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Academic literature on the topic 'Ts-reporter'
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Journal articles on the topic "Ts-reporter"
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LEE, Kuan-Der, Seung Joon BAEK, and Rong-Fong SHEN. "Multiple factors regulating the expression of human thromboxane synthase gene." Biochemical Journal 319, no. 3 (November 1, 1996): 783–91. http://dx.doi.org/10.1042/bj3190783.
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Characterization of the 5.5 kb promoter of human thromboxane synthase (TS) gene revealed a proximal positive regulatory sequence (PPRS, -90 to -25 bp) and several distal repressive elements. The maximal promoter activity was found to reside within the first 285 bp, ∼75% of which was contributed by the PPRS. The sequence between -365 and -665 bp exerted a strong repressive effect (∼55%) on reporter gene expression independent of orientation and position, consistent with properties expected for a silencer. The sequence upstream of -665 bp to -5.5 kb contains mainly repressive elements which further reduce the promoter activity by 30%. The 65 bp PPRS worked in an orientation-independent, but position-dependent, manner and could be further divided into two independent elements, PPRS1 (-90 to -50 bp) and PPRS2 (-50 to -25 bp). While similar nuclear factor(s) from different cell types interact with PPRS2, those interacting with PPRS1 exhibit cell specificity. Internal sequence deletion and oligonucleotide competition established that a binding sequence for NF-E2 in PPRS1 (-60 tgctgattcat -50) was important for enhancing TS promoter activity in HL-60 cells. The presence of NF-E2 mRNA in HL-60 cells was demonstrated by reverse-transcription PCR amplification of the cDNA and Northern blot analysis. A 9-fold transactivation of luciferase (luc) reporter gene expression had been detected when NF-E2 cDNA was co-expressed with a TS promoter/luc construct. Despite the fact that NF-E2 and the cis-elements could alter the efficiency of TS transcription, they were not sufficient for restricting cell-specific TS expression. Analysis of the methylation status at the TS promoter in several human cell lines reveals cell-specific patterns of methylation that might correlate with TS expression. Taken together, these results suggest that the expression of human TS gene is modulated by multiple factors including cis-elements, trans-activator(s), and possibly genomic methylation.
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Siddiqui, Mohammad Aarif, Paradesi Naidu Gollavilli, Vignesh Ramesh, Beatrice Parma, Annemarie Schwab, Maria Eleni Vazakidou, Ramakrishnan Natesan, et al. "Thymidylate synthase drives the phenotypes of epithelial-to-mesenchymal transition in non-small cell lung cancer." British Journal of Cancer 124, no. 1 (October 7, 2020): 281–89. http://dx.doi.org/10.1038/s41416-020-01095-x.
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Abstract Background Epithelial-to-mesenchymal transition (EMT) enhances motility, stemness, chemoresistance and metastasis. Little is known about how various pathways coordinate to elicit EMT’s different functional aspects in non-small cell lung cancer (NSCLC). Thymidylate synthase (TS) has been previously correlated with EMT transcription factor ZEB1 in NSCLC and imparts resistance against anti-folate chemotherapy. In this study, we establish a functional correlation between TS, EMT, chemotherapy and metastasis and propose a network for TS mediated EMT. Methods Published datasets were analysed to evaluate the significance of TS in NSCLC fitness and prognosis. Promoter reporter assay was used to sort NSCLC cell lines in TSHIGH and TSLOW. Metastasis was assayed in a syngeneic mouse model. Results TS levels were prognostic and predicted chemotherapy response. Cell lines with higher TS promoter activity were more mesenchymal-like. RNA-seq identified EMT as one of the most differentially regulated pathways in connection to TS expression. EMT transcription factors HOXC6 and HMGA2 were identified as upstream regulator of TS, and AXL, SPARC and FOSL1 as downstream effectors. TS knock-down reduced the metastatic colonisation in vivo. Conclusion These results establish TS as a theranostic NSCLC marker integrating survival, chemo-resistance and EMT, and identifies a regulatory network that could be targeted in EMT-driven NSCLC.
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Gribaudo, Giorgio, Ludovica Riera, Thomas L. Rudge, Patrizia Caposio, Lee F. Johnson, and Santo Landolfo. "Human cytomegalovirus infection induces cellular thymidylate synthase gene expression in quiescent fibroblasts." Journal of General Virology 83, no. 12 (December 1, 2002): 2983–93. http://dx.doi.org/10.1099/0022-1317-83-12-2983.
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Productive infection of non-proliferating cells by cytomegalovirus (CMV) requires the coordinated stimulation of host biochemical pathways that prepare cells to synthesize DNA. Here we illustrate the ability of human CMV (HCMV) to stimulate cellular thymidylate synthase (TS) gene expression in quiescent human embryonic lung fibroblasts. TS mRNA and protein levels are nearly undetectable in quiescent cells, but are greatly increased following HCMV infection. Inhibition of TS activity was shown to impair HCMV DNA synthesis, demonstrating that TS upregulation is required for efficient HCMV replication in quiescent cells. The increase in TS gene expression was due to an increase in gene transcription, since the expression of a reporter gene driven by the human TS promoter was strongly induced by HCMV infection. Deletion analysis of the human TS promoter identified two positive elements that are important for this increased transcription. We have previously shown that murine CMV (MCMV) stimulates the mouse TS promoter by a mechanism that depends on the presence of an E2F element in the promoter region. However, deletion of the two potential E2F binding sites in the human TS promoter did not prevent the virus-induced increase in TS promoter activity. Our data suggest that HCMV activates human TS gene transcription by mechanisms that are independent of E2F and different from those used by MCMV to stimulate the mouse TS promoter.
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Gribaudo, Giorgio, Ludovica Riera, David Lembo, Marco De Andrea, Marisa Gariglio, Thomas L. Rudge, Lee F. Johnson, and Santo Landolfo. "Murine Cytomegalovirus Stimulates Cellular Thymidylate Synthase Gene Expression in Quiescent Cells and Requires the Enzyme for Replication." Journal of Virology 74, no. 11 (June 1, 2000): 4979–87. http://dx.doi.org/10.1128/jvi.74.11.4979-4987.2000.
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ABSTRACT Herpesviruses accomplish DNA replication either by expressing their own deoxyribonucleotide biosynthetic genes or by stimulating the expression of the corresponding cellular genes. Cytomegalovirus (CMV) has adopted the latter strategy to allow efficient replication in quiescent cells. In the present report, we show that murine CMV (MCMV) infection of quiescent fibroblasts induces both mRNA and protein corresponding to the cellular thymidylate synthase (TS) gene, which encodes the enzyme that catalyzes the de novo synthesis of thymidylic acid. The increase in TS gene expression was due to an increase in gene transcription, since the activity of a reporter gene driven by the mouse TS promoter was induced following MCMV infection. Mutagenesis of the potential E2F-responsive element immediately upstream from the TS essential promoter region abolished the virus-mediated stimulation of the TS promoter, suggesting that the transactivating activity of MCMV infection was E2F dependent. Cotransfection experiments revealed that expression of the viral immediate-early 1 protein was sufficient to mediate the increase in TS promoter activity. Finally, MCMV replication and viral DNA synthesis were found to be inhibited by ZD1694, a quinazoline-based folate analog that inhibits TS activity. These results demonstrate that upregulation of cellular TS expression is required for efficient MCMV replication in quiescent cells.
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Kaytor, M. D., and D. M. Livingston. "Saccharomyces cerevisiae RAD52 alleles temperature-sensitive for the repair of DNA double-strand breaks." Genetics 137, no. 4 (August 1, 1994): 933–44. http://dx.doi.org/10.1093/genetics/137.4.933.
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Abstract We have screened for mutations of the Saccharomyces cerevisiae RAD52 gene which confer a temperature-sensitive (ts) phenotype with respect to either the repair of DNA lesions caused by methyl methanesulfonate (MMS) or the recombination of an intrachromosomal recombination reporter. We were readily able to isolate alleles ts for the repair of lesions caused by MMS but were unable to find alleles with a severe ts deficiency in intrachromosomal recombination. We extensively characterized four strains conferring ts growth on MMS agar. These strains also exhibit ts survival when exposed to gamma-radiation or when the HO endonuclease is constitutively expressed. Although none of the four alleles confers a severe ts defect in intrachromosomal recombination, two confer significant defects in tests of mitotic, interchromosomal recombination carried out in diploid strains. The mutant diploids sporulate, but the two strains with defects in interchromosomal recombination have reduced spore viability. Meiotic recombination is not depressed in the two diploids with reduced spore viability. Thus, in the two strains with reduced spore viability, defects in mitotic and meiotic recombination do not correlate. Sequence analysis revealed that in three of the four ts alleles the causative mutations are in the first one-third of the open reading frame while the fourth is in the C-terminal third.
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Fenn, Kathleen, Veena M. Singh, Shing Mirn Lee, David Cieremans, Andrew B. Lassman, Dawn L. Hershman, Katherine D. Crew, et al. "Diagnosis of leptomeningeal metastasis (LM) through identification of circulating tumor cells (CTCs) in cerebrospinal fluid (CSF)." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 3567. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3567.
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3567 Background: Diagnosis of LM from solid tumors can be challenging. The TargetSelector (TS) CTC detection assay has demonstrated highly specific and sensitive CTC capture both for epithelial (CK+) and non-epithelial (CK-) subsets. The assay utilizes a ten-antibody (ab) capture cocktail followed by biotinylated secondary abs that bind to CTCs, enriched in a microfluidic device. TS targeted next-generation sequencing (NGS) assay detects somatic mutations in 12 breast cancer-related genes. The aim was to determine whether TS can improve sensitivity in the diagnosis of LM compared to CSF cytology by lumbar puncture (LP). Methods: CSF was collected prospectively from patients (pts) with a prior solid tumor diagnosis and suspicion of LM. CTCs were isolated from CSF using the TS platform. Cells were stained with cytokeratin (CK), CD45, streptavidin and DAPI. CTCs captured in a microchannel were classified as CK + or -. Peripheral blood samples obtained at time of LP underwent similar CTC analysis. Cell-free total nucleic acids (cfTNA) were extracted from plasma and CSF followed by NGS. Data analysis used the Ion Torrent Suite with annotation and report curation by Ion Reporter and Oncomine Knowledgebase Reporter software respectively. Results: There were 14 pts (13 women and 1 man), median age 56 years (range 32-75) with cancers of the breast (10), lung (1), colon (1), CNS lymphoma (1) or glioma (1). Pts had received a median of 2.5 lines of systemic metastatic therapy (range 0-8). CSF cytology was not sent for 1 pt and TS was not performed for 1 pt. TS and standard cytology had 89% agreement in pts with metastatic breast cancer (MBC, 8/9). Of the 6 pts for whom CTCs were detected in CSF by TS, 3 pts had + cytology (all MBC), 2 pts had - cytology and 1 pt with MBC was not tested by cytology. Of the 3 pts with + CSF by cytology (all MBC), all were detected by TS (Table). Among 5 MBC pts with CTCs present in CSF, ER status was concordant in 2 of 5 (40%). HER2 status was concordant in 3 of 4 (75%) evaluable pts and not determined in 1 pt. Analysis of cfDNA from CSF identified somatic mutations in 3 pts (TP53, PIK3CA, CCND1, respectively). In 1 of 3 pts, the mutation identified in the CSF (PIK3CA) in HR+/HER2- MBC was also identified in the blood. Conclusions: TargetSelector is a viable platform for the detection of breast cancer CTCs in the CSF. NGS performed on CSF samples can identify potentially actionable mutations. [Table: see text]
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Ratinier, Maxime, Steeve Boulant, Christophe Combet, Paul Targett-Adams, John McLauchlan, and Jean-Pierre Lavergne. "Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1." Journal of General Virology 89, no. 7 (July 1, 2008): 1569–78. http://dx.doi.org/10.1099/vir.0.83614-0.
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Since the first report of frameshifting in HCV-1, its sequence has been the paradigm for examining the mechanism that directs alternative translation of the hepatitis C virus (HCV) genome. The region encoding the core protein from this strain contains a cluster of 10 adenines at codons 8–11, which is thought to direct programmed ribosomal frameshifting (PRF), but formal evidence for this process has not been established unequivocally. To identify the mechanisms of frameshifting, this study used a bicistronic dual luciferase reporter system in a coupled transcription/translation in vitro assay. This approach revealed +1 as well as –1 frameshifting, whereas point mutations, selectively introduced between codons 8 and 11, demonstrated that PRF did not readily account for frameshifting in strain HCV-1. Sequence analysis of cDNAs derived from RNA transcribed by T7 RNA polymerase in the dual luciferase reporter system, as well as in both a subgenomic replicon and an infectious clone derived from strain JFH1, identified additions and deletions of adenines between codons 8 and 11 due to transcriptional slippage (TS). Moreover, RNA isolated from cells infected with virus generated by JFH1 containing the A-rich tract also contained heterogeneity in the adenine sequence, strongly suggesting TS by the NS5B viral polymerase. These findings have important implications for insight into frameshifting events in HCV-1 and demonstrate for the first time the involvement of transcriptional slippage in this recoding event.
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Tomikawa, Junko, Shuji Takada, Kohji Okamura, Miho Terao, Hiroko Ogata-Kawata, Hidenori Akutsu, Satoshi Tanaka, Kenichiro Hata, and Kazuhiko Nakabayashi. "Exploring trophoblast-specific Tead4 enhancers through chromatin conformation capture assays followed by functional screening." Nucleic Acids Research 48, no. 1 (November 28, 2019): 278–89. http://dx.doi.org/10.1093/nar/gkz1034.
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Abstract Tead4 is critical for blastocyst development and trophoblast differentiation. We assayed long-range chromosomal interactions on the Tead4 promoter in mouse embryonic stem (ES) cells and trophoblast stem (TS) cells. Using luciferase reporter assays with ES and TS cells for 34 candidate enhancer regions, we identified five genomic fragments that increased Tead4 promoter activity in a TS-specific manner. The five loci consisted of three intra- and two inter-chromosomal loci relative to Tead4 on chromosome 6. We established five mouse lines with one of the five enhancer elements deleted and evaluated the effect of each deletion on Tead4 expression in blastocysts. By quantitative RT-PCR, we measured a 42% decrease in Tead4 expression in the blastocysts with a homozygous deletion with a 1.5 kb genomic interval on chromosome 19 (n = 14) than in wild-type blastocysts. By conducting RNA-seq analysis, we confirmed the trans effect of this enhancer deletion on Tead4 without significant cis effects on its neighbor genes at least within a 1.7 Mb distance. Our results demonstrated that the genomic interval on chromosome 19 is required for the appropriate level of Tead4 expression in blastocysts and suggested that an inter-chromosomal enhancer-promoter interaction may be the underlying mechanism.
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Sablina, A. A., G. V. Ilyinskaya, S. N. Rubtsova, L. S. Agapova, P. M. Chumakov, and B. P. Kopnin. "Activation of p53-mediated cell cycle checkpoint in response to micronuclei formation." Journal of Cell Science 111, no. 7 (April 1, 1998): 977–84. http://dx.doi.org/10.1242/jcs.111.7.977.
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Inactivation of p53 tumor-suppressor leads to genetic instability and, in particular, to accumulation of cells with abnormal numbers of chromosomes. In order to better define the role of p53 function in maintaining genome integrity we investigated the involvement of p53 in the control of proliferation of micronucleated cells resulting from abnormal chromosome segregation. Using cell lines expressing temperature-sensitive (ts) p53 or containing p53 genetic suppressor element (p53-GSE) we showed that inhibition of p53 function increases the frequency of cells with micronuclei. Immunofluorescence study revealed that in REF52 cell cultures with both spontaneous and colcemid-induced micronuclei the proportion of p53-positive cells is considerably higher among micronucleated variants as compared with their mononuclear counterparts. Analysis of 12(1)ConA cells expressing the beta-galactosidase reporter gene under the control of a p53-responsive promoter showed activation of p53-regulated transcription in the cells with micronuclei. Importantly, the percentage of cells manifesting specific p53 activity in colcemid-treated cultures increased with an augmentation of the number of micronuclei in the cell. Activation of p53 in micronucleated cells was accompanied by a decrease in their ability to enter S-phase as was determined by comparative analysis of 5-bromodeoxyuridine (5-BrdU) incorporation by the cells with micronuclei and their mononuclear counterparts. Inhibition of p53 function in the cells with tetracycline-regulated p53 gene expression, as well as in the cells expressing ts-p53 or p53-GSE, abolished cell cycle arrest in micronucleated cells. These results along with the data showing no increase in the frequency of chromosome breaks in REF52 cells after colcemid treatment suggest the existence of p53-mediated cell cycle checkpoint(s) preventing proliferation of micronucleated cells derived as a result of abnormal chromosome segregation during mitosis.
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Prima, Victor, Lia Gore, Aimee Caires, Theresa Boomer, Miyako Yoshinari, Imaizume Masue, Varella-Garcia Marileila, and Stephen P. Hunger. "Chimeric MEF2D and Dazap1 Fusion Proteins Are Created by a Variant t(1;19)(q23;p13.3) in Acute Lymphoblastic Leukemia (ALL)." Blood 104, no. 11 (November 16, 2004): 548. http://dx.doi.org/10.1182/blood.v104.11.548.548.
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Abstract The t(1;19)(q23;p13) is one of the most common chromosome translocations in ALL. In 90–95% of ALL cases with a t(1;19), the 19p13.3 gene E2A is fused to PBX1 located at 1q23, producing E2A-PBX1 chimeric proteins that possess transforming properties. The molecular abnormalities present in the 5–10% of ALL cases with a t(1;19) but no E2A-PBX1 fusion are unknown. TS-2 is an ALL cell line with a t(1;19)(q23;p13.3) but no E2A-PBX1 fusion. We used fluoresence in situ hybridization to localize the chromosome 19 breakpoint in TS-2 to a region approximately 400 kilobases telomeric to E2A and found that the t(1;19) in TS-2 fuses the 19p13 gene DAZAP1 (deleted in azoospermia associated protein 1) to the 1q23 gene MEF2D (myocte enhancer factor 2D). We cloned and sequenced the fusion genes and found they encode for reciprocal in-frame DAZAP1/MEF2D and MEF2D/DAZAP1 fusion transcripts, both of which are expressed in TS-2. MEF2D is a member of the MEF2 family of DNA binding proteins, which were originally characterized as muscle-specific transcription factors that regulated transcription of genes involved in myogenic differentiation. MEF2 proteins are now recognized to have more diverse functions: they are transcriptional effectors of mitogenic signaling pathways and inflammation, play critical roles in calcium-regulated signaling pathways that mediate survival of neurons and T-lympocytes, and participate in neuronal plasticity. DAZAP1 is a protein with novel RNA binding properties that is expressed most abundantly in testis and to a lesser extent in thymus. MEF2D-DAZAP1 includes the MEF2D MADS (MCM1, agamous, deficiens, and serum response factor) box and adjacent MEF2D domain that mediate sequence-specific DNA binding and protein-protein interactions, as well as one of two MEF2D transcriptional activation domains (TAD) fused to the C-terminus of DAZAP1. The DAZAP1-MEF2D chimera includes an intact first and truncated second RNA recognition motif from DAZAP1 joined to the C-terminus of MEF2D that includes its second TAD. We performed electrophoretic mobility shift assays using cognate and mutant MEF2D DNA recognition sites and found that MEF2D/DAZAP1 binds avidly and specifically to DNA in a manner indistinguishable from that of native MEF2D. We found that MEF2D/DAZAP1 activated transcription of a luciferase reporter gene under control of MEF2D recognition elements with substantially more potency than did wild type MEF2D. We also show that DAZAP1/MEF2D proteins bind RNA in a sequence specific manner analogous to that of wild type DAZAP1. MEF2D has been identified as a candidate oncogene involved in development of leukemia/lymphoma via murine retroviral insertional mutagenesis studies. Our data implicate MEF2D in human cancer and suggest that MEF2D/DAZAP1 and/or DAZAP1/MEF2D contributes to leukemogenesis by altering signaling pathways normally regulated by wild type MEF2D and DAZAP1.
Dissertations / Theses on the topic "Ts-reporter"
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Naňo, Andrej. "Automatické generování testovacích dat informačních systémů." Master's thesis, Vysoké učení technické v Brně. Fakulta informačních technologií, 2021. http://www.nusl.cz/ntk/nusl-445520.
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ISAGENis a tool for the automatic generation of structurally complex test inputs that imitate real communication in the context of modern information systems . Complex, typically tree-structured data currently represents the standard means of transmitting information between nodes in distributed information systems. Automatic generator ISAGENis founded on the methodology of data-driven testing and uses concrete data from the production environment as the primary characteristic and specification that guides the generation of new similar data for test cases satisfying given combinatorial adequacy criteria. The main contribution of this thesis is a comprehensive proposal of automated data generation techniques together with an implementation, which demonstrates their usage. The created solution enables testers to create more relevant testing data, representing production-like communication in information systems.