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bcl1 ccnd1/cyclin d1 sp4  (Thermo Fisher)


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    Structured Review

    Thermo Fisher bcl1 ccnd1/cyclin d1 sp4
    Bcl1 Ccnd1/Cyclin D1 Sp4, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ccnd1+sp4/rabbit+monoclonal+anti+cyclin+d1+thermo+fisher/pm32770124-41-18-23
    Average 90 stars, based on 1 article reviews
    bcl1 ccnd1/cyclin d1 sp4 - by Bioz Stars, 2026-09
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    Related Articles

    other:

    Article Title: Loss of VHL and Hypoxia Provokes PAX2 Up-Regulation in Clear Cell Renal Cell Carcinoma
    Article Snippet: The same antibodies used for Western blot analysis were applied for detection of PAX2 (dilution, 1:500), HIF1α (1:500; Abcam Ltd.), CCND1 (clone SP4, 1:40; Labvision), and WT1 (clone 6F-H2, 1:50; Dako).

    Article Title: CD5(-) diffuse large B-cell lymphoma with peculiar cyclin D1+ phenotype. Pathologic and molecular characterization of a single case.
    Article Snippet: Anatomic Pathology, Foundation IRCCS Policlinico San Matteo and University of Pavia, 27100 Pavia, Italy Human Genetics, University of Pavia, 27100 Pavia, Italy Anatomic Pathology, Ospedale Guglielmo da Saliceto, 29100 Piacenza, Italy Department of Surgery, Foundation IRCCS Policlinico San Matteo, 27100 Pavia, Italy Hematology, Foundation IRCCS Policlinico San Matteo and University of Pavia, 27100 Pavia, Italy



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    Combined MAPK and β-catenin pathway activating mutations define deep penetrating nevi a β-catenin pathway mutations, affecting <t>CTNNB1</t> or APC, and MAPK pathway mutations co-occur in deep penetrating nevi (DPN). Nevi with overlapping features of DPN and blue nevus harbor GNAQ activating mutations and are genetically distinct. BRAF activating mutations are mutually exclusive with MAP2K1 alterations. b CTNNB1 missense mutations affect codons of a critical domain that is phosphorylated and regulates subsequent ubiquitin-mediated degradation. c Indels of MAP2K1 cluster near a highly conserved lysine within the kinase catalytic domain. One small deletion affects the negative regulatory region (NRR). DD, docking domain for ERK1/2; NES, nuclear export signal; AL, activation loop within the kinase catalytic domain; PRD, proline-rich domain within the kinase catalytic domain; DVD, domain of versatile docking. d . MAP2K1 mutations activate MAP kinase signaling, which could be inhibited by the MEK inhibitor trametinib
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    ( A ) Schematic of construct used to generate ND2 : WIP1 transgenic mice, showing a 1-kb portion of the Neurod2 ( ND2 ) promoter (green arrow) driving expression of WIP1 (orange arrow; 1.8-kb). ( B ) DNA gel showing RT-PCR results from tail snips of ND2 : WIP1 transgenic founder mice using primers spanning exons 4 and 5 of WIP1 : expected 2485 base pair (bp) PCR product from endogenous Wip1 ; 180bp PCR product from WIP1 cDNA from expression construct in ( A ). C, empty template control; 1–15, founder mice; D1, PCR product using ND2 : WIP1 construct as template. DNA ladders shown on either side of gel, with notations for 200–2000bp. ( C ) WIP1 expression by real-time RT-PCR in the cerebellum of P7 ND2 : WIP1 transgenic, relative to Gapdh , compared to expression in the cerebellum of P7 wild-type (WT) C57Bl/6 mice, * p <0.005. ( D ) Hematoxylin and eosin stained P5 cerebella of WT and ND2 : WIP1 transgenic mice (left-hand panel). Dotted line, cerebellar lobules (I–X). Quantitation of cerebellar lobules in P5 WT and ND2 : WIP1 transgenic mice (right-hand panel) (n=3 cerebella per genotype), * p <0.05. ( E ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and the downstream marker of hedgehog pathway activation, <t>Cyclin</t> <t>D1</t> <t>(Ccnd1),</t> in the external granule layer (EGL) of lobule X of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice, * p <0.05. Bar, EGL width. ( F ) Immunofluorescent staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and p27 Kip1 (p27), in the external granule layer (EGL) of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice (n=3 cerebella per genotype), * p <0.005. Ki67, red; p27, green; DAPI, blue. Bar, EGL width. ML, molecular layer; IGL, internal granule layer; HPF, high-power field. Error bars, standard deviation (SD) among replicates of at least three per group. Scale bars, 100µm. All experiments were repeated at least three times or in at least three distinct cerebella.
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    ( A ) Schematic of construct used to generate ND2 : WIP1 transgenic mice, showing a 1-kb portion of the Neurod2 ( ND2 ) promoter (green arrow) driving expression of WIP1 (orange arrow; 1.8-kb). ( B ) DNA gel showing RT-PCR results from tail snips of ND2 : WIP1 transgenic founder mice using primers spanning exons 4 and 5 of WIP1 : expected 2485 base pair (bp) PCR product from endogenous Wip1 ; 180bp PCR product from WIP1 cDNA from expression construct in ( A ). C, empty template control; 1–15, founder mice; D1, PCR product using ND2 : WIP1 construct as template. DNA ladders shown on either side of gel, with notations for 200–2000bp. ( C ) WIP1 expression by real-time RT-PCR in the cerebellum of P7 ND2 : WIP1 transgenic, relative to Gapdh , compared to expression in the cerebellum of P7 wild-type (WT) C57Bl/6 mice, * p <0.005. ( D ) Hematoxylin and eosin stained P5 cerebella of WT and ND2 : WIP1 transgenic mice (left-hand panel). Dotted line, cerebellar lobules (I–X). Quantitation of cerebellar lobules in P5 WT and ND2 : WIP1 transgenic mice (right-hand panel) (n=3 cerebella per genotype), * p <0.05. ( E ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and the downstream marker of hedgehog pathway activation, <t>Cyclin</t> <t>D1</t> <t>(Ccnd1),</t> in the external granule layer (EGL) of lobule X of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice, * p <0.05. Bar, EGL width. ( F ) Immunofluorescent staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and p27 Kip1 (p27), in the external granule layer (EGL) of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice (n=3 cerebella per genotype), * p <0.005. Ki67, red; p27, green; DAPI, blue. Bar, EGL width. ML, molecular layer; IGL, internal granule layer; HPF, high-power field. Error bars, standard deviation (SD) among replicates of at least three per group. Scale bars, 100µm. All experiments were repeated at least three times or in at least three distinct cerebella.
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    Image Search Results


    Combined MAPK and β-catenin pathway activating mutations define deep penetrating nevi a β-catenin pathway mutations, affecting CTNNB1 or APC, and MAPK pathway mutations co-occur in deep penetrating nevi (DPN). Nevi with overlapping features of DPN and blue nevus harbor GNAQ activating mutations and are genetically distinct. BRAF activating mutations are mutually exclusive with MAP2K1 alterations. b CTNNB1 missense mutations affect codons of a critical domain that is phosphorylated and regulates subsequent ubiquitin-mediated degradation. c Indels of MAP2K1 cluster near a highly conserved lysine within the kinase catalytic domain. One small deletion affects the negative regulatory region (NRR). DD, docking domain for ERK1/2; NES, nuclear export signal; AL, activation loop within the kinase catalytic domain; PRD, proline-rich domain within the kinase catalytic domain; DVD, domain of versatile docking. d . MAP2K1 mutations activate MAP kinase signaling, which could be inhibited by the MEK inhibitor trametinib

    Journal: Nature Communications

    Article Title: Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi

    doi: 10.1038/s41467-017-00758-3

    Figure Lengend Snippet: Combined MAPK and β-catenin pathway activating mutations define deep penetrating nevi a β-catenin pathway mutations, affecting CTNNB1 or APC, and MAPK pathway mutations co-occur in deep penetrating nevi (DPN). Nevi with overlapping features of DPN and blue nevus harbor GNAQ activating mutations and are genetically distinct. BRAF activating mutations are mutually exclusive with MAP2K1 alterations. b CTNNB1 missense mutations affect codons of a critical domain that is phosphorylated and regulates subsequent ubiquitin-mediated degradation. c Indels of MAP2K1 cluster near a highly conserved lysine within the kinase catalytic domain. One small deletion affects the negative regulatory region (NRR). DD, docking domain for ERK1/2; NES, nuclear export signal; AL, activation loop within the kinase catalytic domain; PRD, proline-rich domain within the kinase catalytic domain; DVD, domain of versatile docking. d . MAP2K1 mutations activate MAP kinase signaling, which could be inhibited by the MEK inhibitor trametinib

    Article Snippet: Immunohistochemical analysis was performed on archival FFPE tumor specimens using the following antibodies: CTNNB1 clone B-catenin 1 (Dako catalog# M3539 or IR702), CCND1 clone EP-12 (Dako, catalog #IR083) or clone SP4 (Thermo Scientific, catalog #RM-9104-R7).

    Techniques: Ubiquitin Proteomics, Activation Assay

    Mutant CTNNB1 confers increased cell volume, pigmentation and cyclin D1 levels in vitro. a Stably transduced melanocytes (melan-a) with BRAF V600E and CTNNB1 S33F demonstrate increased β-catenin activity as measured by TOP flash luciferase expression ( left ; P = 0.03), cell volume ( center ; P = 0.04) and melanin content ( right ; P = 0.007) as compared to melanocytes transduced with BRAF V600E alone. Mean with error bars showing s.e.m., unpaired Student’s t -test, three biological replicates performed. b Representative western blot analysis of melanocytes stably transduced with BRAF V600E and CTNNB1 S33F demonstrate increased cyclin D1 levels as compared to those tranduced with GFP or BRAF V600E . Data shown are representative of at least three independent experiments with similar results

    Journal: Nature Communications

    Article Title: Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi

    doi: 10.1038/s41467-017-00758-3

    Figure Lengend Snippet: Mutant CTNNB1 confers increased cell volume, pigmentation and cyclin D1 levels in vitro. a Stably transduced melanocytes (melan-a) with BRAF V600E and CTNNB1 S33F demonstrate increased β-catenin activity as measured by TOP flash luciferase expression ( left ; P = 0.03), cell volume ( center ; P = 0.04) and melanin content ( right ; P = 0.007) as compared to melanocytes transduced with BRAF V600E alone. Mean with error bars showing s.e.m., unpaired Student’s t -test, three biological replicates performed. b Representative western blot analysis of melanocytes stably transduced with BRAF V600E and CTNNB1 S33F demonstrate increased cyclin D1 levels as compared to those tranduced with GFP or BRAF V600E . Data shown are representative of at least three independent experiments with similar results

    Article Snippet: Immunohistochemical analysis was performed on archival FFPE tumor specimens using the following antibodies: CTNNB1 clone B-catenin 1 (Dako catalog# M3539 or IR702), CCND1 clone EP-12 (Dako, catalog #IR083) or clone SP4 (Thermo Scientific, catalog #RM-9104-R7).

    Techniques: Mutagenesis, In Vitro, Stable Transfection, Activity Assay, Luciferase, Expressing, Transduction, Western Blot

    Model of step-wise progression in DPN-like melanoma. BRAF mutation leads to a common nevus. Subsequent CTNNB1 mutation results in the phenotypic switch to DPN. Additional genetic alterations result full transformation to DPN-like melanoma

    Journal: Nature Communications

    Article Title: Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi

    doi: 10.1038/s41467-017-00758-3

    Figure Lengend Snippet: Model of step-wise progression in DPN-like melanoma. BRAF mutation leads to a common nevus. Subsequent CTNNB1 mutation results in the phenotypic switch to DPN. Additional genetic alterations result full transformation to DPN-like melanoma

    Article Snippet: Immunohistochemical analysis was performed on archival FFPE tumor specimens using the following antibodies: CTNNB1 clone B-catenin 1 (Dako catalog# M3539 or IR702), CCND1 clone EP-12 (Dako, catalog #IR083) or clone SP4 (Thermo Scientific, catalog #RM-9104-R7).

    Techniques: Mutagenesis, Transformation Assay

    ( A ) Schematic of construct used to generate ND2 : WIP1 transgenic mice, showing a 1-kb portion of the Neurod2 ( ND2 ) promoter (green arrow) driving expression of WIP1 (orange arrow; 1.8-kb). ( B ) DNA gel showing RT-PCR results from tail snips of ND2 : WIP1 transgenic founder mice using primers spanning exons 4 and 5 of WIP1 : expected 2485 base pair (bp) PCR product from endogenous Wip1 ; 180bp PCR product from WIP1 cDNA from expression construct in ( A ). C, empty template control; 1–15, founder mice; D1, PCR product using ND2 : WIP1 construct as template. DNA ladders shown on either side of gel, with notations for 200–2000bp. ( C ) WIP1 expression by real-time RT-PCR in the cerebellum of P7 ND2 : WIP1 transgenic, relative to Gapdh , compared to expression in the cerebellum of P7 wild-type (WT) C57Bl/6 mice, * p <0.005. ( D ) Hematoxylin and eosin stained P5 cerebella of WT and ND2 : WIP1 transgenic mice (left-hand panel). Dotted line, cerebellar lobules (I–X). Quantitation of cerebellar lobules in P5 WT and ND2 : WIP1 transgenic mice (right-hand panel) (n=3 cerebella per genotype), * p <0.05. ( E ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and the downstream marker of hedgehog pathway activation, Cyclin D1 (Ccnd1), in the external granule layer (EGL) of lobule X of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice, * p <0.05. Bar, EGL width. ( F ) Immunofluorescent staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and p27 Kip1 (p27), in the external granule layer (EGL) of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice (n=3 cerebella per genotype), * p <0.005. Ki67, red; p27, green; DAPI, blue. Bar, EGL width. ML, molecular layer; IGL, internal granule layer; HPF, high-power field. Error bars, standard deviation (SD) among replicates of at least three per group. Scale bars, 100µm. All experiments were repeated at least three times or in at least three distinct cerebella.

    Journal: Oncogene

    Article Title: WIP1 modulates responsiveness to Sonic Hedgehog signaling in neuronal precursor cells and medulloblastoma

    doi: 10.1038/onc.2016.96

    Figure Lengend Snippet: ( A ) Schematic of construct used to generate ND2 : WIP1 transgenic mice, showing a 1-kb portion of the Neurod2 ( ND2 ) promoter (green arrow) driving expression of WIP1 (orange arrow; 1.8-kb). ( B ) DNA gel showing RT-PCR results from tail snips of ND2 : WIP1 transgenic founder mice using primers spanning exons 4 and 5 of WIP1 : expected 2485 base pair (bp) PCR product from endogenous Wip1 ; 180bp PCR product from WIP1 cDNA from expression construct in ( A ). C, empty template control; 1–15, founder mice; D1, PCR product using ND2 : WIP1 construct as template. DNA ladders shown on either side of gel, with notations for 200–2000bp. ( C ) WIP1 expression by real-time RT-PCR in the cerebellum of P7 ND2 : WIP1 transgenic, relative to Gapdh , compared to expression in the cerebellum of P7 wild-type (WT) C57Bl/6 mice, * p <0.005. ( D ) Hematoxylin and eosin stained P5 cerebella of WT and ND2 : WIP1 transgenic mice (left-hand panel). Dotted line, cerebellar lobules (I–X). Quantitation of cerebellar lobules in P5 WT and ND2 : WIP1 transgenic mice (right-hand panel) (n=3 cerebella per genotype), * p <0.05. ( E ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and the downstream marker of hedgehog pathway activation, Cyclin D1 (Ccnd1), in the external granule layer (EGL) of lobule X of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice, * p <0.05. Bar, EGL width. ( F ) Immunofluorescent staining (left-hand panels) and quantitation (right-hand panels) of Ki-67 and p27 Kip1 (p27), in the external granule layer (EGL) of the cerebellum of P5 wild-type, ND2 : WIP1 , and SmoA1 / SmoA1 mice (n=3 cerebella per genotype), * p <0.005. Ki67, red; p27, green; DAPI, blue. Bar, EGL width. ML, molecular layer; IGL, internal granule layer; HPF, high-power field. Error bars, standard deviation (SD) among replicates of at least three per group. Scale bars, 100µm. All experiments were repeated at least three times or in at least three distinct cerebella.

    Article Snippet: Following antigen retrieval, tissues were blocked and incubated with α-Ki67 (1:500; Vector, VP-RMO4) or Ccnd1 (1:100; Thermo Scientific, SP4) overnight at 4°C, then incubated with biotinylated goat anti-rabbit IgG (1:300; Vector, BA-1000).

    Techniques: Construct, Transgenic Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Control, Quantitative RT-PCR, Staining, Quantitation Assay, Immunohistochemical staining, Marker, Activation Assay, Standard Deviation

    ( A ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67+ and Cyclin D1 (Ccnd1)+ cells in the external granule layer of the cerebellum of P5 Wip1 +/+ and Wip1 −/− mice (n=3 cerebella per genotype), * p <0.005. Scale bar, 100µm. ( B ) Kaplan-Meier curves showing overall, MB-related survival of SmoA1 / SmoA1 ; Wip1 +/+, SmoA1 / SmoA1 ; Wip1 +/−, and SmoA1 / SmoA1 ; Wip1 −/− mice. ( C ) Kaplan-Meier curves showing overall, MB-related survival of Math1 -cre ER ; Ptc1 fl/fl; Wip1 +/+, Math1 -cre ER ; Ptc1 fl/fl; Wip1 +/−, and Math1 -cre ER ; Ptc1 fl/fl; Wip1 −/− mice following treatment with 1mg tamoxifen by oral gavage per mouse at P7.

    Journal: Oncogene

    Article Title: WIP1 modulates responsiveness to Sonic Hedgehog signaling in neuronal precursor cells and medulloblastoma

    doi: 10.1038/onc.2016.96

    Figure Lengend Snippet: ( A ) Immunohistochemical staining (left-hand panels) and quantitation (right-hand panels) of Ki-67+ and Cyclin D1 (Ccnd1)+ cells in the external granule layer of the cerebellum of P5 Wip1 +/+ and Wip1 −/− mice (n=3 cerebella per genotype), * p <0.005. Scale bar, 100µm. ( B ) Kaplan-Meier curves showing overall, MB-related survival of SmoA1 / SmoA1 ; Wip1 +/+, SmoA1 / SmoA1 ; Wip1 +/−, and SmoA1 / SmoA1 ; Wip1 −/− mice. ( C ) Kaplan-Meier curves showing overall, MB-related survival of Math1 -cre ER ; Ptc1 fl/fl; Wip1 +/+, Math1 -cre ER ; Ptc1 fl/fl; Wip1 +/−, and Math1 -cre ER ; Ptc1 fl/fl; Wip1 −/− mice following treatment with 1mg tamoxifen by oral gavage per mouse at P7.

    Article Snippet: Following antigen retrieval, tissues were blocked and incubated with α-Ki67 (1:500; Vector, VP-RMO4) or Ccnd1 (1:100; Thermo Scientific, SP4) overnight at 4°C, then incubated with biotinylated goat anti-rabbit IgG (1:300; Vector, BA-1000).

    Techniques: Immunohistochemical staining, Staining, Quantitation Assay

    Biomarkers used in the study*

    Journal: JNCI Journal of the National Cancer Institute

    Article Title: Quantitative Assessment of Effect of Preanalytic Cold Ischemic Time on Protein Expression in Breast Cancer Tissues

    doi: 10.1093/jnci/djs438

    Figure Lengend Snippet: Biomarkers used in the study*

    Article Snippet: Vendor Biomarkers for companion diagnostic tests Estrogen receptor-alpha (ERα) Mouse 1D5/IgG1kappa M7047 DAKO Rabbit SP1/IgG RM-9101 Thermo Scientific Progesterone receptor (PgR) Mouse PgR636/IgG1kappa M3569 DAKO Rabbit PgRA/B (C89F7) 3153 Cell Signaling Technology HER2, also known as ERBB2 Mouse CB11/IgG1 CM 076 AA Biocare Medical Rabbit polyclonal A0485 DAKO Ki67 Mouse MIB-1/IgG1kappa M7240 DAKO Rabbit SP6/IgG 9106-S0 Lab Vision Markers of cold ischaemia Beta-actin (ACTB) Rabbit 13E5/IgG 13E5/IgG Cell Signaling Technology Beta-tubulin (TUBB) Rabbit pF3/IgG 2128 Cell Signaling Technology Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) Rabbit 14C10/IgG 2118 Cell Signaling Technology Histone 4 (HIST4H4) Mouse L64C1 2935 Cell Signaling Technology Histone 3 (HIST3H3) Mouse 96C10/IgG1, kappa 3680 Cell Signaling Technology Lamin A/C (LMNA) Rabbit polyclonal 2032 Cell Signaling Technology Lactate dehydrogenase A (LDHA) Rabbit IgG, C4B5 3582 Cell Signaling Technology Cytokeratin (KRT X) Mouse AE1/AE3/IgG1 M3515 DAKO Rabbit polyclonal ZO622 DAKO Markers of hypoxia Cyclin D1 (CCND1) Rabbit IgG/SP4 RM-9104 Thermo Fisher Fremont Cyclin B1 (CCNB1) Mouse GNS-11/IgG2 554178 BD Biosciences A kinase (PRKA) anchor protein 13 (AKAP13) Mouse IgG2a/ZX-18 sc-81902 Santa Cruz Biotechnology Cell division cycle 42 (CDC42) Mouse IgG3/B-8 sc-8401 Santa Cruz Biotechnology Cleaved caspase3 (CASP3) Rabbit polyclonal 9661 Cell Signaling Technology Hypoxia inducible factor 1-alpha (HIF1A) Rabbit polyclonal NB 100–449 Novus Biological Hypoxia inducible factor 2-alpha (HIF2A) Mouse ep190b/IgG1 ab8365 abcam Markers of phosphorylated proteins Phosphorylated tyrosine (4G10) Mouse IgG2b 05-1050 Millipore Markers of post-translational modification SMT3 suppressor of mif two 3 homolog 1 (SUMO1) Rabbit Y299/IgG ab32058 abcam Acetylated lysine Rabbit polyclonal, purified 9441 Cell Signaling Technology Neural precursor cell expressed, developmentally down-regulated 8 (NEDD8) Rabbit IgG, 19E3 2754 Cell Signaling Technology Open in a separate window * Antibodies were validated and used for quantitative immunofluorescence assays as described in the Patients and Methods section.

    Techniques: Diagnostic Assay, Modification, Purification

    Summary of the proteins tested on the TMA series and the conventional series of biopsies and resections*

    Journal: JNCI Journal of the National Cancer Institute

    Article Title: Quantitative Assessment of Effect of Preanalytic Cold Ischemic Time on Protein Expression in Breast Cancer Tissues

    doi: 10.1093/jnci/djs438

    Figure Lengend Snippet: Summary of the proteins tested on the TMA series and the conventional series of biopsies and resections*

    Article Snippet: Vendor Biomarkers for companion diagnostic tests Estrogen receptor-alpha (ERα) Mouse 1D5/IgG1kappa M7047 DAKO Rabbit SP1/IgG RM-9101 Thermo Scientific Progesterone receptor (PgR) Mouse PgR636/IgG1kappa M3569 DAKO Rabbit PgRA/B (C89F7) 3153 Cell Signaling Technology HER2, also known as ERBB2 Mouse CB11/IgG1 CM 076 AA Biocare Medical Rabbit polyclonal A0485 DAKO Ki67 Mouse MIB-1/IgG1kappa M7240 DAKO Rabbit SP6/IgG 9106-S0 Lab Vision Markers of cold ischaemia Beta-actin (ACTB) Rabbit 13E5/IgG 13E5/IgG Cell Signaling Technology Beta-tubulin (TUBB) Rabbit pF3/IgG 2128 Cell Signaling Technology Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) Rabbit 14C10/IgG 2118 Cell Signaling Technology Histone 4 (HIST4H4) Mouse L64C1 2935 Cell Signaling Technology Histone 3 (HIST3H3) Mouse 96C10/IgG1, kappa 3680 Cell Signaling Technology Lamin A/C (LMNA) Rabbit polyclonal 2032 Cell Signaling Technology Lactate dehydrogenase A (LDHA) Rabbit IgG, C4B5 3582 Cell Signaling Technology Cytokeratin (KRT X) Mouse AE1/AE3/IgG1 M3515 DAKO Rabbit polyclonal ZO622 DAKO Markers of hypoxia Cyclin D1 (CCND1) Rabbit IgG/SP4 RM-9104 Thermo Fisher Fremont Cyclin B1 (CCNB1) Mouse GNS-11/IgG2 554178 BD Biosciences A kinase (PRKA) anchor protein 13 (AKAP13) Mouse IgG2a/ZX-18 sc-81902 Santa Cruz Biotechnology Cell division cycle 42 (CDC42) Mouse IgG3/B-8 sc-8401 Santa Cruz Biotechnology Cleaved caspase3 (CASP3) Rabbit polyclonal 9661 Cell Signaling Technology Hypoxia inducible factor 1-alpha (HIF1A) Rabbit polyclonal NB 100–449 Novus Biological Hypoxia inducible factor 2-alpha (HIF2A) Mouse ep190b/IgG1 ab8365 abcam Markers of phosphorylated proteins Phosphorylated tyrosine (4G10) Mouse IgG2b 05-1050 Millipore Markers of post-translational modification SMT3 suppressor of mif two 3 homolog 1 (SUMO1) Rabbit Y299/IgG ab32058 abcam Acetylated lysine Rabbit polyclonal, purified 9441 Cell Signaling Technology Neural precursor cell expressed, developmentally down-regulated 8 (NEDD8) Rabbit IgG, 19E3 2754 Cell Signaling Technology Open in a separate window * Antibodies were validated and used for quantitative immunofluorescence assays as described in the Patients and Methods section.

    Techniques: