ceramic hydroxyapatite type 1 ha Search Results


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Focus Technologies Inc hsv-1 hsv-2 igg differentiation immunoblot
Initial selection of HSV-2-specific serological tests
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Initial selection of HSV-2-specific serological tests
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Initial selection of HSV-2-specific serological tests
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Initial selection of HSV-2-specific serological tests
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Cayman Chemical phosphatidylinositol-4-phosphate 5-kinase type 1 gamma
Common genes between the SP-2509 drug resistance associated genes and murine genes affecting nervous system development. Associated disease syndromes for each gene may be crosschecked in the GeneCards/disorders platform. Genes associated to neurological disorders are marked in blue, genes associated to tumorogenesis or malignancies are marked in red, whilst genes involved in neural and/or cancer entities are marked in purple.
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Common genes between the SP-2509 drug resistance associated genes and murine genes affecting nervous system development. Associated disease syndromes for each gene may be crosschecked in the GeneCards/disorders platform. Genes associated to neurological disorders are marked in blue, genes associated to tumorogenesis or malignancies are marked in red, whilst genes involved in neural and/or cancer entities are marked in purple.
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Common genes between the SP-2509 drug resistance associated genes and murine genes affecting nervous system development. Associated disease syndromes for each gene may be crosschecked in the GeneCards/disorders platform. Genes associated to neurological disorders are marked in blue, genes associated to tumorogenesis or malignancies are marked in red, whilst genes involved in neural and/or cancer entities are marked in purple.
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Selleck Chemicals dna topoisomerase i camptothecin
E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various <t>DNA</t> repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and <t>Camptothecin</t> (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.
Dna Topoisomerase I Camptothecin, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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KOKEN CO atelocollagen 0.05%, 0.1%, 0.5%, 1% [w/v]
E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various <t>DNA</t> repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and <t>Camptothecin</t> (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.
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Valentis Inc igf-1 receptor
E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various <t>DNA</t> repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and <t>Camptothecin</t> (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.
Igf 1 Receptor, supplied by Valentis Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various <t>DNA</t> repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and <t>Camptothecin</t> (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.
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E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various <t>DNA</t> repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and <t>Camptothecin</t> (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.
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Image Search Results


Initial selection of HSV-2-specific serological tests

Journal:

Article Title: Performance of Commercially Available Enzyme Immunoassays for Detection of Antibodies against Herpes Simplex Virus Type 2 in African Populations

doi: 10.1128/JCM.42.7.2961-2965.2004

Figure Lengend Snippet: Initial selection of HSV-2-specific serological tests

Article Snippet: In 2001, three tests were approved by the U.S. Food and Drug Administration (FDA) for the diagnosis of HSV-2 infection, including the HerpeSelect (Focus Technologies, Inc., Cypress, Calif.), the HSV-1 and HSV-2 IgG differentiation immunoblot (Focus Technologies), and the POCkit HSV-2 (Diagnology, Ltd., Belfast, Northern Ireland).

Techniques: Selection, Purification, Enzyme-linked Immunosorbent Assay, Recombinant

Common genes between the SP-2509 drug resistance associated genes and murine genes affecting nervous system development. Associated disease syndromes for each gene may be crosschecked in the GeneCards/disorders platform. Genes associated to neurological disorders are marked in blue, genes associated to tumorogenesis or malignancies are marked in red, whilst genes involved in neural and/or cancer entities are marked in purple.

Journal: International Journal of Environmental Research and Public Health

Article Title: Soft Tissue Ewing Sarcoma Cell Drug Resistance Revisited: A Systems Biology Approach

doi: 10.3390/ijerph20136288

Figure Lengend Snippet: Common genes between the SP-2509 drug resistance associated genes and murine genes affecting nervous system development. Associated disease syndromes for each gene may be crosschecked in the GeneCards/disorders platform. Genes associated to neurological disorders are marked in blue, genes associated to tumorogenesis or malignancies are marked in red, whilst genes involved in neural and/or cancer entities are marked in purple.

Article Snippet: PIP5K1C , Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Gamma , Neurogenic Bladder; alcohol use disorder; Cerebellar Ataxia, Cayman Type.

Techniques: Isolation, Derivative Assay, Sterility, Sequencing, Mutagenesis

E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various DNA repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and Camptothecin (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.

Journal: Theranostics

Article Title: Human papillomavirus E6/E7 oncoproteins promote radiotherapy-mediated tumor suppression by globally hijacking host DNA damage repair

doi: 10.7150/thno.78091

Figure Lengend Snippet: E6/E7 viral oncoproteins negatively affects host genome integrity and increases cellular sensitivity to various DNA repair inhibitors. Number of InDels (A) and SNPs (C) detected in DNA of immortalized keratinocytes (HaCaT) transduced or not with HPV16 E6 and E7. For each time interval (P0-P10 and P0-20), the values were normalized to the total number of sequencing reads. The proportions of InDels/SNPs present in coding or non-coding regions are also represented. Transcribed: the variant is on the transcribed strand. Untranscribed: the variant is on the untranscribed strand. Nontranscribed: the variant is in a non-coding region. (B) InDel size distribution (insertions: size >0; deletions: size <0). (D) Relative contribution of the different published SBS signatures (COSMIC v3.3) to the overall detected mutational profile. SBS5 (potentially associated to a deficiency of nucleotide excision repair and/or aging) and 40 (unknown etiology) were responsible for >90% of the mutational burden. The COSMIC SBS1 signature (characterized by C>T mutations) exclusively detected in E6E7-transduced cells should be noticed. (E) Mutational spectrum of COSMIC signatures of interest (SBS1, 5 and 40). (F) Dose-response curves of several HPV E6E7 isogenic cell pairs treated with Niraparib or Veliparib (PARP1/2 inhibitors), RI-1 (RAD51 inhibitor), YU238259 (homology-dependent DNA repair inhibitor) and Camptothecin (DNA topoisomerase I inhibitor) for 72h. Results represent the means ± SEM of four independent experiments. The IC50 and 95% CI of each condition is also indicated. (G) 2D synergy maps highlighting synergistic dose regions (in red). The indicated average synergy score for a specific treatment combination was averaged over all the dose combination measurements. The means of three independent experiments were used to assess the synergy between radiotherapy and each DNA repair inhibitor according to the ZIP method.

Article Snippet: Potent/selective inhibitors of PARP1/2 (Niraparib and Veliparib), RAD51 (RI-1), homology-dependent DNA repair (YU238259) and DNA topoisomerase I (Camptothecin) were purchased from Selleckchem (Houston, TX, USA).

Techniques: Sequencing, Variant Assay