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cip2a expression  (Novus Biologicals)


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    Novus Biologicals cip2a expression
    Figure 1 Model of <t>CIP2A</t> involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.
    Cip2a Expression, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cip2a expression/product/Novus Biologicals
    Average 93 stars, based on 10 article reviews
    cip2a expression - by Bioz Stars, 2026-05
    93/100 stars

    Images

    1) Product Images from "Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy."

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    Journal: BMC cancer

    doi: 10.1186/s12885-015-1300-3

    Figure 1 Model of CIP2A involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.
    Figure Legend Snippet: Figure 1 Model of CIP2A involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.

    Techniques Used: Protein-Protein interactions, Over Expression, Activity Assay

    Figure 2 Immunohistochemical (IHC analysis of CIP2A expression in patients with colorectal cancer. Representative examples of CIP2A expression: (a) strong expression in colorectal liver metastasis, (b) weak expression in colorectal liver metastasis, (c) staining in paired colon cancer, (d) colorectal metastasis tissues, and (e) H-score in paired colon cancer and liver metastasis samples. CIP2A was not consistently overexpressed in colon cancer compared with colorectal liver metastasis in paired tissue specimens.
    Figure Legend Snippet: Figure 2 Immunohistochemical (IHC analysis of CIP2A expression in patients with colorectal cancer. Representative examples of CIP2A expression: (a) strong expression in colorectal liver metastasis, (b) weak expression in colorectal liver metastasis, (c) staining in paired colon cancer, (d) colorectal metastasis tissues, and (e) H-score in paired colon cancer and liver metastasis samples. CIP2A was not consistently overexpressed in colon cancer compared with colorectal liver metastasis in paired tissue specimens.

    Techniques Used: Immunohistochemical staining, Expressing, Staining

    Figure 3 Kaplan–Meier survival plot of overall survival (OS) by KRAS genotype. (a) OS was significantly worse in patients with wild type KRAS and strong CIP2A expression, compared with patients with wild type KRAS and weak CIP2A expression (P = 0.035). (b) No difference in OS associated with CIP2A expression was observed in mutant KRAS patients (P = 0.759).
    Figure Legend Snippet: Figure 3 Kaplan–Meier survival plot of overall survival (OS) by KRAS genotype. (a) OS was significantly worse in patients with wild type KRAS and strong CIP2A expression, compared with patients with wild type KRAS and weak CIP2A expression (P = 0.035). (b) No difference in OS associated with CIP2A expression was observed in mutant KRAS patients (P = 0.759).

    Techniques Used: Expressing, Mutagenesis

    Figure 4 Interaction between CIP2A, KRAS genotype and proliferation in the Caco-2 KRAS wild-type cell line. The result of immunoblot and proliferation assay is shown in (a) and (b), respectively. Column 1 vs. 2: CIP2A knockdown by shCIP2A resulted in decreased CIP2A, KRAS, and pERK expression as well as decreased proliferation; Column 1 vs. 3: KRAS overexpression by pCMV6-KRAS G12D resulted in increased KRAS, CIP2A, and pERK expression, as well as increased proliferation; Column 3 vs. 4: in Caco-2 cells with KRAS overexpression by pCMV6-KRAS G12D, knockdown of CIP2A by shCIP2A resulted in decreased CIP2A and KRAS expression. However, it did not cause significantly decreased pERK expression or decreased proliferation (*P < 0.05).
    Figure Legend Snippet: Figure 4 Interaction between CIP2A, KRAS genotype and proliferation in the Caco-2 KRAS wild-type cell line. The result of immunoblot and proliferation assay is shown in (a) and (b), respectively. Column 1 vs. 2: CIP2A knockdown by shCIP2A resulted in decreased CIP2A, KRAS, and pERK expression as well as decreased proliferation; Column 1 vs. 3: KRAS overexpression by pCMV6-KRAS G12D resulted in increased KRAS, CIP2A, and pERK expression, as well as increased proliferation; Column 3 vs. 4: in Caco-2 cells with KRAS overexpression by pCMV6-KRAS G12D, knockdown of CIP2A by shCIP2A resulted in decreased CIP2A and KRAS expression. However, it did not cause significantly decreased pERK expression or decreased proliferation (*P < 0.05).

    Techniques Used: Western Blot, Proliferation Assay, Knockdown, Expressing, Over Expression

    Figure 5 Silencing of CIP2A in Caco-2 cells leads to decreased resistance to cetuximab. Immunoblot analysis of CIP2A expression in control (shLuc) and CIP2A knockdown (shCIP2A) cells.
    Figure Legend Snippet: Figure 5 Silencing of CIP2A in Caco-2 cells leads to decreased resistance to cetuximab. Immunoblot analysis of CIP2A expression in control (shLuc) and CIP2A knockdown (shCIP2A) cells.

    Techniques Used: Western Blot, Expressing, Control, Knockdown



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    Figure 1 Model of <t>CIP2A</t> involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.
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    Image Search Results


    Figure 1 Model of CIP2A involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.

    Journal: BMC cancer

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    doi: 10.1186/s12885-015-1300-3

    Figure Lengend Snippet: Figure 1 Model of CIP2A involvement in the EGFR-RAS signaling pathways. ETS1 mediates CIP2A overexpression in human cancers with increased EGFR-MEK-ERK pathway activity. A positive feedback loop of CIP2A and MEK/ERK signaling pathways is shown.

    Article Snippet: CIP2A expression was assessed by IHC using monoclonal antibodies to CIP2A (NB100-74663, 1:1200; Novus Biologicals, Littleton, CO, USA).

    Techniques: Protein-Protein interactions, Over Expression, Activity Assay

    Figure 2 Immunohistochemical (IHC analysis of CIP2A expression in patients with colorectal cancer. Representative examples of CIP2A expression: (a) strong expression in colorectal liver metastasis, (b) weak expression in colorectal liver metastasis, (c) staining in paired colon cancer, (d) colorectal metastasis tissues, and (e) H-score in paired colon cancer and liver metastasis samples. CIP2A was not consistently overexpressed in colon cancer compared with colorectal liver metastasis in paired tissue specimens.

    Journal: BMC cancer

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    doi: 10.1186/s12885-015-1300-3

    Figure Lengend Snippet: Figure 2 Immunohistochemical (IHC analysis of CIP2A expression in patients with colorectal cancer. Representative examples of CIP2A expression: (a) strong expression in colorectal liver metastasis, (b) weak expression in colorectal liver metastasis, (c) staining in paired colon cancer, (d) colorectal metastasis tissues, and (e) H-score in paired colon cancer and liver metastasis samples. CIP2A was not consistently overexpressed in colon cancer compared with colorectal liver metastasis in paired tissue specimens.

    Article Snippet: CIP2A expression was assessed by IHC using monoclonal antibodies to CIP2A (NB100-74663, 1:1200; Novus Biologicals, Littleton, CO, USA).

    Techniques: Immunohistochemical staining, Expressing, Staining

    Figure 3 Kaplan–Meier survival plot of overall survival (OS) by KRAS genotype. (a) OS was significantly worse in patients with wild type KRAS and strong CIP2A expression, compared with patients with wild type KRAS and weak CIP2A expression (P = 0.035). (b) No difference in OS associated with CIP2A expression was observed in mutant KRAS patients (P = 0.759).

    Journal: BMC cancer

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    doi: 10.1186/s12885-015-1300-3

    Figure Lengend Snippet: Figure 3 Kaplan–Meier survival plot of overall survival (OS) by KRAS genotype. (a) OS was significantly worse in patients with wild type KRAS and strong CIP2A expression, compared with patients with wild type KRAS and weak CIP2A expression (P = 0.035). (b) No difference in OS associated with CIP2A expression was observed in mutant KRAS patients (P = 0.759).

    Article Snippet: CIP2A expression was assessed by IHC using monoclonal antibodies to CIP2A (NB100-74663, 1:1200; Novus Biologicals, Littleton, CO, USA).

    Techniques: Expressing, Mutagenesis

    Figure 4 Interaction between CIP2A, KRAS genotype and proliferation in the Caco-2 KRAS wild-type cell line. The result of immunoblot and proliferation assay is shown in (a) and (b), respectively. Column 1 vs. 2: CIP2A knockdown by shCIP2A resulted in decreased CIP2A, KRAS, and pERK expression as well as decreased proliferation; Column 1 vs. 3: KRAS overexpression by pCMV6-KRAS G12D resulted in increased KRAS, CIP2A, and pERK expression, as well as increased proliferation; Column 3 vs. 4: in Caco-2 cells with KRAS overexpression by pCMV6-KRAS G12D, knockdown of CIP2A by shCIP2A resulted in decreased CIP2A and KRAS expression. However, it did not cause significantly decreased pERK expression or decreased proliferation (*P < 0.05).

    Journal: BMC cancer

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    doi: 10.1186/s12885-015-1300-3

    Figure Lengend Snippet: Figure 4 Interaction between CIP2A, KRAS genotype and proliferation in the Caco-2 KRAS wild-type cell line. The result of immunoblot and proliferation assay is shown in (a) and (b), respectively. Column 1 vs. 2: CIP2A knockdown by shCIP2A resulted in decreased CIP2A, KRAS, and pERK expression as well as decreased proliferation; Column 1 vs. 3: KRAS overexpression by pCMV6-KRAS G12D resulted in increased KRAS, CIP2A, and pERK expression, as well as increased proliferation; Column 3 vs. 4: in Caco-2 cells with KRAS overexpression by pCMV6-KRAS G12D, knockdown of CIP2A by shCIP2A resulted in decreased CIP2A and KRAS expression. However, it did not cause significantly decreased pERK expression or decreased proliferation (*P < 0.05).

    Article Snippet: CIP2A expression was assessed by IHC using monoclonal antibodies to CIP2A (NB100-74663, 1:1200; Novus Biologicals, Littleton, CO, USA).

    Techniques: Western Blot, Proliferation Assay, Knockdown, Expressing, Over Expression

    Figure 5 Silencing of CIP2A in Caco-2 cells leads to decreased resistance to cetuximab. Immunoblot analysis of CIP2A expression in control (shLuc) and CIP2A knockdown (shCIP2A) cells.

    Journal: BMC cancer

    Article Title: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an independent prognostic marker in wild-type KRAS metastatic colorectal cancer after colorectal liver metastasectomy.

    doi: 10.1186/s12885-015-1300-3

    Figure Lengend Snippet: Figure 5 Silencing of CIP2A in Caco-2 cells leads to decreased resistance to cetuximab. Immunoblot analysis of CIP2A expression in control (shLuc) and CIP2A knockdown (shCIP2A) cells.

    Article Snippet: CIP2A expression was assessed by IHC using monoclonal antibodies to CIP2A (NB100-74663, 1:1200; Novus Biologicals, Littleton, CO, USA).

    Techniques: Western Blot, Expressing, Control, Knockdown

    (A) Quantification of PP2A activity and western blot showing levels of immunoprecipitated PP2A from the protein extracts used in the phosphatase assays. (B) Western blot analysis showing PP2A, phospho-PP2A, CIP2A and SET expression levels; * p < 0.05; ** p < 0.01; N1–3: normal controls corresponding to normal mammary tissue samples obtained from Fundación Jiménez Díaz Biobank (Madrid, Spain).

    Journal: Oncotarget

    Article Title: PP2A inhibition determines poor outcome and doxorubicin resistance in early breast cancer and its activation shows promising therapeutic effects

    doi:

    Figure Lengend Snippet: (A) Quantification of PP2A activity and western blot showing levels of immunoprecipitated PP2A from the protein extracts used in the phosphatase assays. (B) Western blot analysis showing PP2A, phospho-PP2A, CIP2A and SET expression levels; * p < 0.05; ** p < 0.01; N1–3: normal controls corresponding to normal mammary tissue samples obtained from Fundación Jiménez Díaz Biobank (Madrid, Spain).

    Article Snippet: Then, RNA was reversely transcribed to cDNA using Transcriptor Universal cDNA Master (Roche Life Science). cDNA amplification was done in a 7500 Fast Real-Time PCR System (Applied Biosystems) at 40 cycles, and using TaqMan Gene Expression Assays specific for CIP2A and PP2A (Applied Biosystems).

    Techniques: Activity Assay, Western Blot, Immunoprecipitation, Expressing

    (A) Tumor growth and statistical analysis between control, FTY720, doxorubicin and FTY720+doxorubicin groups of treatment (B) Immunohistochemical detection of CIP2A, SET, p-PP2A, p-Histone H3 and cleaved-Caspase 3 expression in tumor samples from the different groups of treatment. (C) Evaluation of differential expression of CIP2A, SET, p-PP2A, p-Histone H3 and cleaved-Caspase 3.

    Journal: Oncotarget

    Article Title: PP2A inhibition determines poor outcome and doxorubicin resistance in early breast cancer and its activation shows promising therapeutic effects

    doi:

    Figure Lengend Snippet: (A) Tumor growth and statistical analysis between control, FTY720, doxorubicin and FTY720+doxorubicin groups of treatment (B) Immunohistochemical detection of CIP2A, SET, p-PP2A, p-Histone H3 and cleaved-Caspase 3 expression in tumor samples from the different groups of treatment. (C) Evaluation of differential expression of CIP2A, SET, p-PP2A, p-Histone H3 and cleaved-Caspase 3.

    Article Snippet: Then, RNA was reversely transcribed to cDNA using Transcriptor Universal cDNA Master (Roche Life Science). cDNA amplification was done in a 7500 Fast Real-Time PCR System (Applied Biosystems) at 40 cycles, and using TaqMan Gene Expression Assays specific for CIP2A and PP2A (Applied Biosystems).

    Techniques: Immunohistochemical staining, Expressing

    (A) Immunohistochemical detection of CIP2A, p-PP2A and SET showing positive and negative staining. The line shows 25 μm. Magnification x400. Kaplan-Meier analyses of overall survival (B) and event-free survival (C) in a cohort of 230 breast cancer patients.

    Journal: Oncotarget

    Article Title: PP2A inhibition determines poor outcome and doxorubicin resistance in early breast cancer and its activation shows promising therapeutic effects

    doi:

    Figure Lengend Snippet: (A) Immunohistochemical detection of CIP2A, p-PP2A and SET showing positive and negative staining. The line shows 25 μm. Magnification x400. Kaplan-Meier analyses of overall survival (B) and event-free survival (C) in a cohort of 230 breast cancer patients.

    Article Snippet: Then, RNA was reversely transcribed to cDNA using Transcriptor Universal cDNA Master (Roche Life Science). cDNA amplification was done in a 7500 Fast Real-Time PCR System (Applied Biosystems) at 40 cycles, and using TaqMan Gene Expression Assays specific for CIP2A and PP2A (Applied Biosystems).

    Techniques: Immunohistochemical staining, Negative Staining