Дисертації з теми "Prb6"
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Bouvet, Alain. "Étude par diffusion inélastique de neutrons des propriétés magnétiques de borures de terre rare : CeB6, PrB6 et YbB12." Université Joseph Fourier (Grenoble ; 1971-2015), 1993. http://www.theses.fr/1993GRE10186.
Повний текст джерелаDagne, Carl. "Implementering av tillståndsmaskiner med PRBS." Thesis, Linköping University, Department of Electrical Engineering, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1841.
Повний текст джерелаTillståndsmaskiner är vanliga komponenter i många digitala konstruktioner. En vanlig typ av tillståndsmaskin är räknare. Räknare är ofta ganska kostsamma att implementera, med avseende på antalet grindar. För att reducera denna kostnad kan istället en PRBS (Pseudo Random Binary Sequence) användas. Denna byggs upp av ett register där en xor - operation utförs mellan två positioner, som beror på längden av registret. Resultatet från denna operation skiftas sedan in i registret. På detta sätt fås en till synes slumpmässig sekvens. Talen är dock inte på något sätt slumpmässiga utan kan hela tiden förutsägas. I detta examensarbete har en undersökning för att konstruera en billig tillståndsmaskin med hjälp av PRBS:er gjorts i MatLab. Tre olika program har skrivits för att beräkna olika kostnader vid implementering av en tillståndsmaskin.
Finite state machines are common components in digital designs. A common type of finite state machine is a counter. Counters are often quite expensive to implement, with respect to the number of gates. To reduce this cost, a PRBS (Pseudo Random Binary Sequence) can be used. It is constructed of a register where a xor - operation is performed between two positions, which depend on the length of the register. The result from this operation is then shifted back into the register yielding a random-like sequence. The numbers are not random, but can always be predicted. In this thesis work finite state machine using PRBS are designed in MatLab. Three different programs have been written to calculate the costs for implementation of a PRBS.
Newton, B. T. "Applied gas tracing or permeable reactive barriers (PRBs)." Thesis, Queen's University Belfast, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602710.
Повний текст джерелаORRU', ROBERTO. "Sequenziamento e Analisi Molecolare di Varianti Alleliche del Gene PRB1." Doctoral thesis, Università degli Studi di Cagliari, 2016. http://hdl.handle.net/11584/266626.
Повний текст джерелаKalpathy, Venkiteswaran Venkatasubramanian. "Development of a Design Framework for Compliant Mechanisms using Pseudo-Rigid-Body Models." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1482232749828813.
Повний текст джерелаSun, Ang. "Anti-cancer Functions and Mechanisms of a pRb2/p130 Peptide Fragment." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/58962.
Повний текст джерелаPh.D.
The spacer region of pRb2/p130 was reported to be able to inhibit the kinase activity of Cdk2. The region responsible for the inhibitory effect was further narrowed down to a 39-amino-acid sequence, which was named as Spa310. In this dissertation, the anti-cancer functions and mechanisms of Spa310 were studied. The synthesized Spa310 peptide was able to inhibit the kinase activities of Cdk2/Cyclin E/A complexes. In vitro kinase assays showed the inhibition occurred in a dose-dependent manner. The half maximal inhibition concentration of the Spa310 in the kinase assay was 1.67mM. In addition, it has been shown that Spa310 peptide is able to inhibit the kinase activities of both Cdk2/Cyclin E and Cdk2/Cyclin A. Intra-cellular distribution study using fluorescein-labeled Spa310 peptide showed that Spa310 was able to localize to the nuclei of A549 cancer cells. Some data indicated the endoplasmic reticulum might play a role in transporting Spa310 peptide from cytoplasm to the nucleus. At high concentration, the treatment of Spa310 peptide was able to arrest cells at the G0/G1 phase of the cell cycle and reduce the growth of xenografted tumors in nude mice. Further studies indicated Spa310 peptide is not a specific inhibitor for Cdk2/Cyclin E/A. It is also able to inhibit the kinase activities of Cdk1/Cyclin B, Cdk4/Cyclin D and Cdk9/Cyclin T/K. Result of a binding assay using GST-Spa310 and in vitro transcribed/translated Cdk2 did not support a direct binding between Spa310 and Cdk2. Additionally, GST-Spa310 was unable to bind to the in vitro transcribed/translated Cyclin E. At first, co-immunoprecipitation experiments indicated a weak binding between Spa310 peptide and Cdk2. However, later this weak binding was proven to be unspecific and only occurred when the concentration of Spa310 peptide was high. Thus, the hypothesized mechanism of the inhibitory effect of Spa310 was not supported. After noticing three classic Cdk phosphorylation sites present in Spa310, it was proven that Spa310 is a substrate for Cdk1, 2, 4 and 9. Results of kinase assays supported the inhibitory effect of Spa310 on the different Cyclin-dependent kinases was resulted from a substrate-competitive mechanism. Although the data generated from this study does not support Spa310 is a potent peptide inhibitor for the Cdks, knowledge gained from and the approach used in this research can be applied to design and develop more potent and specific Cdk2 peptide inhibitors, which have their potentials to work as powerful anti-cancer reagents.
Temple University--Theses
STUCCHI, SIMONE. "Role of glucose and peroxiredoxin 6 in human chondrocytes and novel biomaterial for in vitro three-dimensional chondrocytes culture." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/261927.
Повний текст джерелаOsteoarthritis (OA) is the most common rheumatic disease in the world and represents the first cause of disability in the world. OA results from the loss of balance between degradation and repair inside cartilage, in favor of degradation, with increased activity of catabolic enzymes such as matrix metalloproteinases and decreased production of ECM proteins. Chondrocytes are responsible for the repair and biosynthesis of elements of the extracellular matrix. Experimental findings support the hypothesis that diabetes is an independent risk factors for OA. However, correct molecular mechanisms underlying the diabetes-associated OA phenotype is still largely unknown. Firstly chondrocytes cell growth, ROS levels and apoptosis were analyzed using different glucose concentration. Results shown that chondrocytes prefer 2.5 mM of glucose which was used as normal glucose concentration and 25 mM of glucose was used as high glucose concentration. ROS levels and cell death increase in chondrocytes growth in high glucose environment. Also cytoskeletal network is more disorganized in C28/I2 cells growth at high glucose concentration, this correlates with different RalA-GTP levels which is involved in the regulation of cytoskeletal organization. Experiments were performed even using medium supplemented by ITS (Insulin-transferrin-selenium) to promote chondrocyte differentiation and IL-1β was used to simulate osteoarthritic cartilage environment. Ral A-GTP levels are lower in cells grown in 25 mM of glucose and stimulated with IL1β. Levels of p-ERK1/2 decrease in cells grown at high glucose concentration and in cells stimulated with IL1β. Furthermore, NF-κB, iNOS and LC3II levels were evaluated. Results demonstrate that high glucose media block autophagic process in chondrocytes. Effect of glucose concentration on human primary chondrocytes cells was evaluated after only 24 h to understand which signaling pathways is activated by high glucose environment. Phosphorylation of ERK1/2, p38, Akt and p65 is altered in chondrocytes growth at high glucose concentration and this correlates with an increase secretion of MMP-13. To better analyze the role of ROS levels in the chondrocytes I worked for 6 months in the Dr. Loeser Lab at the School of Medicine in the University of North Carolina at Chapel Hill; one of the best lab in the cartilage biology field. I worked on PRX6 which is involved in the recovery from H2O2. Oxidation state of PRX6 was evaluated in chondrocytes treated with different stimuli, like H2O2, Fn-f, menadione (men) and DMNQ. After this experiment, we wanted to see if PRX6 could impact the MAPK signaling pathways in cells treated with IGF-1, menadione, combination of menadione and IGF-1 and with Fn-f. Localization of PRX6 was analyzed using nuclear and cytoplasm extraction. Then I worked in collaboration with Prof. Laura Cipolla and Prof. Maddalena Collini to develop and characterized a new gelatin-based hydrogel using Diethylsquarate as crosslinker.
Gong, Mingrui. "Multivariable system controller tuning techniques based on sensitivity measures." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312434.
Повний текст джерелаKato, Gabriel Fukunaga. "Avaliação da expressão imuno-histoquímica das proteínas p53 e pRB em ameloblastomas e tumores odontogênicos queratocísticos." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/23/23141/tde-19012016-155909/.
Повний текст джерелаOdontogenic tumors are a comprehensive group of tumor diseases, being ameloblastomas and keratocystic odontogenic tumors the most frequent benign odontogenic tumors. Their biological characteristics are little unknown. The aim of present study was to evaluate the immunohistochemical profile of pRB and p53 proteins in 21 cases of ameloblastomas and 20 cases of keratocystic odontogenic tumors for anti-pRB and anti-p53 antibodies. The quantification of immunostaining was performed manually with high-resolution photographs processed in the ImageJ software to quantify positive cells in a 1000 cells-field. The location of immunostaining for both antibodies was similar. In ameloblastomas, positive cells are located mainly in the peripheral layers, whereas in keratocystic odontogenic tumors the positive cells are located in the suprabasal layers. Quantitatively, the percentage of labeled cells was statistically higher in ameloblastomas for anti-p53 (p = 0.01) and higher in keratocystic odontogenic tumors for anti-pRB (p = 0.04). There was no statistical correlation between the percentage of labeled cells to anti-p53 and anti-pRB in ameloblastomas, however, its correlation was positive and moderate in keratocystic odontogenic tumors (r = 0.537; p = 0.018). It is possible to identify a slight difference in immuno-quantification for anti-p53 and anti-pRB among these lesions. These results must be pondered by the small sample, however, is suggests a different profile in a preponderant key biological mechanisms for odontogenic tumors.
Chan, Ho Man. "Molecular basis of cell cycle control : p300 and pRb." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326430.
Повний текст джерелаSajtar, Eric T. "Toolbox to evaluate treatment technologies for PRB CBM water." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1594485851&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.
Повний текст джерелаLagerholm, Anton, and Staffan Molinder. "Parameter estimation on a closed loop nutrunner system by added PRBS disturbance signal." Thesis, KTH, Maskinkonstruktion (Inst.), 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-168906.
Повний текст джерелаDetta examensarbete undersökte parameterskattning på en elektrisk skruvdragare som reglerades under återkoppling. Syftet med detta var att skapa modeller som senare ska kunna användas vid design av regulatorer för nya åtdragningsstrategier. Systemet delades in i två modeller, en för den elektriska motorn och en för drivlinan, som kunde parameterskattas separat. Data hämtade in dels från kontrollsystemet och med ett externt DAQ system vid körning av verktyget under återkoppling. En PRBS signal adderades till systemet som en störning i syfte att ytterligare excitera så att den interna dynamiken skulle synas i de uppmätta utsignalerna. MATLAB-vertyget Simulink Design Optimization användes för parameterskattningen och resultatet validerades sedan. Valideringen visade att systemet simulerades väl, detta visade på lämpligheten hos den adderade störsignalen.
COMISSO, ELISA. "OCT4 promuove l'aggressività del tumore ovarico sieroso ad alto grado attraverso l'inattivazione di pRB e l'aumento della stabilità genomica." Doctoral thesis, Università degli Studi di Trieste, 2016. http://hdl.handle.net/11368/2908031.
Повний текст джерелаOCT4 (POU5F1) is a member of the POU family of transcription factors and is known to play a crucial role in the maintenance of self-renewal and pluripotency in Embryonic Stem Cells (ESCs). Nowadays, several studies highlight the importance of OCT4 expression in tumors in order to maintain the tumorigenic stem cell-like features. Despite the essential role of OCT4 during embryogenesis and reprogramming of somatic cells, its exact role in tumorigenesis is still not well defined. In this thesis we found that OCT4 drives the expression of Nuclear Inhibitor of Protein Phosphatase type 1 (NIPP1) and Cyclin F (CCNF) that together inhibit Protein Phosphatase 1 (PP1) in High-Grade Serous Ovarian Cancer (HG-SOC). This cause Retinoblastoma protein (pRB) hyper-phosphorylation, accelerated cell proliferation and increased in vitro tumorigenicity of ovarian cancer cells. In parallel, OCT4 and NIPP1/CCNF drive the expression of the central Chromosomal Passenger Complex (CPC) components, Borealin, Survivin and the mitotic kinase Aurora B, that are essential for the maintenance of genomic stability. CPC, in fact, promoting the “centrosomes clustering mechanism”, leads to increased mitotic stability. Loss of OCT4 or NIPP1/CCNF results in severe mitotic defects, multipolar spindles and supernumerary centrosomes, finally leading to the induction of senescence and apoptosis. Importantly, activation of these parallel pathways leads to a dramatically reduced overall survival of HG-SOC patients. In conclusion we demonstrate that OCT4 increases HG-SOC aggressiveness by inactivating the Retinoblastoma tumorsuppressor pathway and enhancing mitotic fidelity in cancer cells, highlighting an unknown role of OCT4 as central regulator of genomic stability and RB tumorsuppressor pathway activity. Thus, targeting the OCT4-NIPP1/CCNF-PP1 pathway could be a promising strategy to manage and treat specifically an aggressive subpopulation of HG-SOC.
Luczynski, Maciej Tomasz. "Structure-guided functional analysis of the pRb N-terminal domain." Thesis, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531336.
Повний текст джерелаZarkowska, Tamara Anna. "Phosphorylation of the retinoblastoma protein, pRB, by CDK4-cyclin D1." Thesis, Institute of Cancer Research (University Of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321951.
Повний текст джерелаFranklin, Phoebe. "Are permeable reactive barriers (PRBS) a viable technology for remediation of diffuse nitrate pollution?" Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523068.
Повний текст джерелаHorton, Lynn Elizabeth. "Studies on cyclin structure and pRb phosphorylation in cell cycle control." Case Western Reserve University School of Graduate Studies / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=case1057684343.
Повний текст джерелаCavallaro, Piera Maria Luisa. "Valutazione di materiali innovativi per l'allestimento di barriere reattive permeabili (PRB)." Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1252.
Повний текст джерелаYang, Zhongyu. "Performance Advantages of Maximum Likelihood Methods in PRBS-Modulated Time-of-flight Energy Loss Spectroscopy." Fogler Library, University of Maine, 2003. http://www.library.umaine.edu/theses/pdf/YangZ2003.pdf.
Повний текст джерелаSeibel, B. [Verfasser]. "Berechnungen von Röntgenabsorptionsspektren an YBa₂Cu₃O₇, PrBa₂Cu₃O₇ und Sr₂RuO₄ / B. Seibel." Karlsruhe : KIT-Bibliothek, 1997. http://d-nb.info/1108447422/34.
Повний текст джерелаLarrotta, Fabian Núñez. "Estudo e implementação de sinais de excitação aplicados em identificação de sistemas multivariáveis." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/3/3139/tde-21062016-135438/.
Повний текст джерелаDue to the Predictive Control based on Model (MPC) rising in other process beyond refining and petrochemical plants, which in general have multiple inputs and outputs, there have been an increase in demand of models generated by system identification. Identify models that accurately represent the dynamics of the process depends largely on the characteristics of the processes excitation signals. Thus, the focus of this work is to perform a study of the typical signals used in identification systems, PRBS and GBN, in a multivariable approach. The study carried out in this work begins on the individual generation characteristics of the signals, and then an analysis is made of input signals cross-correlation, by observing the in uence of this on the identification results. Avoid a high correlation among the input signals allows to determine the effect of each input on the output of the identification process. An important point in the signals design for multivariable system identification is its frequency to get excite the processes in the normal operation frequency regions and thus extract the maximum dynamic information possible of the process. The studied characteristics are evaluated by testing three different simulated plants, categorized as well, medium and ill conditioned. These implementations were made using GBN and PRBS signals of dierent frequencies. Expressions to characterize the excitation signals were evaluated identifying the processes in open and closed-loop. For ill-conditioned plants were implemented signals composed by a fully correlated part and a non-correlated part, known as two-step method. Finally, identification experiments are performed on a real time application in a pilot pH neutralization plant. The tests were made in the plant in order to evaluate the frequency and correlation studies in a real application. The results show that the completely uncorrelated signals condition must not be satisfied to have good results on the identified models, which besides allows greater exibility in the generation of the excitation signals set.
Ali-Khan, Nadeem. "Biochemical characterisation of the eukarytic cell cycle regulatory proteins, E2F and pRB." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270398.
Повний текст джерелаSimpson, Matthew Thomas W. "Caspace-3 deficiency rescues peripheral nervous system defect in pRb nullizygous mice." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6297.
Повний текст джерелаBanerji, Lolita. "The role and regulation of the pRB/E2F pathway in B-lymphocytes." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252407.
Повний текст джерелаKorah, Juliana. "Role of the pRb/E2F pathway in TGF beta-mediated tumour suppression." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=123071.
Повний текст джерелаLa formation de tumeurs est caractérisée par une série d'évènements bien définis qui sont communs à tous les cancers, notamment l'habileté des cellules à atteindre l'immortalisation, maintenir la prolifération, et éviter l'apoptose. Ces procédés cytostatiques et de croissance cellulaire sont normalement régulés par divers facteurs de croissance qui agissent de concert pour maintenir l'homéostasie cellulaire. De ce fait, un dérèglement dans la signalisation de ces facteurs mène à une croissance incontrôlée et à la formation de tumeurs. Plus particulièrement, le facteur de croissance β (TGFβ) exerce un rôle central en agissant comme suppresseur de tumeurs dans quasiment tous les types cellulaires et tissus. Les effets en tant que suppresseur de tumeurs du TGFβ sont illustrés par son habileté à inhiber la croissance cellulaire, induire la mort cellulaire, et prévenir l'immortalisation cellulaire. La capacité du TGFβ à prévenir l'immortalisation cellulaire s'appuie sur le fait qu'il inhibe l'activité de la télomérase. Bien que l'expression de hTERT, la protéine faisant partie du complexe de la télomérase, soit accrue dans la plupart des cellules cancéreuses, des études de notre laboratoire ont révélé que le TGFβ peut réprimer l'expression du gène codant pour hTERT dans les cellules autant normales que cancéreuses à travers des voies de signalisation multiples. Nous avons de plus trouvé que l'inhibition de hTERT par le TGFβ requiert la synthèse d'une molécule intermédiaire que nous avons identifié comme étant le facteur de transcription E2F1, et avons démontré que d'interférer avec l'activité du E2F1 empêche les effets inhibiteurs du TGFβ sur l'activité de la télomérase. La famille des facteurs de transcription E2F joue un rôle central dans la régulation de la progression du cycle cellulaire. La dérégulation de ces facteurs est un évènement commun dans la plupart des cancers. Il a été démontré que le E2F1 possède l'habileté d'induire autant la progression du cycle cellulaire que l'apoptose, cependant, le mécanisme par lequel le E2F1 induit l'apoptose n'est pas complètement élucidé. Le TGFβ est lui-même un facteur pro-apoptotique puissant, car il module l'expression de plusieurs gènes apoptotiques dans une variété de tissus. Cependant, une voie de signalisation commune et centrale, agissant en amont du TGFβ et amenant à la mort cellulaire, reste toujours à démontrer. Des travaux récents de notre laboratoire soulignent le E2F1 comme étant un facteur central en amont de l'apoptose médiée par le TGFβ dans les cellules cancéreuses. En utilisant un modèle de souris où le E2F1 a été inhibé, nous avons pu déterminer que le E2F1 est requis pour l'apoptose médiée par le TGFβ également dans les cellules normales. Nous avons investigué plus en profondeur les mécanismes moléculaires par lesquels le E2F1 contribue à l'apoptose médiée par le TGFβ et avons trouvé qu'un traitement par le TGFβ mène à la formation du complexe transcriptionellement actif E2F1-pRb-P/CAF sur le promoteur de plusieurs gènes pro-apoptotiques pour activer leur transcription. Ces découvertes définissent un nouveau procédé d'activation des gènes par l'axe de signalisation TGFβ-E2F1, et a permis d'élucider la voie pRb/E2F1 comme un médiateur critique et à grande portée du programme apoptotique du TGFβ et ce, dans plusieurs tissus cibles. Nous avons de plus déterminé que le TGFβ induit l'activation de la transcription de gènes autophagiques par le complexe pRb/E2F1. Collectivement, nos études supportent un rôle pour le complexe pRb/E2F1 dans la voie de signalisation du TGFβ et dans ses effets en tant que suppresseur de tumeurs.
Moberg, Kenneth H. (Kenneth Harold) 1967. "Molecular analysis of the role of E2F proteins in the pRB pathway." Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/49676.
Повний текст джерелаIncludes bibliographical references.
The E2F family of transcription factors appear to represent the primary cellular target of the tumor suppressive properties of the retinoblastoma protein. E2F therefore functions in a pathway which is a frequent target in human cancer, and the tumorigenicity of these mutations may be mediated at the transcriptional level by E2F. E2F is also regulated by cell cycle-dependent interactions with the pRB-related proteins p107 and p130. Unlike pRB, mutations in p107 or p130 are not associated with cancer. The different properties of the pRB family may result from the manner in which each protein regulates E2F. To determine how individual E2Fs contribute to the cell cycle regulatory properties of pRB, p107 and p1 30, we have examined the regulation of individual members of the E2F family. Our data suggest that the induction of E2F responsive genes is primarily due to the loss of nuclear repressor complexes at G1/S. This loss correlates with the disappearance of nuclear forms of E2F-4 protein, which represents the majority of pRBbound nuclear E2F during G1. These data suggests that E2F-4, the most abundant E2F in vivo, acts primarily as the DNA-binding component of a G1 transcriptional repressor complex. In contrast, we find that E2F-1, -2 and -3 are present at low levels in vivo and localize to the nucleus by virtue of a nuclear localization signal sequence in the N-terminal domain of these proteins. Their constitutive nuclear localization suggests that these E2F family members will contribute to the activation of responsive gene transcription during S-phase. Together, these data suggest that induction of E2F-responsive genes at G1/S is triggered both by the loss of an abundant transcriptional repressor, E2F-4*pRB, and by the presence of nuclear forms of E2F capable of transcriptional activation. These functional differences among E2Fs may underlie the oncogenic consequences specifically associated with pRB loss. Inactivation of pRB is predicted to both abrogate repression of E2F-responsive genes, and relieve inhibition of nuclear, activatory E2Fs. The combined effect of these forms of transcriptional deregulation of the E2F pathway may be sufficient to promote transformation in vivo.
by Kenneth H. Moberg, Jr.
Ph.D.
Tutton, Stephen Paul. "Repression of E2F-4 Mediated Transcription and Growth by Hypophosphorylated pRb2/p130 in Human Prostate Cancer Cells." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/138637.
Повний текст джерелаPh.D.
A fundamental property of tumor cells is the ability to proliferate in an unscheduled manner, circumventing the cues which would otherwise prevent entry into, and completion of, the cell cycle (Malumbres, Barbacid 2001). The retinoblastoma protein (pRb), and its homologues pRb2/p130 and p107, comprise a gene family which is central in maintaining appropriate cell proliferation and differentiation. The RB proteins bind to and modulate the activity of E2F transcription factors, by way of a unique binding motif termed the pocket domain; as such, RB family genes are often referred to as pocket proteins. E2F -1, -2, and -3 are considered transcriptional activators and have been shown mainly to bind pRB, whereas E2F -4 and -5 are considered transcriptional repressors, and primarily bind p107 and pRb2/p130 (Classon, Dyson 2001, Cobrinik 2005). The commonly accepted model of pRb2/p130 function is that, during quiescence, pRb2/p130, bound to E2F-4 and -5, is an active repressor of E2F responsive S-phase genes, which includes p107 and a number of cyclins (Figure 1). Upon entry into G1, the many phosphoacceptor sites of pRb2/p130 are progressively phosphorylated, disrupting the repressor complex, and allowing the transcription of downstream targets. pRb2/p130 is acted upon by the same early and late G1 kinases which phosphorylate pRb and p107, namely cyclin dependant kinases (cdk) 4 and 6, which partner with cyclin D, and later by cdk2, which requires cyclin E or A. pRb phosphorylation is required to prevent its inhibition of E2F transcription, which would otherwise halt cell cycle progression. E2F transcriptional activity permits the cell to traverse the G1/S restriction point by, among other effects, promoting cdk2 activity, which maintains pocket protein inactivation and E2F activity in a positive feedback fashion. By interacting with different sets of E2F proteins to repress transcription, pRb and pRb2/p130 act in a parallel manner to restrict cell proliferation (Classon, Dyson 2001, Cobrinik 2005, Bartek, Lukas 2001). Preliminary investigation of pRb2/p130 phosphorylation among individual cell lines grown to confluence revealed significant variation. The pattern observed suggests that, in quiescent cells, the state of pRb2/p130 phosphorylation, and thus its functionality, can vary significantly from one cell type to another. This variance likely has significant consequences on cell phenotype, dependant on the fine balance of upstream kinases and inhibitors which regulate pRb2/p130 activity. Further investigation revealed that prostate cancer cell lines which are judged to be more aggressive also resist contact inhibition, and also that there is a higher degree of pocket protein phosphorylation and E2F gene transcription in these cells. The expression and degree of pocket protein phosphorylation in these prostate cancer cells correlates with malignancy, and may impact E2F-mediated transcription and growth. Despite this increased phosphorylation, the more aggressive prostate cells did not appear to have excessive cdk2 or cdk4 expression or kinase activity. These cells did exhibit a progressive loss of cdk inhibitor (CKI) expression in comparison to less invasive cells, which might explain the greater degree of RB protein family phosphorylation. As a modestly invasive cell line containing abundant, hypophosphorylated pRb2/p130, LNCaP was selected for lentiviral infection with siRNA containing plasmids to generate knockdown subclones. Knockdown of pRb2/p130 resulted in increased E2F-dependant gene expression in these cells, supporting the idea that hypophosphorylated pRb2/p130 did in fact repress transcription in this context. However despite this derepression, a growth advantage was not conferred to these cells by pRb2/p130 knockdown.
Temple University--Theses
Jayadeva, Girish. "B55alpha modulates the phosphorylation status of the pRb-related p107 and p130 proteins." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/64785.
Повний текст джерелаPh.D.
The retinoblastoma family of phosphoproteins consisting of the retinoblastoma protein (pRB) and the two structurally related proteins p130 and p107 play an important role in the negative regulation of cell cycle progression. Hypophosphorylated pocket proteins interact with the different members of the E2F family and repress the transcription of E2F-dependent genes and consequently suppress cell cycle progression through the G0/G1 transition and the restriction point in G1. Mitogenic stimulation results in sequential activation of cyclin/CDK complexes in mid to late G1, leading to subsequent hyperphosphorylation at multiple Ser/Thr sites of pocket proteins triggering dissociation of pocket protein/E2F complexes. This disruption leads to de-repression of many E2F dependent genes whose products are essential for cell cycle progression. The traditional view has been that pocket proteins continue to be hyperphosphorylated through the S and G2 phases and following cyclin/CDK inactivation during mitotic exit become dephosphorylated by action of PP1. However, our lab observed that upon treatment of asynchronously growing cells with the CDK inhibitor Flavopiridol or CHX, pocket proteins, are rapidly dephosphorylated correlating with the inactivation of G1/CDKs and down regulation of D-type cyclins, respectively. Pocket protein dephosphorylation was prevented by pre-treating these cells with phosphtase inhibitors at a concentration selective for PP2A, implicating PP2A or PP2A-like serine/threonine phosphatase in this iii process. The involvement of PP2A on pocket protein dephosphorylation was further strengthened by the observation that SV40 small t antigen (ST) delays/prevents p107 dephosphorylation. Moreover, a physical association between PP2A/C and p130/p107 was observed throughout the cell cycle that was not affected by CHX treatment, strongly suggesting that CHX-induced dephosphorylation is not the result of increased pocket protein targeting by PP2A, but rather that a dynamic equilibrium between CDKs and PP2A is shifted to dephosphorylation when CDK activity is compromised. This dynamic equilibrium operates throughout the cell cycle. PP2A is a trimeric enzyme complex consisting of a catalytic C, a structural A and substrate specific B subunit. There are four families of regulatory B subunits designated B, B’, B’’ and B’’’, each with several members encoded by genes with multiple splice variants that mediate substrate specificity and subcellular localization. It has been reported recently that in excess of 200 functional distinct PP2A holoenzymes can assemble with distinct specificities. Therefore, to gain insight into the mechanisms that regulate the steady state phosphorylation of pocket proteins throughout the cell cycle, it was essential to identify the specific holoenzyme complexes involved. To this end, it was identified that a PP2A trimeric holoenzyme containing B55α specifically targets and dephosphorylates p107/p130 both in vitro and in mammalian cells. B55α associates directly with the spacer of p107 and this interaction seems to be indirectly enhanced by the C-terminus of p107. The decreased association of p107 with PP2A/C of the B55α/PP2A holoenzyme complex upon treatment with ST further confirmed the role of B55α in mediating p107-PP2A/C interaction. Our data also revealed an interaction between B55α and p130, but not pRb, which appears to prefer a PR70, suggesting selectivity in the interaction of pocket proteins with distinct PP2A holoenzymes. In accordance with this, recombinant purified B55α dephosphorylates p107 in vitro. Limited ectopic expression of B55α but not other subunits, result in ST sensitive dephosphorylation of p107 and p130 in cells. Further shRNA mediated knockdown of B55α results in hyperphosphorylation of p107 and p130. This suggests that the cellular levels of B55α are critical in modulating the phosphorylation status of p107/p130 rather than just catalyzing the dephosphorylation of these proteins when the activity of CDKs is compromised. Since ST disrupts the B55α/PP2A holoenzyme complex by binding to the PP2A-A-C dimer and leads to hyperphosphorylation of pocket proteins it is conceivable that ST mediates its effects on cell proliferation at least in part, via inactivation of the PP2A holoenzymes that activates pocket proteins. Given the sensitivity of p107 phosphorylation to the cellular levels of B55α, future analyses should ascertain if deregulation of B55α leads to hyperphosphorylation of pocket proteins and abnormal cell cycle progression.
Temple University--Theses
Meza, Maria I. "The use of PRBs (permeable reactive barriers) for attenuation of cadmium and hexavalent chromium from industrial contaminated soil." Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/432.
Повний текст джерелаNorman, Per-Gustaf. "Cloning, Purification and Crystallization of Low PSII Accumultation 19 (LPA19) and Peroxiredoxin-6 (Prx6): A Thorny Road to Diffracting Crystals." Thesis, Umeå universitet, Kemiska institutionen, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111548.
Повний текст джерелаPenglong, Tipparat. "Molecular Basis of Erythroid Cell Proliferation and Differentiation." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T022.
Повний текст джерелаTo ensure the generation of billions of erythrocytes daily, erythropoiesis must be well controlled by proliferation and differentiation processes. These two processes are regulated by expressions of specific genes, coordinated by transcription factors (TFs) and epigenetic factors, such as bromodomain proteins. This study focused on the effects of the binding and dissociation of a key erythroid TF, GATA-1, to the crucial cell cycle TFs, pRb and E2F. In the first part of this thesis, the role of GATA-1 and FOG-2 binding to pRb/E2F in a control balances between cell proliferation and differentiation was studied. Mice bearing a GATA-1 mutation (GATA-1S310A) displayed higher levels of E2F2 sequestration and suffered from fatal anemia when the compensatory pathway of E2F2 production via IGF-1 signaling was also inhibited. The properties described for GATA-1 were found to be common to FOG-2, and the abolition of FOG-2 binding to pRb led to obesity resistance in FOG-2pRb- mice. In the second part of this work, as c-Myc is regulated by GATA-1 and E2F, the first chemical epigenetic inhibitor repressing c-Myc expression to be described, JQ1, was investigated to see if it could control erythropoiesis. The UT7 erythroleukemia cell line, which proliferates without differentiating was used. This cell line stops differentiation at the proerythroblast stage, in response to erythropoietin. JQ1 treatment inhibited UT7 proliferation and restored terminal erythroid differentiation. The molecular mechanism underlying this regulation by JQ1 was shown that the inhibition of c-Myc expression was associated with the inhibition of STAT5 transcription, with no change in the phosphorylation of this protein. It was found that JQ1 had a putative TGF--like activity, which did not involve the Smad pathway. It was shown in the ex vivo studies that JQ1 increased the viability of erythroid cells and accelerated the maturation of these cells in both WT and thalassemic mice. The observed differences between leukemic and normal erythropoiesis involved differential epigenetic modifications that could be at the basis of new strategies regarding cancer treatment.The key role of the association of GATA-1 or FOG-2 had with pRb/E2F, and the dissociation of these factors, in erythropoiesis and adipogenesis, respectively, led us to investigate, in vivo, the physiological consequences of E2F sequestration by pRb. As a result, transgenic mice displaying conditional expression of a peptide containing the N-terminal part of GATA-1 that binds to pRb (GATA-1Nter) were developed. In vitro, this peptide traps E2F in a GATA-1Nter/pRb complex, resulting in the irreversible inhibition of cell proliferation. The yield of transgenic mice expressing the GATA-1Nter peptide in vivo was unsuccessful, as this expression lead to lethality at the embryonic stage. Using an alternative approach, based on the inducible expression of the peptide in adults, chimeric mice with a high frequency of recombination of the GATA-1Nter transgene were obtained for this study. The establishment of a stable mouse line expressing the GATA-1Nter peptide should make it possible to determine the pathophysiological consequences of E2F sequestration in the GATA-1Nter/pRb complex
Luo, Ping. "Quantification of morphological changes in zero valent iron (ZVI) : effect on permeable reactive barrier (PRB) longevity." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503921.
Повний текст джерелаDoherty, R. D. "Modelling of a permeable reactive barrier (PRB) in a manufactured gas plant site, Portadown, Northern Ireland." Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269086.
Повний текст джерелаThunberg, Billy, and Kalle Kurttio. "Radardetektering av stålämnen med hjälp av UWB-radar." Thesis, Högskolan i Gävle, Elektronik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-22538.
Повний текст джерелаThe steel industries Sandvik, Sandviken and SSAB, Borlänge, produces billets (quadratic,long steel units). Billets travelling through the furnace will heat up. At the end of the furnace,the billets will require precision measurements regarding its position, due to the extractingdevice. Sensors that are used today require an unobstructed view, which is achieved by holesin the furnace walls. Maintenance is needed in order to ensure that no impurities are cloggingthe holes. The goal with this thesis is to investigate whether it is possible to detect rectangular billets byusing an UWB-radar system. The broadband characteristics of an UWB-unit makes it asuitable successor, as free sight is not a requirement. This will decrease downtown due tomaintenance and optimize the time required for billets extraction.This involves economic and environmental aspects as well, due to lower energy consumption. This will be tested by collecting radar measurements for further signal processing. The usedradar system is forward scattering radar. The work started with a theoretical study aboutUWB-technique and basics about radar. Thereafter test scenarios were designed to study howthe radar wave is affected by changing environments. The resulting measurements were latersignal processed in Matlab. This work shows that it is possible to detect billets with various dimensions, using UWBradar.The algorithm can also be used as a passage alarm, which can be used in other areasthan furnaces.
Barnes, James Douglas. "The role of the pRb/BAG-1 complex in the regulation of apoptosis in colorectal epithelial cells." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414356.
Повний текст джерелаContu, Simone Santana. "Expressão imunohistoquímica da proteína pRb na mucosa esofágica de indivíduos sob risco para carcinoma epidermóide de esôfago." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2001. http://hdl.handle.net/10183/5078.
Повний текст джерелаMoriéras, Angéline. "Rôle de RBF1, l’homologue de la protein oncosuppressive pRb, dans l’apoptose et l’homéostasie tissulaire chez drosophila melanogaster." Versailles-St Quentin en Yvelines, 2013. http://www.theses.fr/2013VERS0034.
Повний текст джерелаPRb is the first tumor suppressor identified in Human. While its role during cell cycle is well characterized, little is known about its properties on apoptosis regulation and apoptosis-induced cell responses. We generated a punctual mutant form of RBF1. This mutant form conserved the JNK-dependent pro-apoptotic properties of RBF1 and gained the ability of inducing overgrowth phenotypes in adult wings. We show that this overgrowth is a consequence of an abnormal proliferation in wing imaginal discs, which depends on the JNK pathway activation. These results show for the first time that RBF1 could be important to control tissue homeostasis via the regulation of apoptosis induced-proliferation. In parallel, I have used MS/MS to identified a new potential RBF1 partner: PABP, which is implicated in translation activation. This interaction suggests that RBF1 could act as a tumor suppressor in part by regulating translation
Bertin, Joséphine. "Impact des voies pRb/E2F1 et p53 dans la réponse à l'ABT-737 dans les cellules cancéreuses." Nantes, 2011. https://archive.bu.univ-nantes.fr/pollux/show/show?id=2767bce7-a3c4-4dcd-b8eb-25d280da3795.
Повний текст джерелаABT-737 is a functional analogue of ABT-263 (Navitoclax), an anticancer agent inhibitor of some Bcl-2 homologues, for which monotherapy cytotoxicity has been reported in certain instances. ABT-737 by mimicking the BH3 domain structure of the BH3-only Bad, inhibits the formation of complexes between pro- and anti-apoptotic Bcl-2 family members to trigger apoptosis. In our study, we identify an additional, transcription dependent, mechanism that contributes to sensitivity to ABT-737. In cancer cells lacking functional p53, we observe a caspase dependent induction of Noxa, a BH3-only protein, upon treatment with ABT-737. This induction is dependent upon the transcription factor E2F-1 that occupied of the Noxa promoter and, strikingly, upon the E2F-1 regulatory protein pRb, cleaved by caspases upon ABT-737 treatment. Moreover, we have shown that, in cancer cells with functional p53, the sensitivity to ABT-737 is dependent upon p53 and no upon E2F1. In this case, the role of p53, in apoptosis induction by ABT-737, does not require its transcriptional function. Our data suggest that transcription factors, as p53 and E2F1, may allow to sensitive cancer cells to ABT-737. Thus, the use of drug that induced the pRb/E2F1 or p53 pathway, as Nutlin-3a, may have clinical utility in treatment of patient when combined with orally bioavailable compound ABT-263
Lamichhane, Suman. "Physiological and Molecular Dissection of Salinity Tolerance in Arabidopsis and Maize and Nitrogen Uptake in Wheat." Diss., Virginia Tech, 2020. http://hdl.handle.net/10919/97843.
Повний текст джерелаDoctor of Philosophy
In coastal areas, sea-level rise increases the chances of saltwater intrusion into cultivable lands, making a hostile environment for crop growth and production by imposing flooding and salinity stresses simultaneously. Identification of central regulators that regulate the adaptation to both flooding and salinity is a critical step for the development of new crop genotypes with enhanced tolerance to these stresses. Previous studies have characterized the function of the PROTEOLYSIS 6 (PRT6) gene in adaptation to flooding stress in plants. This study assessed whether this gene is involved in adaptation to salinity stress in Arabidopsis and maize by evaluating the growth and survival of their respective prt6 mutants under high salt. Consistent with the flooding tolerance data, our study showed that the PRT6 gene also functions as a negative regulator of salinity stress tolerance in Arabidopsis. The prt6 mutation in Arabidopsis activated the key transcriptional and hormone response pathways associated with adaptation to both salinity/osmotic stress and sodium toxicity, expressed as enhanced tolerance to excess salt at seed germination, seedling, and adult plant stages. In maize, disruption of the PRT6 gene decreased seed germination, primary root elongation, and shoot biomass growth under high salt, which is opposite to our observations in Arabidopsis. Additionally, the maize mutant plants encountered more oxidative stress, as demonstrated by the higher accumulation of malondialdehyde (MDA) under high salt. Moreover, maize prt6 mutants exhibited reduced grain yield under high salt. Overall, these results indicate that disruption of the PRT6 gene confers increased tolerance to high salt in Arabidopsis, whereas it conversely reduced salinity tolerance in maize. In wheat, we compared two genotypes with distinct nitrogen use efficiency (NUE), VA08MAS-369 and VA07W-415, to determine critical traits involved in NUE regulation. Our study showed that grain yield and yield-related parameters were significantly higher in line 369 than line 415 under low N. Moreover, high NUE in line 369 was attributed to efficient N uptake in this genotype under limited N. Our root architecture analysis demonstrated that line 369 was able to maintain root depth, volume, and thickness even under N limitation. Consistently, line 369 highly induced expression of genes associated with nitrogen transport at low N. Altogether, this study identified key traits involved in high NUE in wheat, facilitating the breeding of new wheat genotypes with enhanced NUE.
Khan, Shireen S. "Analysis of the roles of p53, pRb and p19ARF in promoting cell cycle arrest and maintaining genetic stability /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9952660.
Повний текст джерелаQueiroz, Leila Brito de. "Avaliação da expressão das proteínas p53 e prb em cacarcinoma escamocelular e papilomas orais pelo método imuno –histoquímico." Instituto de Ciências da Saúde, 2006. http://repositorio.ufba.br/ri/handle/ri/20017.
Повний текст джерелаMade available in DSpace on 2016-08-09T17:05:57Z (GMT). No. of bitstreams: 1 Dissertação_ICS_ Leila Brito de Queiroz.pdf: 980344 bytes, checksum: f980c569498b36f40b83a68c4a77fda4 (MD5)
A progressão do ciclo celular é regulada por uma variedade de proteínas, como as quinases dependentes de ciclinas, inibidores de quinases dependente de ciclinas e proteínas supressoras de tumor, como a p53 e pRb. Alterações na expressão de proteínas supressoras de tumor podem ser responsáveis pelo desenvolvimento de processos neoplásicos malignos. O HPV, vírus epiteliotrópico, considerado agente causal do câncer de colo de útero produz oncoproteínas E6 e E7 capazes de modificar o comportamento celular das proteínas p53 e pRb, respectivamente. A proposta deste estudo foi avaliar a expressão imuno-histoquimica das proteínas p53 e pRb de biópsias em blocos parafinados (n=56) de carcinoma escamocelular (n=31), papiloma orais (n=19) e tecido histologicamente normal (n=6) e associar os achados à detecção do HPV pelo método de PCR. A imunoexpressão foi avaliada de acordo com a marcação nuclear protéica, em escores 0,1, e 2 (imunoexpressão até 10%; entre 10% e 50% e acima de 50%, respectivamente). Nos Carcinomas, a p53 estava expressa em 61,3% dos casos, assim como para pRb. Nas 19 amostras de papilomas, 5,3% e 26,3%% foram positivos para expressão imuno-histoquímica das proteínas p53 e pRb, respectivamente. Nos tecidos normais, em 50% houve imunoexpressão da p53 e em 16,7% da pRb. Foi estatisticamente significante a correlação entre a detecção da proteína p53 e a natureza da neoplasia (p=0,000), assim como para análise da proteína pRb foi estatisticamente significante a diferença entre os ranks médios do epitélio normal e carcinoma (p=0,014) e papilomas e carcinomas (p=0,003). De acordo com o grau de expressão, o escore 2 (superexpressão) para p53 e pRb foi associado ao desenvolvimento de neoplasias malignas, não sendo este escore detectado nas lesões papilomatosas ou em tecidos histologicamente normais. O presente estudo não permitiu definir o associação do HPV com a imunoexpressão das proteínas p53 e pRb em lesões malignas e benignas na cavidade oral, em função do pequeno número de amostra com resultados positivos.
Ndabambi, Nonkululeko. "Recombinant expression of the pRb- and p53-interacting domains from the human RBBP6 protein for in vitro binding studies." Thesis, University of the Western Cape, 2004. http://etd.uwc.ac.za/index.php?module=etd&.
Повний текст джерелаSvoboda, Devon. "The Role of Pocket Proteins pRb and p107 in Radial Migration and Axon Guidance through Cell Cycle Independent Mechanisms." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32954.
Повний текст джерелаEngel, Brienne E. "Mechanisms and Molecular Biology of Major Tumor Suppressors." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5357.
Повний текст джерелаKhan, Junaid Ali. "Progesterone Receptor Isoforms : functional Selectivity and Pharmacological Targeting." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00769945.
Повний текст джерелаSavvidis, Charalampos, and Zeyang Geng. "Onboard Impedance Diagnostics Method of Li-ion Traction Batteries using Pseudo-Random Binary Sequence." Thesis, Linköpings universitet, Tekniska fakulteten, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-118970.
Повний текст джерелаSoares, Rosilene Calazans. "Estudo da detec??o do DNA do papiloma v?rus humano (HPV) e da express?o imuno-histoqu?mica de prote?na do ciclo celular no carcinoma epiderm?ide oral." Universidade Federal do Rio Grande do Norte, 2005. http://repositorio.ufrn.br:8080/jspui/handle/123456789/17157.
Повний текст джерелаCoordena??o de Aperfei?oamento de Pessoal de N?vel Superior
Oral squamous cell carcinoma (OSCC) is the most common malignancy in oral cavity and human papillomavirus (HPV) may have an important role in its development. The aim of this experiment was to investigate the HPV DNA and viral types in 90 cases of OSCC. Moreover, a comparative analysis between the cases of OSSC with and without HPV DNA was performed by using cell cycle markers p21 and pRb in order to detect a possible correlation of these proteins and HPV infection. DNA was extracted from paraffin embedded tissue and amplified by PCR (polymerase chain reaction) with primers PCO3+ e PCO4+ for a fragment of human β-globin gene. After this procedure, PCR for HPV DNA detection was realized using a pair of generic primers GP5+ e GP6+. Immunohistochemical study was performed by streptoavidin-biotin technique and antibodies against p21 and pRb proteins were employed. Eighty-eight cases were positive for human β-globin gene and HPV DNA was found in 26 (29.5%) of then. It could not be detected significant correlation between HPV and age, sex and anatomical sites of the lesion. The most prevalent viral type was HPV 18 (80.8%). Regarding the immunohistochemical analysis, it was detected significant association between HPV presence and pRb immunoexpression (p=0,044), nevertheless, the same was not observed in relation to p21 protein (p =0,416). It can be concluded that the low detection of HPV DNA in OSCC by the present experiment suggests a possible role of the virus in the development and progression in just a subset of this disease
O carcinoma epiderm?ide oral ? a neoplasia maligna mais freq?ente da cavidade oral e o papilomav?rus humano (HPV) parece ter um relevante papel na indu??o desta les?o. Neste trabalho investigou-se o DNA do HPV e tipos virais em 90 casos de carcinoma epiderm?ide oral (CEO). Realizou-se tamb?m uma an?lise comparativa entre os grupos de CEO com DNA do HPV e sem o DNA do v?rus, empregando-se os marcadores do ciclo celular p21 e pRb, a fim de estabelecer poss?vel correla??o entre a express?o imuno-histoqu?mica dessas prote?nas e a infec??o pelo HPV. O DNA foi extra?do de tecido emblocado em parafina e amplificado por PCR (rea??o em cadeia da polimerase) com um par de primers designados PCO3+ e PCO4+ para um fragmento do gene da β-globina humana. Posteriormente, realizou-se PCR para detec??o do DNA de HPV utilizando-se um par de primers gen?ricos designados GP5+ e GP6+. A tipagem viral foi realizada pela hibridiza??o dot blot. No m?todo imuno-histoqu?mico utilizou-se a t?cnica da streptavidina-biotina com um painel de anticorpos monoclonais para as prote?nas p21 e pRb. Dos 88 casos positivos para o gene da β-globina humana, em 26 (29,5%) foi detectado o DNA do HPV. N?o houve associa??o significativa entre o HPV e as vari?veis idade e sexo dos pacientes e localiza??o anat?mica da les?o. O tipo viral prevalente foi o HPV 18 (80,8%). Quanto ? an?lise imuno-histoqu?mica, foi observada associa??o estatisticamente significativa entre a presen?a do HPV e a express?o imunohistoqu?mica de pRb (p=0,044), entretanto, n?o houve qualquer diferen?a estatisticamente significativa entre a express?o da prote?na p21 e a presen?a do v?rus (p =0,416). P?de-se concluir que o baixo percentual de detec??o do DNA do HPV no carcinoma epiderm?ide oral no presente trabalho, sugere uma poss?vel participa??o do HPV no desenvolvimento e progress?o de apenas um subgrupo dessas les?es
Rekštytė, Toma. "Pienarūgščių bakterijų įtaka akrilamido formavimuisi pusruginės duonos gaminiuose bei kvietinių kepinių kokybės pagerinimo galimybės deaktyvuotų mielių priedu." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130618_094636-54626.
Повний текст джерелаThe aim of this study was to investigate acrylamide formation in semi rye bread fermented with Lactobacillus delbruecki, Pediococcus acidilactici, Pediococcus pentosaceus and Lactobacillus sakei, and, to investigate the influence of RS 190 deactivated yeast on wheat flour technological properties and wheat bread quality. Results show that the amount of acrylamide in bread samples ranged from 37.87 ± 0.55 to 74.64 ± 0.36 µg/kg. Lactofermentation reduce acrylamide formation in semi rye bread. L. delbruecki was found to have a higher effect on acrylamide reduction in bread samples in compare with P. acidilactici, P. pentosaceus and L. sakei. Also, proteolytic activity of LAB have a influence on acrylamide content reduction in bread. Bread made with L. delbruecki (the highest proteolytic activity) contained lower acrylamide content (37.87 ± 0.55 µg/kg), while breads prepared with P. pentosaceus and P. acidilactici (lower proteolytic activity) contained higher acrylamide contents (74.64 ± 0.36 and 63.38 ± 0.98 µg/kg, respectively). Pharinographic analysis of wheat flour with deactivated yeast and without deactivated yeast results shows that the higher water absorbtion have wheat flour with deactivated yeast (59.1 ± 1.18 %) and higher dough stability (5 times higher) but longer dough formation time (1,3 times longer). The addition of deactivated yeast in wheat flour have a significant effect of bread specific volume, porosity and moisture content. In conclusion we could say... [to full text]
Fritah, Asmaà. ""P21WAF1 régule l'activité transcriptionnelle du récepteur des oestrogènes à l'interface prolifération / différenciation"." Paris 6, 2006. http://www.theses.fr/2006PA066173.
Повний текст джерелаFerraz, de Sá Beltrão Monique. "Estudo clínico e genético do Papilomavírus humano sorotipo 16/ Monique Ferraz de Sá Beltrão." Universidade Federal de Pernambuco, 2011. https://repositorio.ufpe.br/handle/123456789/1738.
Повний текст джерелаFaculdade de Amparo à Ciência e Tecnologia do Estado de Pernambuco
O câncer cervical é o segundo tipo de neoplasia que mais acomete as mulheres no Brasil, com alta prevalência em Pernambuco. A associação desta patologia como o papilomavírus humano (HPV) já está bem estabelecida e atualmente, sabe-se que o HPV pode ser encontrado em vários outros locais de infecção, além da região genital. Com o intuito de apontar a distribuição corpórea do HPV pelo corpo humano foi realizada uma revisão da literatura buscando por sítios corpóreos em que o DNA viral já tinha sido identificado. Dentre os tipos virais de alto risco que mais acometem a população brasileira, sabe-se que o HPV16 aparece associado a mais de 50% dos achados. Baseado nisso, uma busca pela presença do DNA do HPV e pelos variantes virais do HPV16 foi realizada em mulheres de Pernambuco que apresentavam lesões genitais. Complementarmente, sabe-se que sistemas de expressão são amplamente utilizados para produção de diversas moléculas biológicas, sendo o bacteriano o mais rápido e fácil de ser utilizado. Visando melhor utilização do sistema de expressão em bactéria, desenvolvemos um método para detectar a produção de -galactosidase em cepas heterólogas de Escherichia coli. Esse sistemas bacterianos vem sendo utilizados para produção de diversas moléculas virais, como oncoproteínas virais. Baseado no levantamento bibliográfico realizado foi possível identificar DNA viral nos mais diferentes sítios corpóreos, inclusive com ausência de lesões clínicas, apontando para a possibilidade do HPV agir como um oportunista. Da população estudada, mais de 50% foram positivas para o HPV, com achados de múltiplas infecções com tipos virais distintos, onde o variante Europeu foi o mais frequente nos casos de HPV16 positivo. A linhagem Origami (DE3) de E.coli demonstrou-se eficiente no ensaio colorimétrico expressando o gene da -galactosidase com baixa produção de proteínas bacterianas. Baseado nisso, esse modelo bacteriano foi utilizado no processo de sub-clonagem do gene E7 do HPV16 permitindo após indução do promotor visualizar uma banda de 15 KDa na eletroforese de proteínas totais, banda provavelmente referente a oncoproteína viral. No entanto, faz-se necessário emprego de testes imunológicos com anticorpos específicos para confirmar sua produção e posterior purificação. A tipagem da população a respeito do variante do HPV mais predominante e produção da proteína E7 permitem o aumento nos conhecimentos dos diferentes mecanismos de interação do vírus com o hospedeiro e favorecem ao desenvolvimento de métodos diagnósticos e terapêuticos mais eficientes e específicos para as diferentes regiões do mundo