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ATCC
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ATCC
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PrimerDesign Inc
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ATCC
hpv 18 ![]() Hpv 18, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/product/hpv18+positive+human+cervical+cancer+cell+line+hela/pm25981999-58-30-31?v=ATCC Average 93 stars, based on 1 article reviews
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Image Search Results
Journal: Brazilian Journal of Microbiology
Article Title: A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens
doi: 10.1007/s42770-019-00137-8
Figure Lengend Snippet: HPV types 16 and 18 prevalence in patients with different types of cervical dysplasia
Article Snippet: Source of plasmids DNA DNA plasmids containing the entire genomes of HPV16 (ATCC 45113D) and
Techniques:
Journal: Brazilian Journal of Microbiology
Article Title: A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens
doi: 10.1007/s42770-019-00137-8
Figure Lengend Snippet: HPV types 16 and 18 overall detection via three different methods
Article Snippet: Source of plasmids DNA DNA plasmids containing the entire genomes of HPV16 (ATCC 45113D) and
Techniques:
Journal: Brazilian Journal of Microbiology
Article Title: A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens
doi: 10.1007/s42770-019-00137-8
Figure Lengend Snippet: Comparison between the results obtained for the identification of HPV 16 and 18, with TSnPCR and with MCHA
Article Snippet: Source of plasmids DNA DNA plasmids containing the entire genomes of HPV16 (ATCC 45113D) and
Techniques: Comparison
Journal: Brazilian Journal of Microbiology
Article Title: A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens
doi: 10.1007/s42770-019-00137-8
Figure Lengend Snippet: Comparison of the results obtained for the identification of HPV 16 and 18, with TSnPCR and with MFHA
Article Snippet: Source of plasmids DNA DNA plasmids containing the entire genomes of HPV16 (ATCC 45113D) and
Techniques: Comparison
Journal: Frontiers in Oncology
Article Title: Loop-Mediated Isothermal Amplification Assay for Detecting Tumor Markers and Human Papillomavirus: Accuracy and Supplemental Diagnostic Value to Endovaginal MRI in Cervical Cancer
doi: 10.3389/fonc.2021.747614
Figure Lengend Snippet: Limits of detection and time to positive for synthetic sequences and clinical samples in Groups 1 and 2 of tumor markers and HPV 16 and 18.
Article Snippet:
Techniques: Marker, Sequencing
Journal: Frontiers in Oncology
Article Title: Loop-Mediated Isothermal Amplification Assay for Detecting Tumor Markers and Human Papillomavirus: Accuracy and Supplemental Diagnostic Value to Endovaginal MRI in Cervical Cancer
doi: 10.3389/fonc.2021.747614
Figure Lengend Snippet: Sensitivity, specificity, positive and negative predictive values of LAMP assays for detection of small volume Stage 1 cervical cancer alone and together with endovaginal MRI.
Article Snippet:
Techniques: Histopathology, Marker
Journal: Epigenetics
Article Title: Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines
doi: 10.1080/15592294.2025.2451551
Figure Lengend Snippet: ALA regulated mRNA expression of DNMT1, DNMT3B, and TET2, as well as the activity of DNMT1 and DNMT3B, in cervical cancer cell lines. HeLa, SiHa, and C33A cell lines were treated with 20, 40, and 80 μM concentrations of ALA for 24 h. The effect of ALA was studied on DNMT1, DNMT3B, and TET2 mRNA expression and activity of DNMT1 and DNMT3B. The values have been plotted as mean ± SD of 3 independent experiments performed in duplicates.
Article Snippet:
Techniques: Expressing, Activity Assay
Journal: Epigenetics
Article Title: Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines
doi: 10.1080/15592294.2025.2451551
Figure Lengend Snippet: ALA modulated mRNA expression of HDAC1, HDAC8, SIRT1, KAT2B, and HAT1 and HDAC1 activity in cervical cancer cell lines. HeLa, SiHa, and C33A cell lines were treated with 20, 40, and 80 μM concentrations of ALA for 24 h. The effect of ALA was studied on HDAC1, HDAC8, SIRT1, KAT2B, and HAT1 mRNA expression and activity of HDAC1. The values were plotted as mean ± SD of three independent experiments performed in duplicates.
Article Snippet:
Techniques: Expressing, Activity Assay
Journal: Epigenetics
Article Title: Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines
doi: 10.1080/15592294.2025.2451551
Figure Lengend Snippet: ALA altered mRNA expression of EZH2, EHMT2, PRMT5, SETD7, PRDM5, KDM1A and KDM6B in cervical cancer cell lines. HeLa, SiHa, and C33A cell lines were treated with 20, 40, and 80 μM concentrations of ALA for 24 h. The effect of ALA was studied on EZH2, EHMT2, PRMT5, SETD7, PRDM5, KDM1A, and KDM6B mRNA expression. The values have been plotted as mean ± SD of three independent experiments performed in duplicates.
Article Snippet:
Techniques: Expressing
Journal: Epigenetics
Article Title: Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines
doi: 10.1080/15592294.2025.2451551
Figure Lengend Snippet: ALA altered mRNA expression of DAPK1, CDH1, RARβ, and hTERT as well as promoter methylation of DAPK1, CDH1, and RARβ in cervical cancer cell lines. HeLa, SiHa, and C33A cell lines were treated with 20, 40, and 80 μM concentrations of ALA for 24 h. The effect of ALA was studied on mRNA and promoter methylation of DAPK1, CDH1, RARβ, and hTERT. the values have been plotted as mean ± SD of three independent experiments performed in duplicates.
Article Snippet:
Techniques: Expressing, Methylation
Journal: Epigenetics
Article Title: Alpha-linolenic acid-mediated epigenetic reprogramming of cervical cancer cell lines
doi: 10.1080/15592294.2025.2451551
Figure Lengend Snippet: ALA reduced global DNA methylation in cervical cancer cell lines. A. HeLa and B. SiHa cell lines were treated with 20, 40, and 80 μM concentrations of ALA for 24 h. The values have been plotted as mean ± SD of three independent experiments performed in duplicates.
Article Snippet:
Techniques: DNA Methylation Assay
Journal: Frontiers in Cell and Developmental Biology
Article Title: Novel Affibody Molecules Targeting the HPV16 E6 Oncoprotein Inhibited the Proliferation of Cervical Cancer Cells
doi: 10.3389/fcell.2021.677867
Figure Lengend Snippet: Immunofluorescence and immunohistochemical staining analyses of the binding specificity of Z HPV16E6 affibodies to HPV16 E6. (A) Representative images showing TC-1, CaSki cells (HPV16 positive), HeLa229 (HPV18 positive), and C666-1 cells (HPV negative) stained with Z HPV16E6 1115, Z HPV16E6 1171, and Z HPV16E6 1235. The Z WT affibody was used as a negative control. The affibody molecule stain is shown in green, while the nuclear stain (PI) is shown in red; magnification at ×400. (B) Representative image of HPV16-positive cervical cancer sections and HPV-negative normal human sections by hematoxylin and eosin (HE) staining and immunohistochemistry (IHC) staining with Z HPV16E6 affibodies. Sections from HPV16-positive cervical cancer sections (upper panel) and HPV-negative normal human sections (lower panel) were labeled with Z HPV16E6 affibodies. Polyclonal HPV16 E6 antibody was used as a positive control. Z WT and PBS were used as negative controls. Magnification at ×400.
Article Snippet: Human HPV-positive CaSki (HPV16),
Techniques: Immunofluorescence, Immunohistochemical staining, Staining, Binding Assay, Negative Control, Immunohistochemistry, Labeling, Positive Control
Journal: Frontiers in Cell and Developmental Biology
Article Title: Novel Affibody Molecules Targeting the HPV16 E6 Oncoprotein Inhibited the Proliferation of Cervical Cancer Cells
doi: 10.3389/fcell.2021.677867
Figure Lengend Snippet: In vivo testing of the target binding ability of Z HPV16E6 affibodies to tumor tissues. Tumor imaging in nude mice bearing TC-1 (A) or HeLa229 (C) xenografts (arrows) by using fluorescence-conjugated affibody molecules. NIR-based imaging was executed at various time points pi with DyLight 755-conjugated Z HPV16E6 affibodies and used DyLight 755-conjugated Z WT affibody as a negative control. Tumor-to-skin ratios were calculated at different time points pi of the indicated agents in nude mice bearing TC-1 (B) and HeLa229 (D) xenografts. Data are shown as the mean ± SD of triplicates.
Article Snippet: Human HPV-positive CaSki (HPV16),
Techniques: In Vivo, Binding Assay, Imaging, Fluorescence, Negative Control
Journal: Frontiers in Cell and Developmental Biology
Article Title: Novel Affibody Molecules Targeting the HPV16 E6 Oncoprotein Inhibited the Proliferation of Cervical Cancer Cells
doi: 10.3389/fcell.2021.677867
Figure Lengend Snippet: Z HPV16E6 1235 inhibits the proliferation of HPV16-positive cell lines by binding to and blocking the intracellular activity of the HPV16 E6 oncoprotein. (A) p53 was up-regulated in a dose-dependent manner by treatment with Z HPV16E6 1235 in CaSki cells. (B) The effect of Z HPV16E6 1235 on the intracellular binding between HPV16 E6 and p53 was assessed by immunoprecipitating the E6/E6AP/p53 trimeric complex using an anti-p53 antibody bound to Protein A/G agarose beads from CaSki cells treated for 24 h. A parallel negative control assay was run for each group by incubating cell lysates with control IgG. The bar graph represents the amount of E6 bound to the relative amount of immunoprecipitated p53 after the quantification of p53 and E6 protein bands with ImageJ software. Data are presented as the mean ± SD of three independent experiments. ** P < 0.01. (C) CaSki cells were treated with 10 μM Z HPV16E6 1235 for the indicated periods and the expression of p53 target genes, including PUMA, BAX and p21, was evaluated by Western blotting. Cells without any treatment (Mock) or treated with 10 μM Z WT for 48 h were used as negative controls. GAPDH served as an internal reference standard. (D) The effects of Z HPV16E6 1235 and Z HPV16E7 384 alone or in combination on the viability of HPV16-positive cancer cells (TC-1, CaSki), HPV18-positive cervical cancer cells (HeLa229) and HPV-negative cancer cells (C666-1) were assessed by CCK-8 assay after 48 h of treatment with the indicated concentrations; these cells were compared to Z WT -treated cells. Data are shown as the mean ± SD of three independent experiments. (E–F) Colony formation assays of HPV16-positive TC-1 and CaSki cells or HPV18-positive HeLa229 cells following treatment with 2.5 μM test affibody molecules for 14 days. The Z WT affibody and medium groups were set as controls. ** P < 0.01, *** P < 0.001 vs. the control group. # P < 0.05 vs. the Z HPV16E6 1235 or Z HPV16E7 384 alone treatment group.
Article Snippet: Human HPV-positive CaSki (HPV16),
Techniques: Binding Assay, Blocking Assay, Activity Assay, Negative Control, Control, Immunoprecipitation, Software, Expressing, Western Blot, CCK-8 Assay
Journal: Frontiers in Cell and Developmental Biology
Article Title: Novel Affibody Molecules Targeting the HPV16 E6 Oncoprotein Inhibited the Proliferation of Cervical Cancer Cells
doi: 10.3389/fcell.2021.677867
Figure Lengend Snippet: Effect of Z HPV16E6 1235 in combination with Z HPV16E7 384 on the cell cycle, apoptosis, and cellular senescence. TC-1 and CaSki cells were treated with 10 μM of test affibody molecules for 24 h and analyzed by flow cytometry assay for the cell cycle (A,B) and apoptosis (C,D) with PI and Annexin V/PI. Data are presented as the mean ± SD in three independent experiments. (E,F) SA-β-gal staining of TC-1 and CaSki cells treated with 10 μM test affibody molecules for 24 h. Representative images taken using a bright-field inverted microscope (100 × magnification) are shown. In all panels, TC-1 and CaSki (HPV16-positive) cells treated with Z WT and HeLa229 (HPV18-positive) treated with selected affibodies were used as negative controls. Significance: * P < 0.05, ** P < 0.01 vs. the control group. # P < 0.05 vs. the Z HPV16E6 1235 or Z HPV16E7 384 alone treatment group.
Article Snippet: Human HPV-positive CaSki (HPV16),
Techniques: Flow Cytometry, Staining, Inverted Microscopy, Control
Journal: International Journal of Molecular Sciences
Article Title: HPV-Mediated Resistance to TNF and TRAIL Is Characterized by Global Alterations in Apoptosis Regulatory Factors, Dysregulation of Death Receptors, and Induction of ROS/RNS
doi: 10.3390/ijms20010198
Figure Lengend Snippet: Pro-inflammatory cytokines TNF and TRAIL increase the production and release of reactive oxygen and nitrogen species (ROS/RNS) in cells expressing HPV oncogenes. The levels of ROS and RNS in the absence or presence of pro-inflammatory cytokines alone (2 nM TNF or 50 ng/mL TRAIL) or in combination (2 nM TNF and 50 ng/mL TRAIL) were determined in cultures of PHKs ( A ), PHKs transduced with HPV16 oncogenes ( B ), and in cervical cancer-derived cell lines SiHa (positive for HPV16) ( C ) and HeLa (positive for HPV18) ( D ) using the OxiSelect™ In Vitro ROS/RNS Assay Kit (Cell Biolabs, Inc.), according to the manufacturer’s instructions. The results presented are representative of three independent experiments. Solid lines represent statistical differences between intracellular samples and dashed lines between supernatant samples as determined by Student’s t -test ( p -value ≤ 0.05).
Article Snippet: Cervical cancer-derived cell lines SiHa (HPV16, ATCC #HTB-35),
Techniques: Expressing, Transduction, Derivative Assay, In Vitro