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Статті в журналах з теми "Translationally controlled tumour protein"

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Bommer, Ulrich-Axel, and Bernd-Joachim Thiele. "The translationally controlled tumour protein (TCTP)." International Journal of Biochemistry & Cell Biology 36, no. 3 (March 2004): 379–85. http://dx.doi.org/10.1016/s1357-2725(03)00213-9.

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Newbery, H. J., M. Brueser, I. Phillips, and C. M. Abbott. "The role of translationally controlled tumour protein in tumourigenesis." European Journal of Cancer Supplements 6, no. 9 (July 2008): 72. http://dx.doi.org/10.1016/s1359-6349(08)71451-4.

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Bommer, Ulrich-Axel. "Cellular Function and Regulation of the Translationally Controlled Tumour Protein TCTP." Open Allergy Journal 5, no. 1 (May 18, 2012): 19–32. http://dx.doi.org/10.2174/1874838401205010019.

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The ‘translationally controlled tumour protein’ TCTP was originally discovered 30 years ago by researchers interested in proteins regulated at the translational level. Cloning and sequencing confirmed the conservation of this protein among all eukaryotic kingdoms, but did not reveal any functional clue, and TCTP was listed in the databases as a ‘family’ of its own. The functional characterisation of this protein extended over more than a decade, leading to a plethora of individual functions and interactions that have been ascribed to this protein. A major addition to the functional characterisation of TCTP was the identification in 1995 of its histamine releasing factor (HRF) activity in allergic conditions, which for the first time described an extracellular activity for TCTP in human disease. This triggered a host of additional publications aimed at characterising this HRF activity, which are discussed in other articles of this issue. Another milestone in the elucidation of TCTP's function was the demonstration of its anti-apoptotic activity in 2001. Evidence is also accumulating for a role of TCTP in the cell cycle and in early development. This article provides an overview of the main cellular activities of TCTP. The second part will summarise our current knowledge on the mechanisms involved in regulating intracellular TCTP levels.
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Kloc, Malgorzata, Jacek Z. Kubiak, and Rafik Mark Ghobrial. "Translationally Controlled Tumor-Associated Protein." Biochemistry Research International 2012 (2012): 1. http://dx.doi.org/10.1155/2012/432590.

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Venugopal, Thayanithy. "Evolution and expression of Translationally Controlled Tumour Protein (TCTP) of fish." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 142, no. 1 (September 2005): 8–17. http://dx.doi.org/10.1016/j.cbpc.2005.04.011.

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Chan, Tim Hon Man, Leilei Chen, and Xin-Yuan Guan. "Role of Translationally Controlled Tumor Protein in Cancer Progression." Biochemistry Research International 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/369384.

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Translationally controlled tumor protein (TCTP) is a highly conserved and ubiquitously expressed protein in all eukaryotes—highlighting its important functions in the cell. Previous studies revealed that TCTP is implicated in many biological processes, including cell growth, tumor reversion, and induction of pluripotent stem cell. A recent study on the solution structure from fission yeast orthologue classifies TCTP under a family of small chaperone proteins. There is growing evidence in the literature that TCTP is a multifunctional protein and exerts its biological activity at the extracellular and intracellular levels. Although TCTP is not a tumor-specific protein, our research group, among several others, focused on the role(s) of TCTP in cancer progression. In this paper, we will summarize the current scientific knowledge of TCTP in different aspects, and the precise oncogenic mechanisms of TCTP will be discussed in detail.
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Branco, Rémi, and Josette Masle. "Systemic signalling through translationally controlled tumour protein controls lateral root formation in Arabidopsis." Journal of Experimental Botany 70, no. 15 (April 30, 2019): 3927–40. http://dx.doi.org/10.1093/jxb/erz204.

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Abstract The plant body plan and primary organs are established during embryogenesis. However, in contrast to animals, plants have the ability to generate new organs throughout their whole life. These give them an extraordinary developmental plasticity to modulate their size and architecture according to environmental constraints and opportunities. How this plasticity is regulated at the whole-organism level is elusive. Here we provide evidence for a role for translationally controlled tumour protein (TCTP) in regulating the iterative formation of lateral roots in Arabidopsis. AtTCTP1 modulates root system architecture through a dual function: as a general constitutive growth promoter enhancing root elongation and as a systemic signalling agent via mobility in the vasculature. AtTCTP1 encodes mRNAs with long-distance mobility between the shoot and roots. Mobile shoot-derived TCTP1 gene products act specifically to enhance the frequency of lateral root initiation and emergence sites along the primary root pericycle, while root elongation is controlled by local constitutive TCTP1 expression and scion size. These findings uncover a novel type for an integrative signal in the control of lateral root initiation and the compromise for roots between branching more profusely or elongating further. They also provide the first evidence in plants of an extracellular function of the vital, highly expressed ubiquitous TCTP1.
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Jandl, Katharina, Christopher D. Gregory, and Grazyna Kwapiszewska. "Translationally Controlled Tumor Protein in Extracellular Vehicles: Dangerous Cargo?" American Journal of Respiratory Cell and Molecular Biology 59, no. 4 (October 2018): 407–9. http://dx.doi.org/10.1165/rcmb.2018-0160ed.

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Hoepflinger, Marion, Johannes Reitsamer, Anja Geretschlaeger, Norbert Mehlmer, and Raimund Tenhaken. "The effect of Translationally Controlled Tumour Protein (TCTP) on programmed cell death in plants." BMC Plant Biology 13, no. 1 (2013): 135. http://dx.doi.org/10.1186/1471-2229-13-135.

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Tuynder, M., G. Fiucci, S. Prieur, A. Lespagnol, A. Geant, S. Beaucourt, D. Duflaut, et al. "Translationally controlled tumor protein is a target of tumor reversion." Proceedings of the National Academy of Sciences 101, no. 43 (October 15, 2004): 15364–69. http://dx.doi.org/10.1073/pnas.0406776101.

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Дисертації з теми "Translationally controlled tumour protein"

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Thaw, Paul. "Structural studies of p23'f'y'p : a translationally controlled tumour protein." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341815.

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Foster, William Swinburne. "Translationally Controlled Tumour Protein as a Novel Therapeutic Target in Pulmonary Arterial Hypertension." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35006.

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Background: Pulmonary arterial hypertension (PAH) is a multifaceted disease characterized by elevated pulmonary arterial pressure, right ventricular hypertrophy, and a poor prognosis. Pathological hallmarks of PAH include pulmonary vascular remodelling, pre-capillary arterial obliteration, and plexiform lesions. Over the past 15 years, pulmonary endothelial cell (EC) apoptosis has been repeatedly implicated as a key trigger of occlusive arterial remodelling in PAH. While it has been hypothesized that pulmonary EC apoptosis gives rise to the emergence of growth-dysregulated, apoptosis- resistant ECs involved in arterial remodelling, the molecular mechanisms linking these two events has not yet been fully elucidated. Recently, our lab identified translationally controlled tumour protein (TCTP) as one of several significantly dysregulated proteins in culture-derived blood-outgrowth endothelial cells (BOECs) isolated from hereditable PAH (HPAH) patients harbouring mutations in the gene encoding for bone morphogenetic protein receptor type 2. Immunohistological analyses indicated that TCTP expression was associated with intra-luminal pulmonary ECs and inflammatory cells in the remodelled vessels of both human PAH patients and SU5416 rats. Furthermore, TCTP silencing abrogated excessive HPAH BOEC proliferation and promoted apoptosis in vitro. Hypothesis: We hypothesized that TCTP represents a central molecular mechanism linking pulmonary arterial EC damage and apoptosis to the emergence of growth- dysregulated lung vascular cells and complex arterial remodelling in PAH.Purpose: The purpose of the present thesis was to examine the effects TCTP inhibition on EC survival and TCTP abundance in vitro as well as on pulmonary hemodynamic changes and arterial remodelling in vivo using a well-validated rat model of severe PAH. Methods: Inhibition of TCTP was accomplished using two TCTP small molecule inhibitors, sertraline and thioridazine. In vitro, rat lung microvascular ECs (RLMVECs) were exposed to thioridazine and assayed for TCTP abundance, survival, and markers of apoptosis. In vivo, PAH was induced in male Sprague Dawley rats using SU5416 combined with 3 weeks of chronic hypoxia (SU/CH). After 4 weeks, right ventricle systolic pressure (RVSP) was measured by direct catheterization and osmotic pumps containing either thioridazine or sertraline were implanted subcutaneously. Following 3 weeks of small molecule delivery, RVSP was re-evaluated, cardiac function/structure was determined using transthoracic echocardiography, and histological analyses of vascular remodelling and inflammation were performed. Results: Our in vitro experiments demonstrated that thioridazine was able to significantly down-regulate TCTP levels and induce an apoptotic phenotype in RLMVECs. In the SU/CH rat model of severe PAH, both thioridazine and sertraline failed to have any effect on pulmonary hemodynamics, right ventricle structure/function, or vascular remodelling. Moreover, neither small molecule was able to detectably down-regulate TCTP levels in the lungs of SU/CH rats. Immunofluorescence staining revealed that TCTP expression occasionally corresponded with the expression of macrophage/monocyte marker CD68 in the lungs of SU/CH rats, consistent with its expression by inflammatory cells; however, no significant differences were found in adventitial cell clearance in the presence or absence of the inhibitors. Conclusions: Our findings support previous reports that thioridazine is able to significantly down-regulate TCTP and induce apoptosis in vitro. In contrast, both small molecule inhibitors failed to down-regulate lung TCTP levels or have any beneficial effects on the progression of PAH in SU/CH rats.
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Hayward, K. L. "Lipotoxicity and the role of translationally controlled tumour protein (TCTP) in pancreatic β-cell survival". Thesis, University of the West of England, Bristol, 2014. http://eprints.uwe.ac.uk/22538/.

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Introduction: Diabetes affects more than 346 million individuals worldwide. Some 90% of diabetics have type 2 diabetes mellitus, which is frequently associated with obesity and hyperlipidemia as well as hyperglycaemia. There is ample evidence that fatty acids become toxic (lipotoxicity) when present at elevated concentrations for prolonged periods of time, although mechanisms are still not fully elucidated. Current diabetic medications do not tackle the underlying issue of β-cell death. New therapeutic strategies to more effectively combat and early deterioration of the β-cell mass and function due to lipotoxicity are thus required. Translationally Controlled Tumour Protein (TCTP) has been identified in a wide range of eukaryotic organisms and linked to many diverse cellular processes including acting as an anti-apoptotic protein. Ideally human islets of Langerhans would be used to investigate diabetes however they are not practical to use due to only being acquirable from cadavers. Rodent islets are more readily available however keeping the rodents require a lot of money, time and a license to ensure they are being cared for correctly. Monolayer cell lines have been created for the use in basic research which can be grown in a suspension forcing the cells to attach to each other forming 3D structures commonly referred to as pseudo-islets, have shown some promising results. Aims: (1) establishing an imaging-based assay for analysing characteristic changes in pancreatic β-cells lipotoxicity, (2) investigate the effect of TCTP in connection with lipotoxicity and (3) investigate possible alternatives to using cultured monolayer cells or isolated islets of Langerhans for diabetes research. Methods: MIN6, INS-1, HIT-T15, alpha TC 1 clone 6 cells and Hans-Wistar rat islets were incubated with were incubated with forskolin, exendin-4, thapsigargin, palmitate and oleate/palmitate (1:1) mix under stimulatory glucose conditions for 8, 24 or 48h to investigate lipid accumulation and/or protein changes. Lipid accumulation and cell death was investigated using ImageXpress 5000a and confocal microscopy. Changes in protein expression were investigated using immunoblots using a mouse monoclonal anti-TCTP antibody. Equal amount of protein was loaded into each lane and glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) or extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) were used as internal controls. Changes in TCTP mRNA expression levels were investigated using TaqMan® with real-time PCR. Pancreatic spheroid formation was investigated using MIN6 and INS-1cells via three methods: agarose overlay, hanging drop/methyl cellulose, and confocal microscopy. Conclusions: Lipid accumulation could successfully be tracked in monolayer cells and islets of Langerhans. Proteomic and biochemical approaches revealed that TCTP level is regulated by glucose, palmitate and exendin-4. Regulation of TCTP by glucose and exendin-4 is cyto-protective. In contrast, high concentration of palmitate causes cell stress, reduction in TCTP protein level and consequently reduced cell viability. This study demonstrated that the cytotoxic effects of palmitate are at least in part mediated by the inhibition of the production of the anti-apoptotic protein TCTP which is reversed with the addition of exendin-4. In contrast, TCTP mRNA was found to be elevated in response to high level of fatty acids both in MIN6 cells and Zucker fatty rat islets of Langerhans suggesting that β-cells try to compensate for the reduced translation of TCTP. The investigation in to an alternative method for spheroid creation failed to produce complete spheroids but a number of areas for future improvements were identified.
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Bruckner, Fernanda Prieto. "The translationally controlled tumor protein is necessary for potyvirus replication." Universidade Federal de Viçosa, 2016. http://www.locus.ufv.br/handle/123456789/11715.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Translationally controlled tumor protein (TCTP) é uma proteína amplamente distribuída em eucariotos. Ela está envolvida na regulação de processos básicos como progressão do ciclo celular, crescimento celular, proteção contra estresses e apoptose. Durante a infecção de tomateiro (Solanum lycopersicum) e Nicotiana benthamiana pelo potyvírus Pepper yellow mosaic virus ocorre aumento dos níveis de seu mRNA. Plantas silenciadas para TCTP acumulam menos vírus do que plantas selvagens, mostrando que esta proteína é importante para a infecção por potyvírus. Neste trabalho, o envolvimento da TCTP na infecção por potyvírus foi analisado detalhadamente utilizando-se o potyvírus Turnip mosaic virus (TuMV). Em plantas de N. benthamiana silenciadas para TCTP também ocorre uma diminuição no acúmulo do TuMV quando comparado com plantas não silenciadas. Além disso, plantas superexpressando TCTP de maneira transiente acumularam mais vírus do que plantas controle, confirmando o efeito positivo desta proteína na infecção por diferentes espécies de potyvírus. Para analisar a localização subcelular de TCTP no contexto da infecção, TCTP fusionada a GFP foi co-expressa com TuMV/6K2:mCherry. TCTP co-localiza-se com as vesículas replicativas e com estrutura a globular perinuclear tipicamente observada em células infectadas. O fracionamento de proteínas celulares demonstrou que TCTP está predominantemente na fração solúvel e uma pequena porção se associa com membranas, tanto em plantas sadias quanto em plantas infectadas. A co- localização com vesículas marcadas por 6K2 e a presença de TCTP em frações membranosas da célula sugerem um possível envolvimento desta proteína na replicação viral. Para verificar esta hipótese, protoplastos obtidos a partir de plantas silenciadas para TCTP foram infectados com TuMV e com o mutante TuMV VNN , o qual não é capaz de replicar-se. Os resultados demonstraram que o acúmulo de TuMV é reduzido em protoplastos silenciados, indicando que TCTP é necessária para a replicação. O acúmulo da proteína TCTP durante a infecção também foi avaliado. A infecção viral induz o aumento dos níveis de mRNA mas não de proteína, sugerindo que o mRNA que codifica TCTP atue na replicação. Desta forma, foi analisado se expressão de um RNA não traduzível de TCTP possui efeito sobre a infecção viral. Os resultados mostraram que apenas a expressão de um RNA traduzível é capaz de aumentar a infecção viral, indicando que a proteína TCTP, ou que a tradução se seu mRNA, é importante para a replicação viral.
The translationally controlled tumor protein (TCTP) is widely distributed among eukaryotes. It is involved in the regulation of basic processes such as cell cycle progression, cell growth, stress protection and apoptosis. During tomato (Solanum lycopersicum) and Nicotiana benthamiana infection by the potyvirus Pepper yellow mosaic virus, an increase of TCTP mRNA levels was observed. Plants silenced for TCTP accumulate fewer viruses than control plants, showing the importance of that gene for potyvirus infection. In this work, TCTP involvement in potyvirus infection was analyzed in details using the potyvirus Turnip mosaic virus (TuMV). N. benthamiana plants silenced for TCTP accumulated fewer viruses than non-silenced plants. In addition, plants overexpressing TCTP transiently accumulated more viruses than control plants, confirming that TCTP has a positive effect on infection by different potyviruses. To study TCTP subcellular localization in potyvirus infected plants, TCTP fused to GFP was co- expressed with TuMV/6K2:mCherry. Confocal analysis has shown that TCTP co- localizes with 6K2-tagged structures such as replicative vesicles and the perinuclear globular structure that is typically observed in potyvirus-infected cells. Cellular fractioning demonstrated that TCTP is mainly present in the soluble fraction but is also associated with membranes. The co-localization of TCTP with 6K2-tagged vesicles and its presence in cellular membranous fractions suggests a possible involvement of TCTP in virus replication. To test this hypothesis, protoplasts obtained from TCTP silenced plants were infected with TuMV and its mutant TuMV VNN , which is defective for replication. The results showed that TuMV accumulation is reduced in silenced protoplasts, indicating that TCTP is necessary for replication. TCTP accumulation during infection was also analyzed. Viral infection induces TCTP mRNA expression, but not protein accumulation, suggesting that the TCTP mRNA and not the protein has a role in viral infection. To check this, we expressed a non-translatable form of TCTP RNA in plants and analyzed its effect in virus accumulation. The results showed that only the expression of a translatable RNA resulting in protein production is able to increase virus infection, indicating that the protein and/or the translation of TCTP is important for potyvirus replication.
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陳漢文 and Hon-man Chan. "Overexpression of translationally controlled tumor protein (TCTP) predisposes to hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/193056.

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Hepatocellular carcinoma (HCC) is the most common tumors worldwide. In contrast to other cancers, the prognosis of HCC is extremely poor, with less that 5% of 5-year survival rate worldwide. From our previous studies, we isolated Chromodomain Helicases/ATPase DNA binding protein1-Like (CHD1L) gene from chromosome 1q21, and characterized it as a specific oncogene in HCC. By using 2D-PAGE and MALDI-TOF mass spectrometry approach, Translationally Controlled Tumor Protein (TCTP) was identified as a CHD1L target, which was preferentially expressed in CHD1L-transfected cells. TCTP is a highly conserved protein and expressed in almost all mammalian tissues. It has been reported that TCTP interacts with microtubules in a cell-cycle-dependent manner, and functions as a prosurvival factor and inhibiting apoptosis. To better understand the molecular mechanisms of HCC progression, the effect of TCTP overexpression in HCC and the mechanism by which TCTP regulated cell-cycle progression were elucidated in this study. CHD1L is a unique oncogene belongs to SNF2-like subfamily. Mechanistic studies found that CHD1L protein directly binds to the promoter region (nt -733 to -1,027) of TCTP and activated TCTP transcription. Investigation of clinical HCC specimens found that overexpression of TCTP was not only significantly associated with the advanced tumor stage (P = 0.037) and overall survival time of HCC patients (P = 0.034), but also an independent marker associated with poor prognostic outcomes. Functional studies demonstrated that TCTP has tumorigenic abilities and overexpression of TCTP contributed to the mitotic defects of tumor cells. Further mechanistic studies demonstrated that TCTP promoted the ubiquitin-proteasome degradation of Cdc25c during mitotic progression, which caused the failure in the dephosphorylation of Cdk1 on Tyr 15 and decreased Cdk1 activity. The consequence of chromosome missegregation and mitotic catastrophe results in aneuploidy, which is frequently observed in cancer. In addition, the correlation between TCTP overexpression and metastatic potential of HCC was elucidated by examined the expression levels of TCTP using a tissue microarray (TMA) containing 60 pairs of primary HCCs and their matched metastases. Further studies demonstrated that overexpression of TCTP shows high incidence of extrahepatic metastasis and positive correlation was found between TCTP and MMP-2 or MMP-9 (Spearmen correlation coefficient=0.466, and 0.352, respectively, P<0.001 for both). In vitro functional studies showed that TCTP protein associated with promoter regions of MMP-2 and MMP-9 and activates their transcriptions. Molecular analyses revealed that TCTP served as a JunD coactivator and formed complexes with JunD and bind with consensus AP-1 sites on MMP-2 and MMP-9 promoters to enhance their expression in HCC cells. More importantly, high co-expression of TCTP and MMP-2 or MMP-9 was significantly associated with poor disease-free survival (log rank= 8.146, and 11.677 respectively, P =0.017 and 0.003 respectively). In summary, two novel molecular mechanisms (CDH1L/TCTP/Cdc25C/Cdk1) and (TCTP/JunD/MMP-2, MMP-9) were revealed during HCC progression and metastasis. Also, the prognostic value of TCTP and MMP-2 or MMP-9 coexpression for HCC was highlight in this study.
published_or_final_version
Clinical Oncology
Doctoral
Doctor of Philosophy
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Karafin, Teele. "Etude de la fonction de Translationally Controlled Tumor Protein (TCTP) dans différents modèles génétiques dans la souris." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS211.

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TCTP est une protéine de 20 kDa que l’on retrouve souvent sous forme de dimère. Elle est fortement conservée dans la phylogénie et on la trouve dans les levures, les plantes, les invertébrés et les mammifères. Elle est localisée dans tous les compartiments de la cellule : noyau, cytoplasme, et membranes. Il s’agit d’une protéine très abondante dans des cellules souches ainsi que des cellules en croissance exponentielle, y compris les cellules tumorales. Sa fonction principale est celle d’une « protéine de survie ». TCTP a été décrite comme interagissant avec de multiples protéines dont p53, MDM2, Bcl-xL et TSAP6. Le but de mon travail est de permettre de mieux caractériser ces fonctions de TCTP et pour cela, nous avons étudié ses interactions in vitro et surtout, in vivo, dans différents modèles génétiques chez la souris
TCTP is a 20 kDa protein frequently encountered as a dimer. It is highly conserved through phylogeny and is present inn yeast, plants, invertebrates and mammals. It is localized in all compartments of the cell: nucleus, cytoplasm, membranes. This protein is highly abundant in stem cells and during the exponential growth, including in cancer cells. It mainly functions as a survivor factor. TCTP has been described as interacting with multiple proteins, including p53, MDM2, Bcl-xL and TSAP6. The purpose of my work is to better characterize these functions of TCTP; we therefore studied its interactions in vitro, but mostly in vivo, using different murine genetic models
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Thébault, Stéphanie. "Etude des complexes entre TCTP (Translationally Controlled Tumor Protein) et ses partenaires." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T024.

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La thématique du laboratoire de l’équipe d’Adam Telerman porte sur la réversion tumorale, un processus rare au cours duquel les cellules cancéreuses perdent leur phénotype malin, et deviennent des cellules dites révertantes. Plusieurs protéines clefs impliquées dans cette transformation ont été mises en évidence, dont TCTP (Translationally Controlled Tumor Protein). La protéine TCTP est également impliquée dans la régulation de l’apoptose en interagissant et en renforçant l’activité anti-apoptotique de Mcl-1 et de Bcl-xl, deux protéines appartenant à la famille des Bcl-2. Ce projet s’attache à comprendre en termes moléculaires le mode d’action de TCTP au cours de l’apoptose
Adam Telerman’s team research focuses on tumor reversion, a rare process in which cancer cells lose their malignant phenotype, and therefore become revertant. Many key proteins were showed to be involved in this transformation, including TCTP (translationally Controlled Tumor Protein). TCTP protein is also involved in apoptosis regulation by interacting and strengthening the anti-apoptotic activity of Mcl-1 and Bcl-xl, two proteins from Bcl-2 family
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Andrade, Patrícia Oliveira. "Involvement of Translationally controlled tumor protein in Tomato yellow spot virus infection." Universidade Federal de Viçosa, 2017. http://www.locus.ufv.br/handle/123456789/21427.

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Fundação de Amparo à Pesquisa do Estado de Minas Gerais
Os vírus são as formas de vida mais abundantes e geneticamente diversas conhecidas em nossa biosfera. Para infectar hospedeiros com sucesso, os vírus manipulam componentes celulares do hospedeiro, recrutando fatores do hospedeiro necessários para replicação, infeção e transmissão. Além disso, os vírus precisam suplantar diversas estratégias de defesa do hospedeiro levando a um complexo mecanismo de coevolução que envolve diversas interações. Diferentes vírus podem interagir com componentes celulares do hospedeiro de forma semelhante. Foi demonstrado que a presença da proteína translationally controlled tumor protein (TCTP) é necessária para o estabelecimento de uma infecção eficiente por potyvírus. TCTP é uma proteína multifuncional encontrada em quase todos os eucariotos envolvida no crescimento celular, homeostase de íons, reparo de danos no DNA e possuí atividade anti-apoptótica. Apesar de inúmeros estudos com TCTP, o envolvimento desta proteína na infecção viral ainda não é totalmente compreendido. Devido a sua diversidade funcional, é possível imaginar que TCTP possa ser um fator do hospedeiro envolvido em infeções causadas por vírus de diferentes grupos. Desta forma, neste trabalho, foi avaliado o efeito de TCTP na infecção por begomovírus. Para isso, plantas de Nicotiana benthamiana com TCTP silenciada por VIGS foram utilizados para estudar o efeito da TCTP na infecção pelo begomovírus Tomato yellow spot virus (ToYSV). O silenciamento de TCTP levou a um maior acúmulo de vírus, sugerindo que TCTP é um fator do hospedeiro envolvido no processo de defesa á infecção viral. Além disso, o mRNA de TCTP é altamente estruturado em mamíferos e está relacionado com a indução de resposta a infecções por diferentes vírus. Por ser um mRNA altamente estruturado é razoável supor que o mRNA de TCTP pode ser alvo do processo de silenciamento pós transcrisional da planta levando à produção de pequenos RNAs de interferência (siRNAs) através da clivagem por proteínas Dicer e os siRNAs gerados podem regular a expressão de genes endógenos do hospedeiro. Desta forma, foi realizada uma análise in silico para avaliar os possíveis siRNAs gerados a partir do silenciamento do mRNA de TCTP e os possíveis alvos desses siRNAs. Genes que podem estar envolvidos em infecção viral, como aqueles que codificam proteína kinases, proteínas envolvidas na via de ubiquitinação, fatores de transcrição e tradução e proteínas de ligação ao cálcio foram alguns dos genes identificados como possíveis alvos destes siRNAs.
Viruses are the most abundant and genetically diverse life forms known in our biosphere. To successfully infect hosts, viruses manipulate host cellular components, recruiting host factors necessary for replication, infection, and transmission. In addition, viruses need to supplant various host defense strategies, leading to a complex coevolution mechanism involving virus-host interactions. Different viruses can interact with host cell components similarly or even antagonistic. The presence of the protein translationally controlled tumor protein (TCTP) has been shown to be necessary for the establishment of an efficient potyvirus infection. TCTP is a multifunctional protein found in almost all eukaryotes and is involved in cell growth; ions homeostasis; DNA damage repair and anti-apoptotic activity. Despite numerous studies with TCTP, the involvement of this protein in viral infection is not yet fully understood. Due to its functional diversity, it is possible to imagine that TCTP may be a host factor involved in infections caused by viruses of different groups. Thus, in this work, the effect of TCTP on begomovirus infection was evaluated. Nicotiana benthamiana plants silenced for TCTP by VIGS experiments were used to study the effect of TCTP expression on infection by the begomovirus Tomato yellow spot virus (ToYSV). TCTP silencing led to higher accumulation of the virus, suggesting that TCTP is a host factor involved in viral infection defense process. Furthermore, TCTP mRNA is highly structured in mammals and is related to the induction of defense response to different viruses. Because it is a highly structured mRNA, it is reasonable to assume that TCTP mRNA may be the target of the plant post transcription gene silencing mechanism, leading to the production of small interfering RNAs (siRNAs) by the cleavage of Dicer proteins and the siRNAs generated might regulate the expression of host endogenous genes involves in virus infection. In silico analysis was performed to evaluate the possible siRNAs generated from the silencing of TCTP mRNA, and the respective targets of this siRNAs. Genes involved in viral infection, such as those encoding protein kinases, proteins involved in the ubiquitination pathway, transcription and translation factors, and calcium binding proteins were some of the genes identified as possible targets of these predicted siRNAs.
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Carvalho, Márcio de [UNESP]. "Estudo do papel da TCTP (Translationally Controlled Tumour Protein) na resposta ao estresses bióticos e abióticos em plantas." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/92453.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
O gene que codifica a TCTP (Translationally Controlled Tumour Protein) está presente em todos os eucariontes e o seu produto está envolvido em diferentes processos celulares. Embora bem caracterizada em mamíferos, poucos são os trabalhos disponíveis na literatura relacionados à análise da TCTP em plantas. No presente trabalho, a expressão do gene que codifica a TCTP em tomateiros foi analisada em situações de estresse biótico e abiótico. No estresse abiótico, as plantas de tomate foram submetidas a dano mecânico nas folhas, e essas coletadas após 4, 8 e 12 horas. No estresse biótico, duas espécies virais foram inoculadas mecanicamente nas plantas de tomate, o Cucumber mosaic virus (CMV) e o Pepper Yellow Mosaic Virus (PepYMV), respectivamente, e as folhas sistemicamente inoculadas foram coletadas após 25 dias. Um aumento na expressão da TCTP foi constatado em resposta ao estresse biótico, sendo de 1,3x em relação ao controle não inoculado na infecção pelo CMV, e de 1,4x na infecção pelo PepYMV. No estresse mecânico, o pico de expressão ocorreu após 4 horas com um aumento de 3,4x em relação ao controle não tratado, com posterior redução nos demais tempos. Adicionalmente, plantas transgênicas de tabaco capazes de superexpressar a TCTP de tomate foram geradas a fim de determinar o papel dessa proteína na infecção pelo PepYMV. Quando as linhagens transgênicas geradas foram inoculadas com o PepYMV observou-se, aos 14 dias após a inoculação (DAI), um aumento na concentração viral (1,8x) em relação às plantas de tabaco não transformadas, sendo o mesmo verificado aos 21 DAI (1,6x). Essa diferença, entretanto, não foi mais observada aos 28 DAI. Esses dados confirmam a relação funcional da TCTP com a resposta de defesa das plantas aos estresses bióticos e abióticos
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Carvalho, Márcio de. "Estudo do papel da TCTP (Translationally Controlled Tumour Protein) na resposta ao estresses bióticos e abióticos em plantas /." Botucatu, 2010. http://hdl.handle.net/11449/92453.

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Orientador: Ivan de Godoy Maia
Banca: Fábio Tebaldi Silveira Nogueira
Banca: Jomar Patricío Monteiro
Resumo: O gene que codifica a TCTP (Translationally Controlled Tumour Protein) está presente em todos os eucariontes e o seu produto está envolvido em diferentes processos celulares. Embora bem caracterizada em mamíferos, poucos são os trabalhos disponíveis na literatura relacionados à análise da TCTP em plantas. No presente trabalho, a expressão do gene que codifica a TCTP em tomateiros foi analisada em situações de estresse biótico e abiótico. No estresse abiótico, as plantas de tomate foram submetidas a dano mecânico nas folhas, e essas coletadas após 4, 8 e 12 horas. No estresse biótico, duas espécies virais foram inoculadas mecanicamente nas plantas de tomate, o Cucumber mosaic virus (CMV) e o Pepper Yellow Mosaic Virus (PepYMV), respectivamente, e as folhas sistemicamente inoculadas foram coletadas após 25 dias. Um aumento na expressão da TCTP foi constatado em resposta ao estresse biótico, sendo de 1,3x em relação ao controle não inoculado na infecção pelo CMV, e de 1,4x na infecção pelo PepYMV. No estresse mecânico, o pico de expressão ocorreu após 4 horas com um aumento de 3,4x em relação ao controle não tratado, com posterior redução nos demais tempos. Adicionalmente, plantas transgênicas de tabaco capazes de superexpressar a TCTP de tomate foram geradas a fim de determinar o papel dessa proteína na infecção pelo PepYMV. Quando as linhagens transgênicas geradas foram inoculadas com o PepYMV observou-se, aos 14 dias após a inoculação (DAI), um aumento na concentração viral (1,8x) em relação às plantas de tabaco não transformadas, sendo o mesmo verificado aos 21 DAI (1,6x). Essa diferença, entretanto, não foi mais observada aos 28 DAI. Esses dados confirmam a relação funcional da TCTP com a resposta de defesa das plantas aos estresses bióticos e abióticos
Abstract: Not available
Mestre
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Частини книг з теми "Translationally controlled tumour protein"

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Senff-Ribeiro, Andrea. "Translationally Controlled Tumor Protein (TCTP/HRF) in Animal Venoms." In Results and Problems in Cell Differentiation, 193–200. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_9.

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Betsch, Léo, Julie Savarin, Mohammed Bendahmane, and Judit Szecsi. "Roles of the Translationally Controlled Tumor Protein (TCTP) in Plant Development." In Results and Problems in Cell Differentiation, 149–72. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_7.

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Bommer, Ulrich-Axel. "The Translational Controlled Tumour Protein TCTP: Biological Functions and Regulation." In Results and Problems in Cell Differentiation, 69–126. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_4.

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Choi, Kwang-Wook, Sung-Tae Hong, and Thao Phuong Le. "Function of Translationally Controlled Tumor Protein in Organ Growth: Lessons from Drosophila Studies." In Results and Problems in Cell Differentiation, 173–91. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_8.

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Zhang, Jie, Grace Shim, Sonia M. de Toledo, and Edouard I. Azzam. "The Translationally Controlled Tumor Protein and the Cellular Response to Ionizing Radiation-Induced DNA Damage." In Results and Problems in Cell Differentiation, 227–53. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_12.

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MacDonald, Susan M. "History of Histamine-Releasing Factor (HRF)/Translationally Controlled Tumor Protein (TCTP) Including a Potential Therapeutic Target in Asthma and Allergy." In Results and Problems in Cell Differentiation, 291–308. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67591-6_16.

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Rasola, Andrea. "Chaperones and protein quality control in the neoplastic process." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr, 239–54. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0017.

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Maintenance of proteome quality control in cells is a vital and extremely complex task, which requires fine-tuning among synthesis, folding, and degradation of proteins and is controlled by an integrated network of subcellular components. A pivotal role in this process is played by chaperones, molecular machines that take part in nearly all cellular functions and make possible the optimal activity of proteins by assisting their folding, conformational changes, and subcellular trafficking, and by controlling protein degradation following unfolding, misfolding, or aggregation. Neoplastic cells undergo major changes in the homeostasis of their proteome, or proteostasis, as a consequence of a profound rewiring of their metabolic circuitries and of exposure to stressful environmental stimuli, such as hypoxia or nutritional and pH fluctuations. These stress conditions also affect protein folding in the endoplasmic reticulum and mitochondrial bioenergetic functions, leading to activation of organelle-restricted, protective signalling pathways called unfolded protein responses, which can subtly regulate the equilibrium among death, dormancy, and aggressiveness of tumour cells. In most cancer types molecular chaperones are overexpressed and exploited to cope with these stress stimuli and to underpin pro-oncogenic biological routines, including cell growth, proliferation, invasion, metastasis, and escape to death stimuli. Chaperone induction has been associated with cancer progression, resistance to chemotherapy, and poor prognosis; therefore, development of chaperone-targeting drugs has emerged as a promising antineoplastic strategy.
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Pepys, Mark B. "The acute phase response and C-reactive protein." In Oxford Textbook of Medicine, edited by Timothy M. Cox, 2199–207. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0239.

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The acute phase response—trauma, tissue necrosis, infection, inflammation, and malignant neoplasia induce a complex series of nonspecific systemic, physiological, and metabolic responses including fever, leucocytosis, catabolism of muscle proteins, greatly increased de novo synthesis and secretion of a number of ‘acute phase’ plasma proteins, and decreased synthesis of albumin, transthyretin, and high- and low-density lipoproteins. The altered plasma protein concentration profile is called the acute phase response. Acute phase proteins—these are mostly synthesized by hepatocytes, in which transcription is controlled by cytokines including interleukin 1, interleukin 6, and tumour necrosis factor. The circulating concentrations of complement proteins and clotting factors increase by up to 50 to 100%; some of the proteinase inhibitors and α‎1-acid glycoprotein can increase three- to fivefold; but C-reactive protein (CRP) and serum amyloid A protein (an apolipoprotein of high-density lipoprotein particles) are unique in that their concentrations can change by more than 1000-fold. C-reactive protein—this consists of five identical, nonglycosylated, noncovalently associated polypeptide subunits. It binds to autologous and extrinsic materials which contain phosphocholine, including bacteria and their products. Ligand-bound CRP activates the classical complement pathway and triggers the inflammatory and opsonizing activities of the complement system, thereby contributing to innate host resistance to pneumococci and probably to recognition and safe ‘scavenging’ of cellular debris. Clinical features—(1) determination of CRP in serum or plasma is the most useful marker of the acute phase response in most inflammatory and tissue damaging conditions. (2) Acute phase proteins may be harmful in some circumstances. Sustained increased production of serum amyloid A protein can lead to the deposition of AA-type, reactive systemic amyloid.
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Тези доповідей конференцій з теми "Translationally controlled tumour protein"

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Lee, Sang-Il, Min-Gyu Jeon, Jung-Yoon Choe, Jinseok Kim, Heewon Lee, and Kyunglim Lee. "02.23 Translationally controlled tumour protein is a critical therapeutic target for rheumatoid arthritis." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211050.23.

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Ho, M., M. Ho, L. M. Julian, W. L. Stanford, and D. J. Stewart. "Disruptive Effect of LAM-Derived Smooth Muscle Cells on Human Lung Progenitors Is Dependent on Expression of Translationally Controlled Tumour Protein." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4280.

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Koo, Namjin, Sangho Oh, and Yong-Min Kim. "Inter-kingdom Comparative Analysis of Translationally Controlled Tumor Protein (TCTP) Provides Clues for Their Lineage-specific Evolution." In 2018 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2018. http://dx.doi.org/10.1109/bibm.2018.8621447.

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Munirathinam, Gnasekar, Andre A. Kajdacsy-Balla, Sushma Kaul, Andrei Scumpu, Terrie Kucynda, Purvi Patel, Michelle Zheng, and Paul F. Lindholm. "Abstract 541: Cadmium activates translationally controlled tumor protein (TCTP) and p38 MAPK as possible pathways for prostate cancer cell aggressiveness." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-541.

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