissues (glioma) and their matched adjacent normal tissues. GAPDH was used as loading control. (f) The reverse relationship between IGFBP2 and miR-592 expression was explored by Spearman’s correlation in glioma tissues (n = 44; *p < 0.05 and **p < 0.01).

    Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    Article Title: MiR-592 functions as a tumor suppressor in glioma by targeting IGFBP2.

    doi: 10.1177/1010428317719273

    Figure Lengend Snippet: Figure 4. IGFBP2 is a specific target gene of miR-592 in glioma. (a) Putative binding sites of miR-592 within the 3′-UTR region of IGFBP2 mRNA, and the sequences of wild-type and mutant-type were shown. (b) The relative luciferase activity was determined in the U87 cells cotransfected with wild-type/mutant-type IGFBP2 3′-UTR vector and miR-592/miR-NC. Firefly luciferase activity was normalized to Renilla luciferase. (c and d) IGFBP2 expression on mRNA and protein levels was determined in U87 cells after being transfected with miR-592 mimic or miR-NC. GAPDH was used as loading control. (e) IGFBP2 mRNA level was determined in glioma tissues (glioma) and their matched adjacent normal tissues. GAPDH was used as loading control. (f) The reverse relationship between IGFBP2 and miR-592 expression was explored by Spearman’s correlation in glioma tissues (n = 44; *p < 0.05 and **p < 0.01).

    Article Snippet: The levels of IGFBP2 were measured using a rabbit polyclonal anti-human IGFBP2 antibody at a dilution of 1:1000 (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA) by western blotting as previously described.19 Normalization was performed by blotting the same samples with an antibody against GAPDH (Santa Cruz Biotechnology Inc.).

    Techniques: Binding Assay, Mutagenesis, Luciferase, Activity Assay, Plasmid Preparation, Expressing, Transfection, Control

    Figure 5. IGFBP2 overexpression reverses the inhibitory effects of miR-592 in glioma. (a) IGFBP2 protein expression was measured in U87 cells transfected with miR-592 mimic with/without IGFBP2 overexpression plasmid. GAPDH was used as an internal control. (b–f) Cell proliferation, colony formation, cell-cycle stage, migration, and invasion were determined in U87 cells transfected with miR-592 mimic with/without IGFBP2 overexpression plasmid (*p < 0.05 and **p < 0.01).

    Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    Article Title: MiR-592 functions as a tumor suppressor in glioma by targeting IGFBP2.

    doi: 10.1177/1010428317719273

    Figure Lengend Snippet: Figure 5. IGFBP2 overexpression reverses the inhibitory effects of miR-592 in glioma. (a) IGFBP2 protein expression was measured in U87 cells transfected with miR-592 mimic with/without IGFBP2 overexpression plasmid. GAPDH was used as an internal control. (b–f) Cell proliferation, colony formation, cell-cycle stage, migration, and invasion were determined in U87 cells transfected with miR-592 mimic with/without IGFBP2 overexpression plasmid (*p < 0.05 and **p < 0.01).

    Article Snippet: The levels of IGFBP2 were measured using a rabbit polyclonal anti-human IGFBP2 antibody at a dilution of 1:1000 (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA) by western blotting as previously described.19 Normalization was performed by blotting the same samples with an antibody against GAPDH (Santa Cruz Biotechnology Inc.).

    Techniques: Over Expression, Expressing, Transfection, Plasmid Preparation, Control, Migration

    Figure 6. MiR-592 inhibits tumor growth in vivo. (a) Tumor growth curve in xenograft mouse model. (b) Photographs of tumor tissues. (c) The weight of tumor tissues. (d) MiR-592 expression in tumor tissues was detected by qRT-PCR. (e) IGFBP2 protein expression in tumor tissues was measured by western blot. GAPDH was used as an internal control (**p < 0.01).

    Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    Article Title: MiR-592 functions as a tumor suppressor in glioma by targeting IGFBP2.

    doi: 10.1177/1010428317719273

    Figure Lengend Snippet: Figure 6. MiR-592 inhibits tumor growth in vivo. (a) Tumor growth curve in xenograft mouse model. (b) Photographs of tumor tissues. (c) The weight of tumor tissues. (d) MiR-592 expression in tumor tissues was detected by qRT-PCR. (e) IGFBP2 protein expression in tumor tissues was measured by western blot. GAPDH was used as an internal control (**p < 0.01).

    Article Snippet: The levels of IGFBP2 were measured using a rabbit polyclonal anti-human IGFBP2 antibody at a dilution of 1:1000 (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA) by western blotting as previously described.19 Normalization was performed by blotting the same samples with an antibody against GAPDH (Santa Cruz Biotechnology Inc.).

    Techniques: In Vivo, Expressing, Quantitative RT-PCR, Western Blot, Control