Academic literature on the topic 'Antropologia molecolare, DNA, Biologia'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Antropologia molecolare, DNA, Biologia.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Antropologia molecolare, DNA, Biologia"
1
Francisco, Raffaela Arrabaça, Ricardo Henrique Alves da Silva, Josabeth Mendonça Pereira, Edson Garcia Soares, Euclides Matheucci Júnior, Edna Sadayo Miazato Iwamura, and Marco Aurelio Guimarães. "A antropologia forense como triagem para as análises da genética forense." Saúde, Ética & Justiça 18, no. 1 (June 25, 2013): 128. http://dx.doi.org/10.11606/issn.2317-2770.v18i1p128-133.
Full textAbstract:
<p class="Default"><span class="A2"><span>A Genética Forense hoje é uma das principais ferramentas utilizadas em casos de identificação humana. Esta emprega as técnicas da biologia molecular para auxiliar na elucidação de crimes, principalmente na determinação da autoria deste. Contudo é sabido que a análise do DNA ainda é um exame de alto custo e que muitas vezes, em centros que não possuem um laboratório para esse fim, os mesmos têm que enviar as suas amostras para serem analisadas em outros locais, o que pode demorar meses até a obtenção do resultado. Como uma técnica aliada para a identificação humana, podemos incluir a Antropologia Forense, que vem a ser uma área de conhecimento que aplica os métodos da antropologia física e arqueologia para coleta e análise de evidências legais, buscando estabelecer a identidade de um ser humano. O exame antropológico forense consiste em traçar um perfil bioantropológico da vítima, incluindo: sexo, ancestralidade, idade, estatura, mão dominante (lateralidade), características dentárias, anomalias ósseas, patologias ósseas e características individuais. Com isso espera-se reduzir o número de análises de DNA forense, uma vez que a análise antropológica forense fornece dados que permite o direcionamento e a aplicação do exame de DNA para um indivíduo ou um grupo específico de pessoas. Com isto, também é possível a redução dos gastos de um laboratório de Genética Forense, pois também há a otimização dos resultados. A aplicação do protocolo para análise de ossadas do Laboratório de Antropologia Forense (LAF) serve como triagem para o exame de DNA forense. Este protocolo já é utilizado na Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo (FMRP/USP) e foi criado em 2005, em um projeto entre a University of Sheffield (UK) e o Centro de Medicina Legal (CEMEL) da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo (FMRP/USP). Com os resultados bioantropológicos de um exame de antropologia forense é possível reduzir o número de amostras para que seja feito um exame de DNA, sendo possível reduzir o tempo e o custo de um exame dessa natureza. Isso é demonstrado na análise de caso apresentada aqui.</span></span></p>
2
Gonçalves Salignac, Luana. "JUSTIÇA DE TRANSIÇÃO: AS “AVÓS DA PRAÇA DE MAIO” COMO INSTRUMENTOS DO DIREITO À IDENTIDADE E À VERDADE HISTÓRICA ARGENTINA." Revista Transgressões 5, no. 2 (October 17, 2017): 53. http://dx.doi.org/10.21680/2318-0277.2017v5n2id13011.
Full textAbstract:
O artigo pretende comprovar a eminente contribuição das “Avós da Praça de Maio” para a Justiça de Transição e, consequentemente, para a sociedade argentina, tendo em vista seus trabalhos dedicados à descoberta da verdade, com destaque à histórica e à biológica, as quais possibilitam a restituição do direito à identidade das crianças sequestradas pelo Estado durante a ditadura militar argentina (1976-1983). Para tanto, utiliza-se o método dialógico, abordando o tema em conjunto com diversas áreas do conhecimento além do direito, como com a antropologia, com a biologia, com a história e com a sociologia. Combatendo o crime de apropriação, as “Avós da Praça de Maio” são respaldadas jurídica e cientificamente para realizarem investigações, coleta de dados, pesquisas, exames de DNA e reparação psicológica daqueles que tiveram a identidade restituída, o que consagra sua organização como modelo internacional de um ativismo restaurador da memória e garantidor da justa transição à democracia.
3
Salvatore, Domenico, Angela Celetti, Nicole Fabien, Christian Paulin, Maria Luisa Martelli, Caterina Battaglia, Daniela Califano, et al. "Low frequency of p53 mutations in human thyroid tumors; p53 and Ras mutation in two out of fifty-six thyroid tumours." European Journal of Endocrinology 134, no. 2 (February 1996): 177–83. http://dx.doi.org/10.1530/eje.0.1340177.
Full textAbstract:
Salvatore D, Celetti A, Fabien N, Paulin C, Martelli ML, Battaglia C, Califano D, Monaco C, Viglietto G, Santoro M, Fusco A. Low frequency of p53 mutations in human thyroid tumors; p53 and Ras mutation in two out of fifty-six thyroid tumours. Eur J Endocrinol 1996;134:177–83. ISSN 0804–4643 Objective: p53 is a well-known nuclear phosphoprotein encoded by a suppressor gene known to be mutated in various kinds of human tumours. A relationship between p53 gene mutation and tumour progression seems to be a common feature of several neoplasias. Desing: In order to investigate the role of p53 mutations in human thyroid tumours, DNA samples derived from fifty-six neoplastic tissues, ranging from benign adenomas to undifferentiated carcinomas, were examined for the presence of p53 gene mutations. Methods: The analysis has been conducted using polymerase chain reaction (PCR) amplification of the exons 5–9 of the p53 gene followed by single strand conformation polymorphism (SSCP) and sequence analyses. Results: One anaplastic carcinoma and one papillary carcinoma showed p53 gene mutations in exons 5 and 8, respectively. A cell line established from the papillary carcinoma showed the same mutation present in the original tumour. Both p53 mutations were heterozygous. The p53 positive samples were analysed for other genetic alterations frequently detected in human thyroid carcinomas (mutations of the RET, TRK, and ras oncogenes): both p53-mutated samples proved to be mutated at level of codon 13 of the c-Ki-ras gene. Conclusions: Our data confirm that p53 gene alterations are rare in well-differentiated thyroid tumours, that they are an important requirement for the establishment in culture of human thyroid carcinoma cell lines, and that they can be associated with other genetic alterations, namely ras mutations, in the malignant progression of thyroid tumours. Alfredo Fusco, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia, via S. Pansini 5, 80131, Napoli, Italy
Dissertations / Theses on the topic "Antropologia molecolare, DNA, Biologia"
1
Maffioletti, G. L. "La DNA elicasi Sgs 1 di lievito previene l’accumulo di intermedi ricombinanti durante la replicazione del DNA danneggiato." Doctoral thesis, Università degli Studi di Milano, 2004. http://hdl.handle.net/2434/64585.
Full text
2
Hirano, Sota <1991>. "Development and validation of experimental workflows for a DNA foundry." Doctoral thesis, Università Ca' Foscari Venezia, 2022. http://hdl.handle.net/10579/22069.
Full textAbstract:
Synthetic biology aims to exploit the development of foundational technologies in the current expansion of biotechnology applications that makes the design and manufacturing of engineered biological systems easier and more reliable. Instrumental to fulfil this vision is the decoupling between design and fabrication. Decoupling is defined as breaking down a complex task into simpler and independent ones such that the resulting work can eventually be recombined to produce a functioning whole. This is in stark contrast with the traditional setting where individual researchers needed to carry out different tasks ranging from DNA design to assembly and quality controls. Thus, decoupling enables a team of complementary experts to leverage individual specializations to achieve better outcomes. By decoupling design from fabrication, we empower researchers to design complex constructs irrespective of and independently from the manufacturing technique thus unlocking the full potential of synthetic biology. A typical example is plasmid assembly where the large number of standard plasmid architectures (e.g., SEVA, MoClo, GoldenGate, RFC10) and related assembly techniques actually hinders researchers’ design capabilities rather than enabling it. In this PhD project I focused on the development and validation of DNA fabrication workflows capable of handling multiple assembly techniques completely independent from the design input. The set of workflows developed allows researchers to submit their DNA design without any constraints related to fabrication techniques. The work presented here represents the foundational technology to enable a truly automated DNA foundry for synthetic biology.
3
MERONI, ALICE. "RNA IN DNA: FROM STRUCTURE TO GENOME INSTABILITY." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/570097.
Full textAbstract:
The presence of RNA in the genome of living cells is one of the emerging topics of the last two decades and has been implicated in many biological processes. I focused my attention on ribonucleotides (rNMPs) embedded into DNA during genome duplication, as a threat to its integrity. In fact, rNMPs have been classified as the most frequent non-canonical nucleotides introduced during genome duplication by DNA polymerases. Such high incorporation frequency has been related to a physiological role in mismatch repair, but it can be easily turned into a source of genomic instability if rNMPs are not removed from DNA. This task is performed by RNase H activities that enable error-free repair of embedded single and multiple ribonucleotides.
I first approached the issue of ribonucleotides incorporation into DNA from a physical point of view. Utilizing Atomic Force Microscopy I studied how ribonucleotides intrusions impact on DNA structure. The results obtained provided new insights on the structural changes imposed by ribonucleotides persistence into DNA. The other part of my Ph.D. project concerned the study of rNMPs incorporation in vivo, using the budding yeast S. cerevisiae as a model organism. The second aim was to unravel the function of the Translesion Synthesis polymerase η (Pol η) when the genome contains residual ribonucleotides and when deoxyribonucleotides (dNTPs) pools are depleted. We found that DNA polymerase η is responsible for the cell lethality observed when dNTPs are scarce and RNase H activities are defective. Therefore, I explored and characterized this unexpected toxic activity. We propose a model where Pol η supports cell survival in low dNTPs conditions by promoting DNA replication using ribonucleotides. While this activity is normally beneficial to wild type cells, it is highly toxic to cells defective for RNase H activities.
4
Gravina, Silvia <1979>. "Mechanisms of cell senescence: p21 and DNA damage response in aging and longevity." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/996/1/Tesi_Gravina_Silvia.pdf.
Full textAbstract:
Theory of aging postulates that aging is a remodeling process where the body of survivors progressively adapts to internal and external damaging agents they are exposed to during several decades. Thus , stress response and adaptation mechanisms play a fundamental role in the aging process where the capability of adaptating effects, certainly, also is related the lifespan of each individual. A key gene linking aging to stress response is indeed p21, an induction of cyclin-dependent kinase inhibitor which triggers cell growth arrest associated with senescence and damage response and notably is involved in the up-regulation of multiple genes that have been associated with senescence or implicated in age-related . This PhD thesis project that has been performed in collaboration with the Roninson Lab at Ordway Research Institute in Albany, NY had two main aims: -the testing the hypothesis that p21 polymorphisms are involved in longevity
-Evaluating age-associated differences in gene expression and transcriptional response to p21 and DNA damage In the first project, trough PCR-sequencing and Sequenom strategies, we we found out that there are about 30 polymorphic variants in the p21 gene. In addition, we found an haplotpype located in -5kb region of the p21 promoter whose frequency is ~ 2 fold higher in centenarians than in the general population (Large-scale analysis of haplotype frequencies is currently in progress). Functional studies I carried out on the promoter highilighted that the ―centenarian‖ haplotype doesn’t affect the basal p21 promoter activity or its response to p53.
However, there are many other possible physiological conditions in which the centenarian allele of the p21 promoter may potentially show a different response (IL6, IFN,progesterone, vitamin E, Vitamin D etc). In the second part, project #2, trough Microarrays we seeked to evaluate the differences in gene expression between centenarians, elderly, young in dermal fibroblast cultures and their response to p21 and DNA damage. Microarray analysis of gene expression in dermal fibroblast cultures of individuals of different ages yielded a tentative "centenarian signature". A subset of genes that were up- or downregulated in centenarians showed the same response to ectopic expression of p21, yielding a putative "p21-centenarian" signature. Trough RQ-PCR (as well Microarrays studies whose analysis is in progress) we tested the DNA damage response of the p21-centenarian signature genes showing a correlation stress/aging in additional sets of young and old samples treated with p21-inducing drug doxorubicin thus finding for a subset of of them , a response to stress age-related.
5
Gravina, Silvia <1979>. "Mechanisms of cell senescence: p21 and DNA damage response in aging and longevity." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/996/.
Full textAbstract:
Theory of aging postulates that aging is a remodeling process where the body of survivors progressively adapts to internal and external damaging agents they are exposed to during several decades. Thus , stress response and adaptation mechanisms play a fundamental role in the aging process where the capability of adaptating effects, certainly, also is related the lifespan of each individual. A key gene linking aging to stress response is indeed p21, an induction of cyclin-dependent kinase inhibitor which triggers cell growth arrest associated with senescence and damage response and notably is involved in the up-regulation of multiple genes that have been associated with senescence or implicated in age-related . This PhD thesis project that has been performed in collaboration with the Roninson Lab at Ordway Research Institute in Albany, NY had two main aims: -the testing the hypothesis that p21 polymorphisms are involved in longevity
-Evaluating age-associated differences in gene expression and transcriptional response to p21 and DNA damage In the first project, trough PCR-sequencing and Sequenom strategies, we we found out that there are about 30 polymorphic variants in the p21 gene. In addition, we found an haplotpype located in -5kb region of the p21 promoter whose frequency is ~ 2 fold higher in centenarians than in the general population (Large-scale analysis of haplotype frequencies is currently in progress). Functional studies I carried out on the promoter highilighted that the ―centenarian‖ haplotype doesn’t affect the basal p21 promoter activity or its response to p53.
However, there are many other possible physiological conditions in which the centenarian allele of the p21 promoter may potentially show a different response (IL6, IFN,progesterone, vitamin E, Vitamin D etc). In the second part, project #2, trough Microarrays we seeked to evaluate the differences in gene expression between centenarians, elderly, young in dermal fibroblast cultures and their response to p21 and DNA damage. Microarray analysis of gene expression in dermal fibroblast cultures of individuals of different ages yielded a tentative "centenarian signature". A subset of genes that were up- or downregulated in centenarians showed the same response to ectopic expression of p21, yielding a putative "p21-centenarian" signature. Trough RQ-PCR (as well Microarrays studies whose analysis is in progress) we tested the DNA damage response of the p21-centenarian signature genes showing a correlation stress/aging in additional sets of young and old samples treated with p21-inducing drug doxorubicin thus finding for a subset of of them , a response to stress age-related.
6
De, Magis Alessio <1989>. "G-quadruplex binders cause DNA damage by inducing R-loops in human cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/8442/1/DeMagis_Alessio_tesi.pdf.
Full textAbstract:
G-Quadruplexes (G4s) and R-loops are non-B DNA structures that can regulate transcription and replication. G4s are formed from four guanine residues that are held together in the same plane by Hoogsteen hydrogen bonds and further stabilized by the presence of monovalent cations. R-loops are triple-strand structures that contain an RNA-DNA hybrid and displaced single-stranded DNA. One of the most important features that influence these DNA structures is the GC content. Indeed, R-loop structures can be favoured by a high guanine density in the non-template DNA strand and this is specifically due to the higher thermodynamic stability of RNA-DNA hybrid. R-loops and G4s are generally regarded as highly deleterious, indeed the structures can block both transcription and DNA replication, creating replicative stress and potentially causing DNA damage. Here, we used immunofluorescence analysis in order to identify the increase of G4s and R-loops in cancer cells treated with specific G4 binders at long and very short time. At long time, the increase of these two non-B DNA structures triggers genomic DNA damage as established by the formation of γH2AX foci and other markers of cellular DNA damage response. Interestingly, stable and transient overexpression of RNaseH, an enzyme that specifically removes R-loop structures, induce a rescue of G4 binder-induced DNA damage and genome instability. Our study provides the first direct evidence of a mechanistic link between G4s and R-loops in human cancer cells.
7
Duardo, Renee Concetta <1994>. "Unbalanced R-loops and micronuclei induced by DNA topoisomerase I poisons in cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10182/1/Duardo_Ren%C3%A9e_Concetta_thesis.pdf.
Full textAbstract:
Topoisomerase I (Top1) poisons are among the most clinically-effective drugs used for colon, ovary and lung cancers. Unpublished data from our lab have recently revealed that the structurally-unrelated Top1 poisons, Camptothecin (CPT) and Indimitecan (LMP776), induce the formation of micronuclei (MNi) in human cancer cells. In addition, MNi trigger an innate immune gene response by stimulating the cGAS/STING pathway. As the mechanisms of MNi formation are not fully determined, our aim is here to establish how MNi form after Top1 poisoning. Using immunofluorescence assays and EdU labelling of nascent DNAs, our results show that, after 24 hours of recovery, a short treatment with sub-cytotoxic doses of Top1 poisons induces the formation of MNi that do not contain newly synthetized (EdU+) DNA. We also saw that Top1 poisons delay replication machinery reducing EdU incorporation and produce significant levels of the damage markers γH2AX and p53BP1 in S-phase cells but not in G1 and G2/M cells. The results also show that MNi formation is dependent on R-loops, as RNaseH1 overexpression markedly reduces Top1 induced MNi. Genome-wide mapping of R-loops by DRIP-seq technique revealed that R-loop levels are both decreased and increased by CPT. In particular, increased R-loops are mainly found at active genes and always overlapped with Top1cc sites. We also found that increased R-loops overlap with lamina-associated chromatin domains while decreased R-loops correlate with replication origin sites. Overall, our data are consistent with the formation of MNi due to R-loop increase and under-replication at specific regions caused by Top1 poisons. These results will eventually help in developing new strategies for effective personalized interventions by using Top1-targeted compounds as immuno-modulators in cancer patients.
8
Baranello, Laura <1981>. "Transcriptional functions of DNA Topoisomerases at a genome-wide scale and a single gene levels." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2970/1/Laura_Baranello_Transcriptional_functions_of_DNA_Topoisomerases_at_a_genome-wide_scale_and_a_single_gene_levels.pdf.
Full textAbstract:
The DNA topology is an important modifier of DNA functions. Torsional stress is generated when right handed DNA is either over- or underwound, producing structural deformations which drive or are driven by processes such as replication, transcription, recombination and repair. DNA topoisomerases are molecular machines that regulate the topological state of the DNA in the cell. These enzymes accomplish this task by either passing one strand of the DNA through a break in the opposing strand or by passing a region of the duplex from the same or a different molecule through a double-stranded cut generated in the DNA. Because of their ability to cut one or two strands of DNA they are also target for some of the most successful anticancer drugs used in standard combination therapies of human cancers. An effective anticancer drug is Camptothecin (CPT) that specifically targets DNA topoisomerase 1 (TOP 1).
The research project of the present thesis has been focused on the role of human TOP 1 during transcription and on the transcriptional consequences associated with TOP 1 inhibition by CPT in human cell lines. Previous findings demonstrate that TOP 1 inhibition by CPT perturbs RNA polymerase (RNAP II) density at promoters and along transcribed genes suggesting an involvement of TOP 1 in RNAP II promoter proximal pausing site. Within the transcription cycle, promoter pausing is a fundamental step the importance of which has been well established as a means of coupling elongation to RNA maturation. By measuring nascent RNA transcripts bound to chromatin, we demonstrated that TOP 1 inhibition by CPT can enhance RNAP II escape from promoter proximal pausing site of the human Hypoxia Inducible Factor 1 (HIF-1) and c-MYC genes in a dose dependent manner. This effect is dependent from Cdk7/Cdk9 activities since it can be reversed by the kinases inhibitor DRB. Since CPT affects RNAP II by promoting the hyperphosphorylation of its Rpb1 subunit the findings suggest that TOP 1inhibition by CPT may increase the activity of Cdks which in turn phosphorylate the Rpb1 subunit of RNAP II enhancing its escape from pausing.
Interestingly, the transcriptional consequences of CPT induced topological stress are wider than expected. CPT increased co-transcriptional splicing of exon1 and 2 and markedly affected alternative splicing at exon 11. Surprisingly despite its well-established transcription inhibitory activity, CPT can trigger the production of a novel long RNA (5’aHIF-1) antisense to the human HIF-1 mRNA and a known antisense RNA at the 3’ end of the gene, while decreasing mRNA levels. The effects require TOP 1 and are independent from CPT induced DNA damage. Thus, when the supercoiling imbalance promoted by CPT occurs at promoter, it may trigger deregulation of the RNAP II pausing, increased chromatin accessibility and activation/derepression of antisense transcripts in a Cdks dependent manner. A changed balance of antisense transcripts and mRNAs may regulate the activity of HIF-1 and contribute to the control of tumor progression
After focusing our TOP 1 investigations at a single gene level, we have extended the study to the whole genome by developing the “Topo-Seq” approach which generates a map of genome-wide distribution of sites of TOP 1 activity sites in human cells. The preliminary data revealed that TOP 1 preferentially localizes at intragenic regions and in particular at 5’ and 3’ ends of genes. Surprisingly upon TOP 1 downregulation, which impairs protein expression by 80%, TOP 1 molecules are mostly localized around 3’ ends of genes, thus suggesting that its activity is essential at these regions and can be compensate at 5’ ends. The developed procedure is a pioneer tool for the detection of TOP 1 cleavage sites across the genome and can open the way to further investigations of the enzyme roles in different nuclear processes.
9
Baranello, Laura <1981>. "Transcriptional functions of DNA Topoisomerases at a genome-wide scale and a single gene levels." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2970/.
Full textAbstract:
The DNA topology is an important modifier of DNA functions. Torsional stress is generated when right handed DNA is either over- or underwound, producing structural deformations which drive or are driven by processes such as replication, transcription, recombination and repair. DNA topoisomerases are molecular machines that regulate the topological state of the DNA in the cell. These enzymes accomplish this task by either passing one strand of the DNA through a break in the opposing strand or by passing a region of the duplex from the same or a different molecule through a double-stranded cut generated in the DNA. Because of their ability to cut one or two strands of DNA they are also target for some of the most successful anticancer drugs used in standard combination therapies of human cancers. An effective anticancer drug is Camptothecin (CPT) that specifically targets DNA topoisomerase 1 (TOP 1).
The research project of the present thesis has been focused on the role of human TOP 1 during transcription and on the transcriptional consequences associated with TOP 1 inhibition by CPT in human cell lines. Previous findings demonstrate that TOP 1 inhibition by CPT perturbs RNA polymerase (RNAP II) density at promoters and along transcribed genes suggesting an involvement of TOP 1 in RNAP II promoter proximal pausing site. Within the transcription cycle, promoter pausing is a fundamental step the importance of which has been well established as a means of coupling elongation to RNA maturation. By measuring nascent RNA transcripts bound to chromatin, we demonstrated that TOP 1 inhibition by CPT can enhance RNAP II escape from promoter proximal pausing site of the human Hypoxia Inducible Factor 1 (HIF-1) and c-MYC genes in a dose dependent manner. This effect is dependent from Cdk7/Cdk9 activities since it can be reversed by the kinases inhibitor DRB. Since CPT affects RNAP II by promoting the hyperphosphorylation of its Rpb1 subunit the findings suggest that TOP 1inhibition by CPT may increase the activity of Cdks which in turn phosphorylate the Rpb1 subunit of RNAP II enhancing its escape from pausing.
Interestingly, the transcriptional consequences of CPT induced topological stress are wider than expected. CPT increased co-transcriptional splicing of exon1 and 2 and markedly affected alternative splicing at exon 11. Surprisingly despite its well-established transcription inhibitory activity, CPT can trigger the production of a novel long RNA (5’aHIF-1) antisense to the human HIF-1 mRNA and a known antisense RNA at the 3’ end of the gene, while decreasing mRNA levels. The effects require TOP 1 and are independent from CPT induced DNA damage. Thus, when the supercoiling imbalance promoted by CPT occurs at promoter, it may trigger deregulation of the RNAP II pausing, increased chromatin accessibility and activation/derepression of antisense transcripts in a Cdks dependent manner. A changed balance of antisense transcripts and mRNAs may regulate the activity of HIF-1 and contribute to the control of tumor progression
After focusing our TOP 1 investigations at a single gene level, we have extended the study to the whole genome by developing the “Topo-Seq” approach which generates a map of genome-wide distribution of sites of TOP 1 activity sites in human cells. The preliminary data revealed that TOP 1 preferentially localizes at intragenic regions and in particular at 5’ and 3’ ends of genes. Surprisingly upon TOP 1 downregulation, which impairs protein expression by 80%, TOP 1 molecules are mostly localized around 3’ ends of genes, thus suggesting that its activity is essential at these regions and can be compensate at 5’ ends. The developed procedure is a pioneer tool for the detection of TOP 1 cleavage sites across the genome and can open the way to further investigations of the enzyme roles in different nuclear processes.
10
Bertozzi, Davide <1983>. "RNA non-codificanti indotti da danno al DNA regolano il fattore di trascrizione HIF-1α." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4746/1/bertozzi_davide_tesi.pdf.
Full textAbstract:
Recenti analisi sull’intero trascrittoma hanno rivelato una estensiva trascrizione di RNA non codificanti (ncRNA), le quali funzioni sono tuttavia in gran parte sconosciute. In questo lavoro è stato dimostrato che alte dosi di camptotecina (CPT), un farmaco antitumorale inibitore della Top1, aumentano la trascrizione di due ncRNA antisenso in 5’ e 3’ (5'aHIF-1α e 3'aHIF-1α rispettivamente) al locus genico di HIF-1α e diminuiscono i livelli dell’mRNA di HIF-1α stesso. Gli effetti del trattamento sono Top1-dipendenti, mentre non dipendono dal danno al DNA alla forca di replicazione o dai checkpoint attivati dal danno al DNA. I ncRNA vengono attivati in risposta a diversi tipi di stress, il 5'aHIF-1α è lungo circa 10 kb e possiede sia il CAP in 5’ sia poliadenilazione in 3’ (in letteratura è noto che il 3'aHIF-1α è un trascritto di 1,7 kb, senza 5’CAP né poliadenilazione). Analisi di localizzazione intracellulare hanno dimostrato che entrambi sono trascritti nucleari. In particolare 5'aHIF-1α co-localizza con proteine del complesso del poro nucleare, suggerendo un suo possibile ruolo come mediatore degli scambi della membrana nucleare. È stata dimostrata inoltre la trascrizione dei due ncRNA in tessuti di tumore umano del rene, evidenziandone possibili ruoli nello sviluppo del cancro. È anche noto in letteratura che basse dosi di CPT in condizioni di ipossia diminuiscono i livelli di proteina di HIF-1α. Dopo aver dimostrato su diverse linee cellulari che i due ncRNA sopracitati non potessero essere implicati in tale effetto, abbiamo studiato le variazioni dell’intero miRnoma alle nuove condizioni sperimentali. In tal modo abbiamo scoperto che il miR-X sembra essere il mediatore molecolare dell’abbattimento di HIF-1α dopo trattamento con basse dosi di CPT in ipossia. Complessivamente, questi risultati suggeriscono che il fattore di trascrizione HIF-1α venga finemente regolato da RNA non-codificanti indotti da danno al DNA.Whole transcriptome analyses revealed a broad transcription of non-coding RNAs (ncRNA), which functions are largely unknown. In this work it was shown that high doses of camptothecin (CPT), an antitumor inhibitor of Top1, increase the transcription of two ncRNA antisense 5 'and 3' (5'aHIF-1α and 3'aHIF-1α respectively) respect to the locus HIF-1α gene and decreased HIF-1α mRNA levels. Treatment effects are Top1-dependent, while are not dependent by the replication fork-mediated DNA damage or by DNA damage-activated checkpoints. The ncRNAs are activated in response to different stress types, the 5'aHIF-1α is about 10 kb length and it has both 5’CAP and polyadenylation (in literature it is known that the 3'aHIF-1α is a transcript of 1.7 kb, with no 5'CAP and no polyadenylation). Intracellular localization have shown that both ncRNAs are nuclear transcripts. In particular 5'aHIF-1α co-localizes with nuclear pore complex proteins, suggesting its possible role as a traffic-mediator of the nuclear membrane. It has been demonstrated also the transcription of the two ncRNAs in human kidney tumor tissues, highlighting it possible roles in cancer development. It is also known that low doses of CPT in hypoxia conditions decrease the HIF-1α protein levels. Having demonstrated on several cell lines that the two ncRNA above could not be implicated in this effect, we studied the entire human miRnoma variations under our experimental conditions. Thus we found that miR-X seems to be the molecular mediator of HIF-1α abatement after low doses CPT treatment in hypoxia conditions. Overall, these results suggest that HIF-1α transcription factor is finely regulated by non-coding RNA induced by DNA damage.
Books on the topic "Antropologia molecolare, DNA, Biologia"
1
Baiamonte, Salvatore. ESTRAZIONE DI DNA DALLA FRUTTA: Esperimento Scientifico Di Biologia Molecolare per Ragazzi. Independently Published, 2017.
Find full text
2
Baiamonte, Salvatore. DNA : la Prova Certa?: Biologia Molecolare Forense per Ragazzi e per Adulti Appassionati Di Scienza e Diritto. Independently Published, 2016.
Find full text
3
Baiamonte, Salvatore. DNA, la Prova Certa?: Biologia Molecolare e Processo Penale Trattati in Maniera Semplice per Ragazzi e Adulti Appassionati Di Scienza. Independently Published, 2016.
Find full textConference papers on the topic "Antropologia molecolare, DNA, Biologia"
1
Martins, Letícia, Marianny Rodrigues Costa Amorim, and Andreia Juliana Rodrigues Caldeira. "ORIGEM E IMPORTÂNCIA FILOGENÉTICA DO DNA MITOCONDRIAL." In I Congresso Nacional On-line de Biologia Celular e Estrutural. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1942.
Full textAbstract:
Introdução: A molécula do DNA mitocondrial (mtDNA) é muito utilizada em estudos envolvendo estrutura populacional, relações filogenéticas e o entendimento de vários aspectos biológicos e evolutivos de uma grande variedade de organismos. Mas, apesar desse destaque em estudos moleculares, ainda existem muitas dúvidas sobre a organela. Objetivo: Realizar uma revisão bibliográfica sobre a origem e importância filogenética do mtDNA.Material e método: Foi realizada uma busca de artigo embase dados como SciELO Brasil e Web of Science. Resultados: A mitocôndria é uma organela responsávelpela respiração celular e tem origem endossimbiótica, que pode ser evidenciada pela presença de um DNA própriocircular, semelhante à células ancestrais procariotas. O mtDNA é pequeno (aproximadamente 16 kb nos animais), com raras exceções; possui poucos genes, 37 no total, que codifica para apenas 5% dos produtos necessários para o funcionamento da mitocôndria. É considerado como um genoma compacto, com poucas seqüências espaçadoras, seqüências repetitivas, pseudogenes e introns e aindaausência de recombinação, embora exceções sejam descritas. O conteúdo gênico é conservado, e a ordem em que esses genes se encontram organizados no genomacostuma ser também conservada. A taxa evolutiva do mtDNA é alta, quando comparada a do genoma nuclear. O mtDNA é capaz de ligar pessoas à sua linhagem materna, já que este possui herança exclusivamente materna além disso, é considerado um marcador genético, pois apresenta mais de 5 mil cópias numa única célula. Conclusão: A análise desse tipo de DNA é excepcional em estudo de tecidos antigos e até arqueológicos, como dentes e ossos epodem ser amplamente usados em estudo de evolução e antropologia. Na atualidade, o mtDNA ganhou destaque na área forense, favorecendo a coleta evidencias que elucidam as situações de crimes.