tfpi-2 promoter Search Results


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  • 98
    Thermo Fisher mspi
    Mspi, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 913 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore pp2a
    CaBP4 phosphorylation by mouse retinal lysates is inhibited by <t>PP2A</t> inhibitors. Dephosphorylation of GST-CaBP4 due to the endogenous phosphatase in lysates from light-adapted mouse retinas ( A – F ) or HEK293 cells ( F ) was determined by autoradiography
    Pp2a, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1121 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    OriGene tfpi 2
    Treatment with 5-aza-dC restores <t>TFPI-2</t> expression in 3 NPC cell lines . TFPI-2 mRNA expression level was evaluated by RT-PCR. GAPDH was amplified as an internal control. NNE8 was used as positive control. A water blank control was also included.
    Tfpi 2, supplied by OriGene, used in various techniques. Bioz Stars score: 89/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    PrimerDesign Inc tfpi 2 cpg island
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Tfpi 2 Cpg Island, supplied by PrimerDesign Inc, used in various techniques. Bioz Stars score: 86/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TaKaRa tetracycline responsive promoter
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Tetracycline Responsive Promoter, supplied by TaKaRa, used in various techniques. Bioz Stars score: 88/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Promega promoter less luciferase expression vector pgl3
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Promoter Less Luciferase Expression Vector Pgl3, supplied by Promega, used in various techniques. Bioz Stars score: 92/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher mspi restriction endonuclease
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Mspi Restriction Endonuclease, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Promega pgl4 10
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Pgl4 10, supplied by Promega, used in various techniques. Bioz Stars score: 94/100, based on 1884 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Beyotime dna isolation kit
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Dna Isolation Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Epigenomics roadmap epigenomics project
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Roadmap Epigenomics Project, supplied by Epigenomics, used in various techniques. Bioz Stars score: 94/100, based on 3284 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Roche x tremegene 9 dna transfection reagent
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    X Tremegene 9 Dna Transfection Reagent, supplied by Roche, used in various techniques. Bioz Stars score: 92/100, based on 3070 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Roche generation amplicon deep sequencing
    Bisulfite sequencing of the <t>TFPI-2</t> <t>CpG</t> island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.
    Generation Amplicon Deep Sequencing, supplied by Roche, used in various techniques. Bioz Stars score: 86/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    NEONC Technologies neo212
    <t>NEO212</t> reverses the EMT phenotype of GSCs in vitro An EMT PCR array was performed in mesenchymal USC02 and proneural USC04 cells treated with NEO212 or vehicle. The graphs show those genes that were modulated (threshold = 4-fold change) in NEO212-treated cells vs vehicle-treated cells. (A,B) Genes related to an epithelial phenotype upregulated with NEO212 treatment in USC02 (A) and USC04 (B) cells. (C,D) Genes related to a mesenchymal phenotype whose expression was more than 4 fold regulated by NEO212 treatment in USC02 (C) and USC04 (D) cells. Results are expressed as fold change, relative to vehicle-treated cells.
    Neo212, supplied by NEONC Technologies, used in various techniques. Bioz Stars score: 93/100, based on 149 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    OriGene pcmv6 ac gfp
    <t>NEO212</t> reverses the EMT phenotype of GSCs in vitro An EMT PCR array was performed in mesenchymal USC02 and proneural USC04 cells treated with NEO212 or vehicle. The graphs show those genes that were modulated (threshold = 4-fold change) in NEO212-treated cells vs vehicle-treated cells. (A,B) Genes related to an epithelial phenotype upregulated with NEO212 treatment in USC02 (A) and USC04 (B) cells. (C,D) Genes related to a mesenchymal phenotype whose expression was more than 4 fold regulated by NEO212 treatment in USC02 (C) and USC04 (D) cells. Results are expressed as fold change, relative to vehicle-treated cells.
    Pcmv6 Ac Gfp, supplied by OriGene, used in various techniques. Bioz Stars score: 89/100, based on 385 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Virapur cytomegalovirus
    <t>NEO212</t> reverses the EMT phenotype of GSCs in vitro An EMT PCR array was performed in mesenchymal USC02 and proneural USC04 cells treated with NEO212 or vehicle. The graphs show those genes that were modulated (threshold = 4-fold change) in NEO212-treated cells vs vehicle-treated cells. (A,B) Genes related to an epithelial phenotype upregulated with NEO212 treatment in USC02 (A) and USC04 (B) cells. (C,D) Genes related to a mesenchymal phenotype whose expression was more than 4 fold regulated by NEO212 treatment in USC02 (C) and USC04 (D) cells. Results are expressed as fold change, relative to vehicle-treated cells.
    Cytomegalovirus, supplied by Virapur, used in various techniques. Bioz Stars score: 92/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Covance p14arf
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
    P14arf, supplied by Covance, used in various techniques. Bioz Stars score: 91/100, based on 75 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Novo Nordisk concizumab
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
    Concizumab, supplied by Novo Nordisk, used in various techniques. Bioz Stars score: 92/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TaKaRa gc buffer i
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
    Gc Buffer I, supplied by TaKaRa, used in various techniques. Bioz Stars score: 91/100, based on 581 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TaKaRa mcf 7 tet off cells
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
    Mcf 7 Tet Off Cells, supplied by TaKaRa, used in various techniques. Bioz Stars score: 94/100, based on 70 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore bisulfite treated dna
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
    Bisulfite Treated Dna, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 267 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TaKaRa pcr cloning
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
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    Biocolor Ltd super taq dna polymerase
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
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    TaKaRa tet system approved fetal bovine serum fbs
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
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    Millipore jumpstart red taq dna polymerase
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
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    BIOTAGE psq assay design
    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by <t>p14ARF</t>
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    Image Search Results


    CaBP4 phosphorylation by mouse retinal lysates is inhibited by PP2A inhibitors. Dephosphorylation of GST-CaBP4 due to the endogenous phosphatase in lysates from light-adapted mouse retinas ( A – F ) or HEK293 cells ( F ) was determined by autoradiography

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Protein Phosphatase 2A Dephosphorylates CaBP4 and Regulates CaBP4 Function

    doi: 10.1167/iovs.12-11319

    Figure Lengend Snippet: CaBP4 phosphorylation by mouse retinal lysates is inhibited by PP2A inhibitors. Dephosphorylation of GST-CaBP4 due to the endogenous phosphatase in lysates from light-adapted mouse retinas ( A – F ) or HEK293 cells ( F ) was determined by autoradiography

    Article Snippet: Because OA inhibits not only PP2A but also PP4, PP5, and PP6, we also analyzed whether CaBP4 phosphorylation is promoted by fostriecin, which is a more selective inhibitor of PP2A.

    Techniques: De-Phosphorylation Assay, Autoradiography

    Recombinant PP2A B and C subunits interact with CaBP4. GST or GST-CaBP4 immobilized on glutathione magnetic beads was incubated with lysates of HEK293 cells cotransfected with epitope-tagged PP2A subunits: HA-tagged Aα ( A ), c-myc–tagged

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Protein Phosphatase 2A Dephosphorylates CaBP4 and Regulates CaBP4 Function

    doi: 10.1167/iovs.12-11319

    Figure Lengend Snippet: Recombinant PP2A B and C subunits interact with CaBP4. GST or GST-CaBP4 immobilized on glutathione magnetic beads was incubated with lysates of HEK293 cells cotransfected with epitope-tagged PP2A subunits: HA-tagged Aα ( A ), c-myc–tagged

    Article Snippet: Because OA inhibits not only PP2A but also PP4, PP5, and PP6, we also analyzed whether CaBP4 phosphorylation is promoted by fostriecin, which is a more selective inhibitor of PP2A.

    Techniques: Recombinant, Magnetic Beads, Incubation

    Recombinant PP2A subunits enhance CaBP4 dephosphorylation in HEK293 cells. HEK293 cells were not transfected ( lane 1 ) or cotransfected with rPP2A Aα, Bα, and Cβ ( lane 2 ). ( A ) Western blot analysis of the recombinant epitope-tagged

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Protein Phosphatase 2A Dephosphorylates CaBP4 and Regulates CaBP4 Function

    doi: 10.1167/iovs.12-11319

    Figure Lengend Snippet: Recombinant PP2A subunits enhance CaBP4 dephosphorylation in HEK293 cells. HEK293 cells were not transfected ( lane 1 ) or cotransfected with rPP2A Aα, Bα, and Cβ ( lane 2 ). ( A ) Western blot analysis of the recombinant epitope-tagged

    Article Snippet: Because OA inhibits not only PP2A but also PP4, PP5, and PP6, we also analyzed whether CaBP4 phosphorylation is promoted by fostriecin, which is a more selective inhibitor of PP2A.

    Techniques: Recombinant, De-Phosphorylation Assay, Transfection, Western Blot

    PP2A subunits are expressed in the retina and interact with CaBP4. ( A ) Detection of PP2A subunits A, B, and C in mouse retina and HEK293 cells. Mouse retinas or HEK293 cells were homogenized and analyzed by SDS-PAGE followed by transfer onto immobilon-P

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Protein Phosphatase 2A Dephosphorylates CaBP4 and Regulates CaBP4 Function

    doi: 10.1167/iovs.12-11319

    Figure Lengend Snippet: PP2A subunits are expressed in the retina and interact with CaBP4. ( A ) Detection of PP2A subunits A, B, and C in mouse retina and HEK293 cells. Mouse retinas or HEK293 cells were homogenized and analyzed by SDS-PAGE followed by transfer onto immobilon-P

    Article Snippet: Because OA inhibits not only PP2A but also PP4, PP5, and PP6, we also analyzed whether CaBP4 phosphorylation is promoted by fostriecin, which is a more selective inhibitor of PP2A.

    Techniques: SDS Page

    Treatment with 5-aza-dC restores TFPI-2 expression in 3 NPC cell lines . TFPI-2 mRNA expression level was evaluated by RT-PCR. GAPDH was amplified as an internal control. NNE8 was used as positive control. A water blank control was also included.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: Treatment with 5-aza-dC restores TFPI-2 expression in 3 NPC cell lines . TFPI-2 mRNA expression level was evaluated by RT-PCR. GAPDH was amplified as an internal control. NNE8 was used as positive control. A water blank control was also included.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Amplification, Positive Control

    TFPI-2 inhibits cell mobility in NPC cells . The cell motility of the CNE2-empty vector and CNE2- TFPI-2 was determined by wound healing assay. At 24 h after scratching, the CNE2- TFPI-2 cells spread significantly slower than did CNE2 empty vector cells. All experiments were performed in triplicate, and data from representative experiments are shown.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: TFPI-2 inhibits cell mobility in NPC cells . The cell motility of the CNE2-empty vector and CNE2- TFPI-2 was determined by wound healing assay. At 24 h after scratching, the CNE2- TFPI-2 cells spread significantly slower than did CNE2 empty vector cells. All experiments were performed in triplicate, and data from representative experiments are shown.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Plasmid Preparation, Wound Healing Assay

    TFPI-2 inhibits colony formation in NPC cells . Top: CNE2 cells were transfected with empty vector or TFPI-2 -expressing plasmids and selected with G418 for 2 weeks. The experiment was done in triplicate and the error bars represent standard deviations ( p

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: TFPI-2 inhibits colony formation in NPC cells . Top: CNE2 cells were transfected with empty vector or TFPI-2 -expressing plasmids and selected with G418 for 2 weeks. The experiment was done in triplicate and the error bars represent standard deviations ( p

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Transfection, Plasmid Preparation, Expressing

    TFPI-2 induces apoptosis in NPC cells . A: CNE2 cells were transfected with empty vector and TFPI-2 , then stained with annexin V-FITC and PI and subjected to flow cytometry. Fluorescence dot blots of annexin V-positive (horizontal axis) and PI-positive (vertical axis) cells are shown. B: Cells that were positively stained by annexin V-FITC only (early apoptosis) and positive for both annexin V-FITC and PI (late apoptosis) were quantitated, and both subpopulations were considered as apoptotic cells. The bar graph shows the average in 5 experiments. Error bars show standard deviations.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: TFPI-2 induces apoptosis in NPC cells . A: CNE2 cells were transfected with empty vector and TFPI-2 , then stained with annexin V-FITC and PI and subjected to flow cytometry. Fluorescence dot blots of annexin V-positive (horizontal axis) and PI-positive (vertical axis) cells are shown. B: Cells that were positively stained by annexin V-FITC only (early apoptosis) and positive for both annexin V-FITC and PI (late apoptosis) were quantitated, and both subpopulations were considered as apoptotic cells. The bar graph shows the average in 5 experiments. Error bars show standard deviations.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Transfection, Plasmid Preparation, Staining, Flow Cytometry, Cytometry, Fluorescence

    Methylation status of the TFPI-2 promoter region in NPC cell lines and normal nasopharyngeal epithelia (NNE) . The data are representative of 2 independent experiments. In vitro -methylated DNA was used as a methylation-positive control and DNA from normal lymphocytes was used as an unmethylated-positive control. Water was included as a blank control. MSP: methylation-specific PCR; U: unmethylated alleles; M: methylated alleles. PC: positive control.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: Methylation status of the TFPI-2 promoter region in NPC cell lines and normal nasopharyngeal epithelia (NNE) . The data are representative of 2 independent experiments. In vitro -methylated DNA was used as a methylation-positive control and DNA from normal lymphocytes was used as an unmethylated-positive control. Water was included as a blank control. MSP: methylation-specific PCR; U: unmethylated alleles; M: methylated alleles. PC: positive control.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Methylation, In Vitro, Positive Control, Polymerase Chain Reaction

    Methylation-specific PCR analysis of the TFPI-2 promoter region in NPC primary tumors and normal nasopharyngeal epithelia (NNE) . Four NPC primary tumors (NPC 13, 16, 24 and 34) and 4 NNE (NNE3, 7, 9 and 12) are shown as examples. U: unmethylated alleles; M: methylated alleles. The data are representative of 2 independent experiments.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: Methylation-specific PCR analysis of the TFPI-2 promoter region in NPC primary tumors and normal nasopharyngeal epithelia (NNE) . Four NPC primary tumors (NPC 13, 16, 24 and 34) and 4 NNE (NNE3, 7, 9 and 12) are shown as examples. U: unmethylated alleles; M: methylated alleles. The data are representative of 2 independent experiments.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Methylation, Polymerase Chain Reaction

    Bisulphite genomic sequencing of NPC cells, tumor biopsies and NNEs . Bisulphite genomic sequencing of the methylation status of the 31 CpG sites within the TFPI-2 promoter in 2 NPC cell lines (CNE2 and C666-1), 2 NPC biopsies (NPC24 and NPC34) and 1NNE biopsy (NNE7). Five randomly selected clones were sequenced for each sample. Open and filled circles represent unmethylated and methylated CpG sites, respectively. Circles were partially filled according to the percentage of methylation of the CpG site. The frames show the CpG pairs covered by methylation-specific PCR primers.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: Bisulphite genomic sequencing of NPC cells, tumor biopsies and NNEs . Bisulphite genomic sequencing of the methylation status of the 31 CpG sites within the TFPI-2 promoter in 2 NPC cell lines (CNE2 and C666-1), 2 NPC biopsies (NPC24 and NPC34) and 1NNE biopsy (NNE7). Five randomly selected clones were sequenced for each sample. Open and filled circles represent unmethylated and methylated CpG sites, respectively. Circles were partially filled according to the percentage of methylation of the CpG site. The frames show the CpG pairs covered by methylation-specific PCR primers.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Genomic Sequencing, Methylation, Clone Assay, Polymerase Chain Reaction

    TFPI-2 inhibits NPC cell proliferation . A: RT-PCR validation of stable transfectance of CNE2-TFPI-2 or CNE2-Empty vector. B: Proliferation curves of CNE2 cells, stable transfectants of CNE2- TFPI-2 and CNE2-empty vector. Cells were counted every 24 h for 6 days.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: TFPI-2 inhibits NPC cell proliferation . A: RT-PCR validation of stable transfectance of CNE2-TFPI-2 or CNE2-Empty vector. B: Proliferation curves of CNE2 cells, stable transfectants of CNE2- TFPI-2 and CNE2-empty vector. Cells were counted every 24 h for 6 days.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Plasmid Preparation

    RT-PCR analysis of mRNA expression of TFPI-2 in NPC cell lines and normal nasopharyngeal epithelia (NNE) samples . The data are representative of 2 independent experiments. Glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ) and water were used as internal and blank controls, respectively.

    Journal: BMC Cancer

    Article Title: TFPI-2 is a putative tumor suppressor gene frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma

    doi: 10.1186/1471-2407-10-617

    Figure Lengend Snippet: RT-PCR analysis of mRNA expression of TFPI-2 in NPC cell lines and normal nasopharyngeal epithelia (NNE) samples . The data are representative of 2 independent experiments. Glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ) and water were used as internal and blank controls, respectively.

    Article Snippet: Moreover, TFPI-2 was completely restored by demethylation treatment in all 3 TFPI-2 -silenced NPC cell lines.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing

    Bisulfite sequencing of the TFPI-2 CpG island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.

    Journal: PLoS ONE

    Article Title: Epigenetic Silencing of TFPI-2 in Canine Diffuse Large B-Cell Lymphoma

    doi: 10.1371/journal.pone.0092707

    Figure Lengend Snippet: Bisulfite sequencing of the TFPI-2 CpG island. Each box indicates a CpG dinucleotide and each line of boxes represents analysis of a single dog. Color gradation indicated the methylation level of each CpG site (0–1); 0, totally unmethylated; 1 totally methylated.

    Article Snippet: In silico Prediction of TFPI-2 CpG Island and Primer Design In order to identify putative CpG island on promoter region, TFPI-2 genomic sequence (ENSCAFG00000002040), as stored on Ensembl genome browser ( http://www.ensembl.org/index.html ), including 1000 bp upstream the ATG site was employed as query sequence.

    Techniques: Methylation Sequencing, Methylation

    Schematic representation of of the TFPI-2 gene and CpG island. The black boxes indicate exons, +1 indicates the translation start site. Each vertical bar represents a CpG dinucleotide. From −284 to +586 is the location of the CpG island, the grey box (from −196 to +16) indicates the region analyzed by Bis-seq.

    Journal: PLoS ONE

    Article Title: Epigenetic Silencing of TFPI-2 in Canine Diffuse Large B-Cell Lymphoma

    doi: 10.1371/journal.pone.0092707

    Figure Lengend Snippet: Schematic representation of of the TFPI-2 gene and CpG island. The black boxes indicate exons, +1 indicates the translation start site. Each vertical bar represents a CpG dinucleotide. From −284 to +586 is the location of the CpG island, the grey box (from −196 to +16) indicates the region analyzed by Bis-seq.

    Article Snippet: In silico Prediction of TFPI-2 CpG Island and Primer Design In order to identify putative CpG island on promoter region, TFPI-2 genomic sequence (ENSCAFG00000002040), as stored on Ensembl genome browser ( http://www.ensembl.org/index.html ), including 1000 bp upstream the ATG site was employed as query sequence.

    Techniques:

    NEO212 reverses the EMT phenotype of GSCs in vitro An EMT PCR array was performed in mesenchymal USC02 and proneural USC04 cells treated with NEO212 or vehicle. The graphs show those genes that were modulated (threshold = 4-fold change) in NEO212-treated cells vs vehicle-treated cells. (A,B) Genes related to an epithelial phenotype upregulated with NEO212 treatment in USC02 (A) and USC04 (B) cells. (C,D) Genes related to a mesenchymal phenotype whose expression was more than 4 fold regulated by NEO212 treatment in USC02 (C) and USC04 (D) cells. Results are expressed as fold change, relative to vehicle-treated cells.

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: NEO212 reverses the EMT phenotype of GSCs in vitro An EMT PCR array was performed in mesenchymal USC02 and proneural USC04 cells treated with NEO212 or vehicle. The graphs show those genes that were modulated (threshold = 4-fold change) in NEO212-treated cells vs vehicle-treated cells. (A,B) Genes related to an epithelial phenotype upregulated with NEO212 treatment in USC02 (A) and USC04 (B) cells. (C,D) Genes related to a mesenchymal phenotype whose expression was more than 4 fold regulated by NEO212 treatment in USC02 (C) and USC04 (D) cells. Results are expressed as fold change, relative to vehicle-treated cells.

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: In Vitro, Polymerase Chain Reaction, Expressing

    The cytotoxic and anti-migratory effects of NEO212 are independent (A–C) USC02 cells recover their ability to migrate after removal of NEO212. (A) Representative images taken 72 h after performing the wound healing assay. Primary cultures of USC02 cells were treated with the indicated concentrations of NEO212 for 24 h, and medium was replaced with fresh medium without compound in half of the cells (upper panel), while in the other half the medium was not changed (lower panel). Scale bar, 200 μm. (B) After 72 h, the remaining wound area was quantified and compared to the corresponding initial area. (C) Cell viability after 72 h, relative to vehicle-treated cells whose medium was not changed after 24 h. (D-F) NEO212 losses its cytotoxic effects, but not its ability to block cell migration after 24 h of incubation in medium without cells. (D) Cell viability of USC02 after 120 h treatments with increasing concentrations of fresh NEO212 (black line) or NEO212 previously incubated for 24 h in medium at 37 °C and then added to the cells (grey line). (E) Wound healing assay performed with the indicated concentrations of fresh NEO212 (NEO212-0h, black bars) or NEO212 previously incubated in medium for 24 h at 37 °C (NEO212-24h, grey bars). After 24 h, the remaining wound area was quantified, and represented as relative to each corresponding initial area. (F) Representative images taken at 0 h (upper panel) and 24 h (lower panel), of the wound healing assay performed with USC02 cells at the indicated concentrations of NEO212 previously pre-incubated during 24 h at 37 °C. Scale bar, 200 μm. In all cases, the bar graphs represent the average ± SEM of at least three independent experiments performed in quadruplicate. *, P

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: The cytotoxic and anti-migratory effects of NEO212 are independent (A–C) USC02 cells recover their ability to migrate after removal of NEO212. (A) Representative images taken 72 h after performing the wound healing assay. Primary cultures of USC02 cells were treated with the indicated concentrations of NEO212 for 24 h, and medium was replaced with fresh medium without compound in half of the cells (upper panel), while in the other half the medium was not changed (lower panel). Scale bar, 200 μm. (B) After 72 h, the remaining wound area was quantified and compared to the corresponding initial area. (C) Cell viability after 72 h, relative to vehicle-treated cells whose medium was not changed after 24 h. (D-F) NEO212 losses its cytotoxic effects, but not its ability to block cell migration after 24 h of incubation in medium without cells. (D) Cell viability of USC02 after 120 h treatments with increasing concentrations of fresh NEO212 (black line) or NEO212 previously incubated for 24 h in medium at 37 °C and then added to the cells (grey line). (E) Wound healing assay performed with the indicated concentrations of fresh NEO212 (NEO212-0h, black bars) or NEO212 previously incubated in medium for 24 h at 37 °C (NEO212-24h, grey bars). After 24 h, the remaining wound area was quantified, and represented as relative to each corresponding initial area. (F) Representative images taken at 0 h (upper panel) and 24 h (lower panel), of the wound healing assay performed with USC02 cells at the indicated concentrations of NEO212 previously pre-incubated during 24 h at 37 °C. Scale bar, 200 μm. In all cases, the bar graphs represent the average ± SEM of at least three independent experiments performed in quadruplicate. *, P

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: Wound Healing Assay, Blocking Assay, Migration, Incubation

    NEO212 suppresses invasion of mesenchymal (A, B, E) and proneural (C, D, F) GSCs (A) Representative images of invasion assay through a Matrigel-coated Boyden Chamber, performed with USC02 cells and 15 μM treatments. Scale bar, 200 μm. (B) After overnight treatments with 15 μM NEO212, the number of invaded cells per field was counted. The bar graph represents the average ± SEM of at least three independent experiments performed in triplicate. *, P

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: NEO212 suppresses invasion of mesenchymal (A, B, E) and proneural (C, D, F) GSCs (A) Representative images of invasion assay through a Matrigel-coated Boyden Chamber, performed with USC02 cells and 15 μM treatments. Scale bar, 200 μm. (B) After overnight treatments with 15 μM NEO212, the number of invaded cells per field was counted. The bar graph represents the average ± SEM of at least three independent experiments performed in triplicate. *, P

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: Invasion Assay

    NEO212 blocks the activation of the FAK/Src signaling pathway (A) Representative western blots of phosphorylated FAK (P-FAK), total FAK, phosphorylated Src (P-Src) and total Src, from experiments performed with equimolar concentrations of TMZ, POH, TMZ+POH and NEO212, in mesenchymal USC02 and proneural USC04 GSCs. (B) Data correspond to the average ± SEM of three independent experiments. *, P

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: NEO212 blocks the activation of the FAK/Src signaling pathway (A) Representative western blots of phosphorylated FAK (P-FAK), total FAK, phosphorylated Src (P-Src) and total Src, from experiments performed with equimolar concentrations of TMZ, POH, TMZ+POH and NEO212, in mesenchymal USC02 and proneural USC04 GSCs. (B) Data correspond to the average ± SEM of three independent experiments. *, P

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: Activation Assay, Western Blot

    NEO212 decreases tumor progression and GSC invasion in an in vivo mesenchymal-GSC (USC02) tumor model (A) Kaplan-Meier survival analysis of mice treated with vehicle (red line), TMZ 5 mg/kg (light green line), TMZ 25 mg/kg (dark green line), NEO212 5 mg/kg (light blue line) and NEO212 25 mg/kg (dark blue line). *, P

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: NEO212 decreases tumor progression and GSC invasion in an in vivo mesenchymal-GSC (USC02) tumor model (A) Kaplan-Meier survival analysis of mice treated with vehicle (red line), TMZ 5 mg/kg (light green line), TMZ 25 mg/kg (dark green line), NEO212 5 mg/kg (light blue line) and NEO212 25 mg/kg (dark blue line). *, P

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: In Vivo, Mouse Assay

    NEO212 reduces migration of GSCs (A) Representative images of the wound healing assay performed with mesenchymal USC02 cells treated with 15 μM of each drug. Scale bar, 200 μm. (B) After 24 h of treatment, the remaining wound area was quantified and compared to the initial wound. The bar graph represents the average ± SEM of at least three independent experiments performed in quadruplicate. *, P

    Journal: Molecular cancer therapeutics

    Article Title: NEO212 Inhibits Migration and Invasion of Glioma Stem Cells

    doi: 10.1158/1535-7163.MCT-17-0591

    Figure Lengend Snippet: NEO212 reduces migration of GSCs (A) Representative images of the wound healing assay performed with mesenchymal USC02 cells treated with 15 μM of each drug. Scale bar, 200 μm. (B) After 24 h of treatment, the remaining wound area was quantified and compared to the initial wound. The bar graph represents the average ± SEM of at least three independent experiments performed in quadruplicate. *, P

    Article Snippet: Here, we show that NEO212 effectively reverses the EMT process, mainly by upregulating several genes that are normally downregulated during EMT , such as cell-cell adhesion molecules CDH1, DSC2, DSP; epithelial cytokeratins KRT7 and KRT19[ , ]; secreted factors that promote an epithelial-like phenotype[ ] like FGFBP1, IL1RN, SPP1, TFPI-2, ESR1 and MST1R; as well as BMP2 and Wnt11, both related to cell differentiation and development[ , ].

    Techniques: Migration, Wound Healing Assay

    The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by p14ARF

    Journal: Cancer research

    Article Title: p14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway

    doi: 10.1158/0008-5472.CAN-13-1951

    Figure Lengend Snippet: The silencing of SP1 and c-JUN reverses the inhibition of plasma clotting by p14ARF

    Article Snippet: Given that P14ARF is known to exert some of its tumor suppressive functions through raising the levels of P53, we considered the involvement of p53 transcriptional activity in the regulation of TFPI2 .

    Techniques: Inhibition, Coagulation

    P14ARF inhibits plasma clotting by upregulating TFPI2 expression

    Journal: Cancer research

    Article Title: p14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway

    doi: 10.1158/0008-5472.CAN-13-1951

    Figure Lengend Snippet: P14ARF inhibits plasma clotting by upregulating TFPI2 expression

    Article Snippet: Given that P14ARF is known to exert some of its tumor suppressive functions through raising the levels of P53, we considered the involvement of p53 transcriptional activity in the regulation of TFPI2 .

    Techniques: Coagulation, Expressing

    TFPI2 is upregulated by P14ARF in a P53 independent manner

    Journal: Cancer research

    Article Title: p14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway

    doi: 10.1158/0008-5472.CAN-13-1951

    Figure Lengend Snippet: TFPI2 is upregulated by P14ARF in a P53 independent manner

    Article Snippet: Given that P14ARF is known to exert some of its tumor suppressive functions through raising the levels of P53, we considered the involvement of p53 transcriptional activity in the regulation of TFPI2 .

    Techniques:

    P14ARF upregulates TFPI2 gene expression through c-JUN and SP1

    Journal: Cancer research

    Article Title: p14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway

    doi: 10.1158/0008-5472.CAN-13-1951

    Figure Lengend Snippet: P14ARF upregulates TFPI2 gene expression through c-JUN and SP1

    Article Snippet: Given that P14ARF is known to exert some of its tumor suppressive functions through raising the levels of P53, we considered the involvement of p53 transcriptional activity in the regulation of TFPI2 .

    Techniques: Expressing

    Induction of the hTFPI2 promoter activity by P14ARF

    Journal: Cancer research

    Article Title: p14ARF suppresses tumor-induced thrombosis by regulating the tissue factor pathway

    doi: 10.1158/0008-5472.CAN-13-1951

    Figure Lengend Snippet: Induction of the hTFPI2 promoter activity by P14ARF

    Article Snippet: Given that P14ARF is known to exert some of its tumor suppressive functions through raising the levels of P53, we considered the involvement of p53 transcriptional activity in the regulation of TFPI2 .

    Techniques: Activity Assay