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Добірка наукової літератури з теми "YAE1"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "YAE1"

Merlin, Christophe, Gregory Gardiner, Sylvain Durand, and Millicent Masters. "The Escherichia coli metD Locus Encodes an ABC Transporter Which Includes Abc (MetN), YaeE (MetI), and YaeC (MetQ)." Journal of Bacteriology 184, no. 19 (October 1, 2002): 5513–17. http://dx.doi.org/10.1128/jb.184.19.5513-5517.2002.

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ABSTRACT We report that the genes abc, yaeC, and yaeE comprise metD, an Escherichia coli locus encoding a dl-methionine uptake system. MetD is an ABC transporter with Abc the ATPase, YaeE the permease, and YaeC the likely substrate binding protein. Expression of these genes is regulated by l-methionine and MetJ, a common repressor of the methionine regulon. We propose to rename abc, yaeE, and yaeC as metN, metI, and metQ, respectively.

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Prusty, Nihar Ranjan, Francesca Camponeschi, Simone Ciofi-Baffoni, and Lucia Banci. "The human YAE1-ORAOV1 complex of the cytosolic iron-sulfur protein assembly machinery binds a [4Fe-4S] cluster." Inorganica Chimica Acta 518 (April 2021): 120252. http://dx.doi.org/10.1016/j.ica.2021.120252.

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Wiatrowski, Heather A., and Marian Carlson. "Yap1 Accumulates in the Nucleus in Response to Carbon Stress in Saccharomyces cerevisiae." Eukaryotic Cell 2, no. 1 (February 2003): 19–26. http://dx.doi.org/10.1128/ec.2.1.19-26.2003.

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ABSTRACT Yap1 is a transcription factor of the AP-1 family that is required for the adaptive response to oxidative stress in Saccharomyces cerevisiae. We recovered Yap1 in a two-hybrid screen for proteins that interact with the Sip2 subunit of the Snf1 protein kinase, which is required for the adaptation of cells to glucose limitation. Yap1 becomes enriched in the nucleus when cells are subjected to oxidative stress. We show that the localization of Yap1 is similarly sensitive to carbon stress. When glucose-grown cells were shifted to medium containing glycerol or no added carbon source, green fluorescent protein (GFP)-Yap1 accumulated in the nucleus. After adaptation to growth in glycerol, GFP-Yap1 was again primarily cytoplasmic. Nuclear accumulation was independent of respiration and of the Snf1, PKA, TOR, and Yak1 pathways, and the mechanism is distinct from that involved in the response to hydrogen peroxide. Addition of glutathione to the medium inhibited nuclear accumulation of GFP-Yap1 in response to carbon stress but did not affect the relocalization of Gal83 or Mig1. Other stresses such as increased temperature, acidic pH, and ionic stress did not cause nuclear enrichment of GFP-Yap1. These findings suggest a role for Yap1 in the response to carbon stress.

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Ben, Chi, Xiaojing Wu, Atsushi Takahashi-Kanemitsu, Christopher Takaya Knight, Takeru Hayashi, and Masanori Hatakeyama. "Alternative splicing reverses the cell-intrinsic and cell-extrinsic pro-oncogenic potentials of YAP1." Journal of Biological Chemistry 295, no. 41 (August 6, 2020): 13965–80. http://dx.doi.org/10.1074/jbc.ra120.013820.

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In addition to acting as a transcriptional co-activator, YAP1 directly mediates translocalization of the pro-oncogenic phosphatase SHP2 from the cytoplasm to nucleus. In the cytoplasm, SHP2 potentiates RAS–ERK signaling, which promotes cell proliferation and cell motility, whereas in the nucleus, it mediates gene regulation. As a result, elucidating the details of SHP2 trafficking is important for understanding its biological roles, including in cancer. YAP1 comprises multiple splicing isoforms defined in part by the presence (as in YAP1-2γ) or absence (as in YAP1-2α) of a γ-segment encoded by exon 6 that disrupts a critical leucine zipper. Although the disruptive segment is known to reduce co-activator function, it is unclear how this element impacts the physical and functional relationships between YAP1 and SHP2. To explore this question, we first demonstrated that YAP1-2γ cannot bind SHP2. Nevertheless, YAP1-2γ exhibits stronger mitogenic and motogenic activities than does YAP1-2α because the YAP1-2α–mediated delivery of SHP2 to the nucleus weakens cytoplasmic RAS–ERK signaling. However, YAP1-2γ confers less in vivo tumorigenicity than does YA1-2α by recruiting tumor-inhibitory macrophages. Mechanistically, YAP1-2γ transactivates and the YAP1-2α–SHP2 complex transrepresses the monocyte/macrophage chemoattractant CCL2. Thus, cell-intrinsic and cell-extrinsic pro-oncogenic YAP1 activities are inversely regulated by alternative splicing of exon 6. Notably, oncogenic KRAS down-regulates the SRSF3 splicing factor that prevents exon 6 skipping, thereby creating a YAP1-2α–dominant situation that supports a “cold” immune microenvironment.

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Gál, József, Attila Szvetnik, Róbert Schnell, and Miklós Kálmán. "The metDd-Methionine Transporter Locus of Escherichia coli Is an ABC Transporter Gene Cluster." Journal of Bacteriology 184, no. 17 (September 1, 2002): 4930–32. http://dx.doi.org/10.1128/jb.184.17.4930-4932.2002.

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ABSTRACT The metD d-methionine transporter locus of Escherichia coli was identified as the abc-yaeE-yaeC cluster (now renamed metNIQ genes). The abc open reading frame is preceded by tandem MET boxes bracketed by the −10 and −35 boxes of a promoter. The expression driven by this promoter is controlled by the MetJ repressor and the level of methionine.

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Kawauchi, Daisuke, Kristian Pajtler, Yiju Wei, Konstantin Okonechnikov, Patricia Silva, David Jones, Mikio Hoshino, Stefan Pfister, Marcel Kool, and Wei Li. "TB-06 MOLECULAR MECHANISM OF BRAIN TUMOUR FORMATION DRIVEN BY SUPRATENTORIAL EPENDYMOMA-SPECIFIC YAP1 FUSION GENES." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii11. http://dx.doi.org/10.1093/noajnl/vdz039.048.

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Abstract YAP1 fusion-positive supratentorial ependymomas predominantly occur in infants, but the molecular mechanisms of oncogenesis are unknown. Here we show YAP1-MAMLD1 fusions but not YAP1 wildtype are sufficient to drive malignant transformation of neural progenitors in the developing cerebral cortex in mice, and the resulting tumours share histo-molecular characteristics of human ependymomas. Nuclear localization of YAP1-MAMLD1 protein is associated with its oncogenicity and is mediated by the nuclear localization signal of MAMLD1 in a YAP1-Ser127 phosphorylation-independent manner. Chromatin immunoprecipitation-sequencing analyses of human YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and TEAD transcription factor binding site motifs in YAP1-bound regulatory elements, hypothesizing the important role of these transcription factors in YAP1-MAMLD1-driven tumourigenesis. Indeed, co-immunoprecipitation assays revealed physical interactions of TEADs and NFIA/B with the YAP1 and MAMLD1 domains of the fusion protein, respectively. Mutation of the TEAD binding site in the YAP1 fusion or repression of NFI targets prevents tumour induction in mice. Together, these results demonstrate that the YAP1-MAMLD1 fusion functions as an oncogenic driver of ependymoma through recruitment of TEADs and NFIs, indicating a rationale for preclinical studies to block the interaction between YAP1 fusions and NFI and TEAD transcription factors.

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Kim, Yong Sook, Mira Kim, Dong Im Cho, Soo Yeon Lim, Ju Hee Jun, Mi Ra Kim, Bo Gyeong Kang, et al. "PSME4 Degrades Acetylated YAP1 in the Nucleus of Mesenchymal Stem Cells." Pharmaceutics 14, no. 8 (August 9, 2022): 1659. http://dx.doi.org/10.3390/pharmaceutics14081659.

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Intensive research has focused on minimizing the infarct area and stimulating endogenous regeneration after myocardial infarction. Our group previously elucidated that apicidin, a histone deacetylase (HDAC) inhibitor, robustly accelerates the cardiac commitment of naïve mesenchymal stem cells (MSCs) through acute loss of YAP1. Here, we propose the novel regulation of YAP1 in MSCs. We found that acute loss of YAP1 after apicidin treatment resulted in the mixed effects of transcriptional arrest and proteasomal degradation. Subcellular fractionation revealed that YAP1 was primarily localized in the cytoplasm. YAP1 was acutely relocalized into the nucleus and underwent proteasomal degradation. Interestingly, phosphor-S127 YAP1 was shuttled into the nucleus, suggesting that a mechanism other than phosphorylation governed the subcellular localization of YAP1. Apicidin successfully induced acetylation and subsequent dissociation of YAP1 from 14-3-3, an essential molecule for cytoplasmic restriction. HDAC6 regulated both acetylation and subcellular localization of YAP1. An acetylation-dead mutant of YAP1 retarded nuclear redistribution upon apicidin treatment. We failed to acquire convincing evidence for polyubiquitination-dependent degradation of YAP1, suggesting that a polyubiquitination-independent regulator determined YAP1 fate. Nuclear PSME4, a subunit of the 26 S proteasome, recognized and degraded acetyl YAP1 in the nucleus. MSCs from PSME4-null mice were injected into infarcted heart, and aberrant sudden death was observed. Injection of immortalized human MSCs after knocking down PSME4 failed to improve either cardiac function or the fibrotic scar area. Our data suggest that acetylation-dependent proteasome subunit PSME4 clears acetyl-YAP1 in response to apicidin treatment in the nucleus of MSCs.

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Hartley, A. D., M. P. Ward, and S. Garrett. "The Yak1 protein kinase of Saccharomyces cerevisiae moderates thermotolerance and inhibits growth by an Sch9 protein kinase-independent mechanism." Genetics 136, no. 2 (February 1, 1994): 465–74. http://dx.doi.org/10.1093/genetics/136.2.465.

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Abstract The growth defect associated with the loss of yeast A kinase activity can be alleviated by the overexpression or deletion of two other kinases, Sch9 and Yak1, respectively. Using tests of epistasis, we have shown that Sch9 and Yak1 define separate signaling pathways and must, therefore, suppress the A kinase defect by different mechanisms. Nevertheless, the Yak1 kinase appears to regulate cellular processes that are under A kinase control. For example, acquisition of heat resistance is correlated with Yak1 kinase activity, such that YAK1-overexpressing cells are over 200-fold more resistant than isogenic yak1 strains. These results, for the first time, associate a phenotype, other than suppression of the A kinase growth defect, with the loss of Yak1 activity and argue a broader role for the Yak1 kinase in cell growth.

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Zeng, Cheng, Pei-Li Wu, Zhao-Tong Dong, Xin Li, Ying-Fang Zhou, and Qing Xue. "YAP1 inhibits ovarian endometriosis stromal cell invasion through ESR2." Reproduction 160, no. 3 (September 2020): 481–90. http://dx.doi.org/10.1530/rep-19-0565.

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Endometriosis is an estrogen-dependent disease, and estrogen receptor 2 (ESR2) plays a critical role in the pathogenesis of ovarian endometriosis by promoting cell invasion. Yes-associated protein 1 (YAP1) plays suppressive roles in several types of tumors. However, the relationship between YAP1 and ESR2 is not fully understood. The aim of this study was to investigate the regulatory mechanism of YAP1 in terms of ESR2 and YAP1 regulation of endometriotic stromal cell (ECSC) invasion in ovarian endometriosis. Our results demonstrated that YAP1 mRNA and protein levels in eutopic endometrium (EU) tissues were higher than those in paired ectopic endometrium (EC) tissues. ECSCs transfected with siYAP1 exhibited a significant increase in both ESR2 mRNA levels and protein expression. Simultaneously, YAP1 overexpression in ECSCs yielded the opposite results. Co-IP assays demonstrated YAP1-NuRD complex formation by YAP1, CHD4 and MTA1 in ECSCs. YAP1 bound to two sites, (-539, -533) and (-158, -152), upstream of the ESR2 transcription initiation site. YAP1 binding to the two sites of the ESR2 promoter in ECSCs was significantly lower than that in eutopic endometrial stromal cells (EUSCs) from EU tissues. ECSCs transfected with siYAP1 exhibited increased invasion activity, while ECSCs transfected with siESR2 showed inhibition of invasion. However, transfection with siYAP1 and siESR2 together decreased the number of invading cells compared with transfection with siYAP1 alone. Therefore, we conclude that decreased levels of YAP1 in ovarian endometriomas enhance ESR2 expression via formation of a YAP1-NuRD complex, which further binds to the ESR2 promoters. Furthermore, YAP1 inhibits ECSCs invasion.

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Szulzewsky, Frank, Pia Hoellerbauer, Hua-Jun Wu, P. J. Cimino, Franziska Michor, Patrick Paddison, Valeri Vasioukhin, and Eric Holland. "GENE-04. THE ONCOGENIC FUNCTIONS OF YAP1-GENE FUSIONS CAN BE INHIBITED BY DISRUPTION OF YAP1-TEAD INTERACTION." Neuro-Oncology 21, Supplement_6 (November 2019): vi98. http://dx.doi.org/10.1093/neuonc/noz175.406.

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Abstract Supratentorial ependymoma can be sub-stratified into clinically relevant subtypes characterized by distinct molecular features. The subtype defined by high YAP1 activity harbored two distinct YAP1 gene fusions, YAP1-MAMLD1 and YAP1-FAM118B. In addition, YAP1 gene fusions have been detected in several other cancer types, including Epithelioid Hemangioendothelioma and Endocervical Adenocarcinoma. YAP1 is a key transcriptional co-activator and proto-oncogene that is negatively regulated by the Hippo pathway. Here, we show that both YAP1-MAMLD1 and YAP1-FAM118B, as well as additional YAP1 fusion genes found in other cancer types, are potent oncogenic drivers that cause tumor formation in the brain and the hindlimb in mice upon overexpression by somatic cell gene transfer. Using different in vitro assays, including Luciferase, RNA-, and ChIP Seq, we show that both the N-terminal YAP1 part and the C-terminal fusion partners exert activity. We can show that the YAP1 activity still relies on the binding to TEAD transcription factors, whereas the C terminal activity does not. Furthermore, the different fusion proteins have become independent from negative Hippo pathway signaling by constitutive nuclear localization and protection from degradation. In addition, by introducing point mutations and truncations to block the YAP1 and the MAMLD1 function we can show that the activity of both halves contributes to the oncogenic function of YAP1-MAMLD1. Using in vitro and in vivo assays we can show that pharmacological and genetic ablation of YAP-TEAD interaction diminishes the oncogenic potential of the fusions, indicating that this might be a potential therapeutic approach for these tumors in the future.

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Більше джерел

Дисертації з теми "YAE1"

Shah, Nupur R. "Functional studies of YAP1 in cancer and embryonic development." Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=238733.

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The Hippo pathway is a master regulator of cell proliferation and organ size, namely through regulation of transcriptional co-activators YAP and TAZ which bind TEAD1-4 transcription factors. The Hippo effector YAP is dysregulated in many human solid tumours including rhabdomyosarcoma and oesophageal cancer. Additionally, persistent hyperactivity of YAP in activated but not quiescent satellite cells can give rise to embryonal rhabdomyosarcoma. However, the question of exactly how YAP acts as an oncogene and actively gives rise to tumour progression in these cancers remains unknown. In this thesis I characterised the mechanisms which determine the functional role of YAP in driving instability in the genome. Secondly, lentiviral mediated knockdown of YAP is performed to determine and investigate its effect on tumorigenesis. Thirdly, gene sets from constitutive YAP S127A induced mouse ERMS tumours subjected to array-CGH were further analysed. Finally, I cloned chicken Yap1, Tead1 and Fstl5 to identify its role during chick embryonic development, by the retroviral mediated loss of function approach. The results demonstrated that constitutive YAP S127A expression in-vitro as well as in-vivo induces chromosomal instability by increasing the rate of mitotic chromosome segregation errors and copy number alterations of oncogenes and other cancer related genes. Recurrent copy number gains of the p53 inhibitor Mdm2 were observed in YAP S127A-driven ERMS tumours. Moreover, lentiviral mediated YAP knockdown showed significant reduction in proliferation, migration and invasion as well as transformation potential in human cultured cancer cells. Moreover, retroviral YAP S127A expression during early stages of chick embryo development did not lead to an overt phenotype and showed poor survival. Additionally, I have cloned RCAS-RNAi vectors to study the loss of function effect on Hippo targets and Fstl5 during chicken embryo development. Collectively, my data provides insight into the mechanisms with which YAP could drive tumorigenesis and that YAP knockdown can be considered a potential therapeutic target to reduce cancer progression.

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Schlegelmilch, Karin [Verfasser]. "YAP1 and the Hippo Signaling Pathway Regulate Progenitor Proliferation / Karin Schlegelmilch." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1042186170/34.

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金原, 和江. "膜結合型プロテアーゼYaeLの機能解析". 京都大学 (Kyoto University), 2003. http://hdl.handle.net/2433/148589.

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Caetano, Soraia Cristina Marques. "O Yap1 no stress causado pelo excesso de cobalto em S. cerevisiae." Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/8214.

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Mestrado em Biotecnologia
A capacidade dos organismos em alterar os seus padrões de expressão de genes em resposta a perturbações do meio ambiente é essencial para a sua viabilidade. Neste trabalho, utilizando Saccharomyces cerevisiae como organismo eucariota modelo, foi estudada a relevância do factor de transcrição da família Yap, o Yap1, na desintoxicação do excesso de cobalto. Os resultados obtidos neste trabalho demonstram que, após a incubação das células com cobalto, o factor de transcrição Yap1 é acumulado no núcleo, através de um mecanismo independente de Orp1/Gpx3. Verificámos que o cobalto tem a capacidade de ligar-se directamente ao Yap1, sugerindo que, à semelhança do que acontece com outros metais, seja este o mecanismo de retenção nuclear após o stress. Confirmámos que uma vez no núcleo, o Yap1 medeia a indução de genes envolvidos na regulação do stress oxidativo em levedura (tais como GPX2, SOD1, TRR1 e TRX2) e constatámos que a presença de cobalto aumenta os níveis de carbonilação das proteínas, sendo esse aumento mais acentuado na ausência de Yap1. Verificámos ainda que os níveis de cobalto estão levemente diminuídos no mutante yap1 ao contrário do ferro que está em concentrações mais elevadas neste mutante relativamente à estirpe selvagem, quer na presença como na ausência de cobalto. Este facto leva-nos a propor que o cobalto altere a homeostase do ferro e que em consequência, conjuntamente com a diminuição das defesas anti-oxidantes, gere stress oxidativo. Foi descrito que a glutationa (GSH) é importante na homeostase do ferro e o excesso de cobalto leva ao aumento dos níveis de ferro intracelulares. Verificámos não só que a expressão de GSH1 está diminuída aos 30 minutos de tratamento do mutante yap1 com cobalto mas também que a adição de GSH faz recuperar os fenótipos de crescimento na presença deste metal. Finalmente apresentámos um modelo de acção do factor Yap1 no stress provocado pelo cobalto.
The ability of organisms to reprogram gene expression in response to changes in the environment is essential for their viability. In this work, using Saccharomyces cerevisiae as a eukaryotic model organism, we studied the relevance of the transcription factor, Yap1, in the detoxification of cobalt excess. The results here reported show that after incubation of cells with cobalt, Yap1 accumulates in the nucleus, through a mechanism independent of the peroxidase Orp1/Gpx3. We found that cobalt has the ability to directly bind to Yap1, suggesting that this is the mechanism for its nuclear retention after cobalt treatment. We confirmed that, once in the nucleus, Yap1 mediates the induction of genes involved in the regulation of oxidative stress in yeast (such as GPX2, SOD1, TRX2 and TRR1). Moreover, we found that the presence of cobalt increases the levels of protein carbonylation, being the damage more pronounced in the absence of Yap1. It was also found that cobalt levels are slightly decreased in the yap1 mutant. In contrast, the iron concentration is higher in this mutant than in the wild type, in the presence and absence of cobalt. This led us to propose that the cobalt alters iron homeostasis and iin consequence generate oxidative stress. It was reported that glutathione (GSH) is important in the homeostasis of iron. As the excess of cobalt leads to increased levels of intracellular iron, we found not only that in the yap1 mutant GSH1 expression is decreased after 30 minutes of treatment with cobalt but also, the addition of GSH can recover the growth phenotypes in the presence of this metal. . Finally we present a working model of the transcription factor Yap1 in stress caused by cobalt.

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Sha, Wei. "Microarray data analysis methods and their applications to gene expression data analysis for Saccharomyces cerevisiae under oxidative stress." Diss., Virginia Tech, 2006. http://hdl.handle.net/10919/27840.

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Oxidative stress is a harmful condition in a cell, tissue, or organ, caused by an imbalance between reactive oxygen species or other oxidants and the capacity of antioxidant defense systems to remove them. These oxidants cause wide-ranging damage to macromolecules, including proteins, lipids, DNA and carbohydrates. Oxidative stress is an important pathophysiologic component of a number of diseases, such as Alzheimerâ s disease, diabetes and certain cancers. Cells contain effective defense mechanisms to respond to oxidative stress. Despite much accumulated knowledge about these responses, their kinetics, especially the kinetics of early responses is still not clearly understood. The Yap1 transcription factor is crucial for the normal response to a variety of stress conditions including oxidative stress. Previous studies on Yap1 regulation started to measure gene expression profile at least 20 minutes after the induction of oxidative stress. Genes and pathways regulated by Yap1 in early oxidative stress response (within 20 minutes) were not identified in these studies. Here we study the kinetics of early oxidative stress response induced by the cumene hydroperoxide (CHP) in Saccharomyces cerevisiae wild type and yap1 mutant. Gene expression profiles after exposure to CHP were obtained in controlled conditions using Affymetrix Yeast Genome S98 arrays. The oxidative stress response was measured at 8 time points along 120 minutes after the addition of CHP, with the earliest time point at 3 minute after the exposure. Statistical analysis methods, including ANOVA, k-means clustering analysis, and pathway analysis were used to analyze the data. The results from this study provide a dynamic resolution of the oxidative stress responses in S. cerevisiae, and contribute to a richer understanding of the antioxidant defense systems. It also provides a global view of the roles that Yap1 plays under normal and oxidative stress conditions.
Ph. D.

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Fechtner, Tim [Verfasser]. "Charakterisierung der neuen, potentiellen Adhäsine Yaa1, Yaa2 und Yaa3 von Chlamydia pneumoniae / Tim Fechtner." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1036261921/34.

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Hegerfeldt, Yael [Verfasser], and Peter [Akademischer Betreuer] Friedl. "Kollektive Invasion in Melanomexplantaten: Bedeutung von Zell-Matrix-Interaktionen / Yael Hegerfeldt. Betreuer: Peter Friedl." Würzburg : Universitätsbibliothek der Universität Würzburg, 2012. http://d-nb.info/1028326785/34.

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Molina-Castro, Silvia. "Study of the Hippo/YAP1 signaling pathway in gastric carcinogenesis induced by Helicobacter pylori." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0623/document.

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Le cancer gastrique (CG) est une maladie multifactorielle, fréquemment associée à l’infection chronique par des souches CagA+ d’Helicobacter pylori. La transition épithélio-mésenchymateuse (EMT) est un processus réversible dans lequel une cellule épithéliale polarisée acquiert un phénotype mésenchymateux. L’EMT est à l’émergence de cellules souches cancéreuses (CSC) qui expriment CD44 et présentent une activité ALDH élevée. L’infection des cellules épithéliales gastriques humaines (CEGs) par CagA+ H. pylori induit des cellules CD44+ avec des propriétés des CSCs via une EMT. La voie Hippo est composée par les kinases MST et LATS, et leurs cibles, les YAP1 et TAZ. Suite à la phosphorylation, YAP1 et TAZ sont inhibés. YAP1 et TAZ activés lient les facteurs TEAD pour promouvoir la croissance cellulaire et l’inhibition de l’apoptose.Notre premier objectif était de rechercher si H. pylori change l’état d’activation de la voie Hippo et l'effet sur l’EMT et les CSC in vitro et in vivo. Le deuxième but est la caractérisation du rôle de YAP1/TEAD dans les propriétés de CSCs gastriques in vitro et les conséquences de son inhibition dans la croissance tumorale in vivo.Pour étudier la régulation de la voie Hippo pendant l’infection par H. pylori, LATS2, YAP1 et CD44 ont été évalués dans la muqueuse gastrique de sujets non-infectés et infectés par H. pylori, qui ont été augmentés avec l’infection et leur surexpression a été associée avec la gastrite et la métaplasie intestinale. Dans les CEGs l’expression de gènes de la voie Hippo a été altérée par l’infection. La régulation de la voie Hippo par H. pylori a une cinétique diphasique et dépendante de CagA. Dans l’infection précoce, H. pylori déclenche l’activité transcriptionelle de YAP1. Cette période d’inactivité de la voie Hippo est suivi de son activation progressive, soutenue par l’accumulation de LATS2 et la phosphorylation inhibitrice de YAP1. La répression de LATS2 avec siRNAs a accéléré l’acquisition du phénotype mésenchymateux après l’infection, l’augmentation de marqueurs de l’EMT (Zeb1 et Snail1), et la diminution des miR-200 épithéliaux. Les CSC induites par H. pylori ont été potentialisées par l’inhibition de LATS2, ce qui suggère que LATS2 limite l’EMT et le phénotype de CSC acquis pendant l’infection. L’inhibition de LATS2 ou YAP1 diminue l’expression de ces deux protéines, révélant ainsi une boucle de régulation positive. Dans des coupes de tissu de CG, l’expression de LATS2 et YAP1 est hétérogène et positivement corrélée, fait qui a été confirmé dans 38 CEGs de la CCLE. L’expression LATS2 est fortement corrélée à celle de CTGF et CYR61, ce qui suggère que LATS2 peut aussi être un gène cible de YAP1/TEAD.La verteporfine (VP) est capable d’interrompre l’interaction YAP1/TEAD, et donc d’inhiber son activité transcriptionelle. In vitro, utilisant CEGs et des cellules de tumeurs de patients amplifiées chez la souris (patient-derived xenograft PDX), le traitement à la VP a diminué la croissance cellulaire, l’expression de gènes cible de YAP1/TAZ/TEAD, l’activité du rapporteur TEAD-luciférase et la capacité de formation de sphères. L’activité de la VP a été testée in vivo par injection péri-tumorale dans un modèle de greffe sous-cutanés des CEGs MKN45 et MKN74 et le PDX GC10 chez la souris NSG. La croissance tumorale a été diminuée. Le poids des tumeurs, l’analyse par IHC (CD44, ALDH, Ki67) et la capacité de formation de sphères des CSCs résiduelles ont été diminuées. Ces résultats montrent une activité inhibitrice de la VP sur les CSCs gastriques in vitro et in vivo.Ce travail montre pour la première fois que l’axe LATS2/YAP1/TEAD est précocement activé pendant l’infection chronique avec H. pylori et que celui-ci contrôle l’EMT et les propriétés de CSC. Le ciblage de la voie Hippo a été montré comme étant efficace dans la prévention de la croissance tumorale, mettant en évidence le potentiel de son inhibition dans le traitement du cancer gastrique
Gastric cancer (GC) is a multifactorial disease, most frequently associated to chronic infection with CagA-positive Helicobacter pylori strains. Epithelial-to-mesenchymal transition (EMT) is reversible process in which polarized epithelial cells acquire a mesenchymal phenotype. EMT is at the origin of cancer stem cells (CSC). In GC, CSCs express CD44 and high aldehyde-dehydrogenase (ALDH) activity. Infection with H. pylori of human gastric cancer cell lines (hGECs) in vitro induces the emergence of a population of CD44+ cells with CSC-properties through an EMT process in a CagA-dependent manner. The Hippo pathway is composed by the kinases MST and LATS, and their phosphorylation targets,YAP1 and TAZ. Upon phosphorylation by LATS, YAP1 and TAZ are inhibited. Active YAP1 and TAZ bind to TEAD transcription factors to promote the expression of genes that regulate cell growth and apoptosis.The first aim of this work was to investigate whether H. pylori affects the activation state of the Hippo pathway, and its effect on the EMT process and the CSCs. Second, we intended to characterize the role of YAP1/TEAD in gastric CSC properties in vitro and the consequences of its pharmacological inhibition on tumor growth in vivo.To study the Hippo pathway regulation during infection, LATS2, YAP1 and CD44 were evaluated in gastric mucosae of non-infected or H. pylori-infected patients. They were upregulated in infected mucosae and were associated to pathology. Hippo pathway regulation by H. pylori infection has biphasic kinetics and is CagA-dependent. Early in infection, H. pylori transiently triggered YAP1 expression and co-transcriptional activity, along with LATS2. This period of Hippo pathway inactivity is followed by a progressive activation, sustained by LATS2 accumulation and inhibitory YAP1Ser127-phosphorylation. LATS2 siRNA-mediated repression accelerated the acquisition of the EMT-phenotype upon infection, the up-regulation of EMT-markers ZEB1 and Snail1, and the decrease of the epithelial miR-200. H. pylori-induced CD44 upregulation, invasion and sphere-forming capacity were further enhanced upon LATS2 knockdown, suggesting that LATS2 restricts the EMT and CSC-like phenotype in hGECs upon H. pylori infection. Inhibition of either LATS2 or YAP1 reduced the expression of both proteins, revealing a positive feedback loop. In tissue sections of GC, LATS2 and YAP1 were heterogeneous and co-expressed. The positive correlation between LATS2 and YAP1 was confirmed in the 38 hGECs of the CCLE. The expression of CTGF and CYR61 was also strongly correlated to LATS2, suggesting that LATS2 could also be a YAP1/TEAD target gene.hGECs of the CCLE. The expression of CTGF and CYR61 was also strongly correlated to LATS2, suggesting that LATS2 could also be a YAP1/TEAD target gene.Verteporfin (VP) disrupts the YAP1/TEAD interaction inhibiting its transcriptional activity. In vitro, using hGECs and cells from patient derived primary tumor xenogratfs (PDXs), we showed that treatment with VP decreased cell growth, expression of YAP1/TAZ/TEAD target genes, TEAD-luciferase reporter activity and sphere-forming capacity. The activity of VP was tested in vivo, by peritumoral injection in a model of subcutaneous graft of hGECs (MKN45 and MKN74) and PDX (GC10) in NGS mice. Tumor growth was followed and a decrease was observed. Tumor weight measurement, IHC analysis (CD44, ALDH and Ki67), and CSCs were decreased in treated tumors. These results show the CSC-inhibitory activity of VP both in vitro and in vivo.We showed for the first time that the LATS2/YAP1/TEAD axis is early activated during the carcinogenesis process induced by chronic H. pylori infection and controls the subsequent EMT and CSC-like features. Targeting the Hippo pathway efficiently prevented tumor growth in a PDX model, highlighting the potential of its inhibition to be implemented in gastric cancer therapy

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Stegmeier, Johannes Friedrich. "Study of Omp85 family proteins YaeT and YtfM and multidrug export machineries in Escherichia coli." Doctoral thesis, [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980586682.

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Guzzo, Cristiane Rodrigues. "Estudo estrutural e funcional das proteínas PilZ e YaeQ do fitopatógeno Xanthomonas axonopodis pv citri." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-26042010-134457/.

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O trabalho aqui desenvolvido teve como objeto o estudo estrutural e funcional de várias proteínas do fitopatógeno Xanthomonas axonopodis pv citri (Xac), dentre as quais se destacam as proteínas hipotéticas conservadas YaeQ e SufE, as proteínas RpfC, RpfF e RpfG envolvidas em quorum sensing e proteínas PilZ, FimX e PilB envolvidas na biogênese do pilus tipo IV. Para o desenvolvimento deste trabalho foram utilizadas diferentes técnicas incluindo: clonagem, expressão, purificação, desnaturação térmica, cristalografia, difração de raios-X, RMN, ensaios de 2-híbrido, produção de nocautes, mutação sítio dirigida, Western- e Far- Western, entre outras. Dentre os resultados mais importantes obtidos temos a determinação estrutural das proteínas YaeQ e PilZ pela técnica MAD. Em ambos os casos, as estruturas representaram topologias inéditas. Com base nos dados estruturais, mostramos que YaeQ pertence à família PD-(D/E)XK presente em endonucleases dependentes de magnésio, e a partir de ensaios funcionais obtivemos evidências que sugerem que YaeQ está envolvida em alguma via de reparo de DNA em Xac. A estrutura tridimensional de PilZ revelou uma inesperada variedade estrutural dentro da família PilZ e mostrou de forma clara porque ortólogos não interagem com o segundo mensageiro bacteriano, c-diGMP. A cadeia principal de PilZ foi assinalada por RMN e a estrutura secundária de PilZ em solução é consistente com aquela determinada por cristalografia. Duas proteínas que interagem com PilZ foram identificadas: PilB e FimX. Como PilZ, ambos exercem papéis na biogênese do pilus tipo IV (T4P). Mostramos que PilZ interage especificamente com o domínio EAL de FimX e que resíduos conservados na região do C-terminal de PilZ estão envolvidos na interação com PilB, mas não com FimX. Ensaios de mutação sítio dirigida mostraram que a Y22 de PilZ pode estar envolvida na regulação da interação de PilZ com FimX e com PilB. Apesar de PilZ não interagir com c-diGMP seu parceiro, FimX, interage. PilZ consegue interagir com PilB ao mesmo tempo em que interage com FimX, formando um complexo ternário que é independente da interação de FimX com c-diGMP. Com base em todos estes resultados propusemos possíveis mecanismos de ação de PilZ e FimX no controle da biogênese do T4P. Além dos resultados acima descritos, determinamos a estrutura de SufE e mostramos que esta aumenta a atividade cisteína dessulfarase de seu parceiro, SufS, em torno de 10 vezes, como ocorre com SufE-SufS de E.coli. Clonamos, expressamos, purificamos e fizemos ensaios de cristalização de algumas proteínas envolvidas no controle de quorum sensing em Xac. Tivemos êxito na cristalização do domínio HPT (histidina fosfotransferase) da proteína chave deste sistema, RpfC
The aim of the project was to perform structural and functional studies of different Xanthomonas axonopodis pv citri (Xac) proteins including the hypothetical proteins YaeQ and SufE; RpfC, RpfF and RpfG involved in the quorum sensing and PilZ, FimX and PilB that play roles in type IV pilus (T4P) biogenesis. Several experimental techniques were employed including cloning, expression and purification of recombinant proteins, thermal denaturation, protein crystallography, X-ray diffraction, NMR, two-hybrid assays, Western- and Far-Western Blotting assays, site direct mutagenesis, and the production of Xac knockouts strains. The most important results include the determination of the three-dimensional crystal structures of PilZ and YaeQ using the MAD technique. In both cases, the structures reveled new protein topologies. The comparison of the YaeQ structure with others deposited in public databases revealed that YaeQ proteins represent a new variation within the PD-(D/E)XK magnesium dependent endonucleases superfamily. Functional assays suggest that YaeQ may be envolved in DNA repair in Xac. The PilZ three-dimensional structure revealed an unexpected structural variation within the PilZ domain superfamily and showed why PilZ orthologs are not able to bind the important bacterial second messenger, c-diGMP. We assigned the PilZ main chain by NMR and used this information to demonstrate that the PilZ secondary structure in solution is consistent with the PilZ crystal structure. We identified two proteins that interact with PilZ: PilB and FimX. As with PilZ, both PilB and FimX are involved in T4P biogenesis. PilZ binds specifically to the EAL domain of FimX and the conserved residues located in the PilZ unstructured C-terminal region contribute to binding with PilB but not with FimX. Site direct mutagenesis studies showed that PilZ residue Y22 is necessary for its capability to interact with both PilB and FimX. Although PilZ does not bind c-diGMP, her partner, FimX, does. We present evidence that PilZ can bind simultaneously to FimX and PilB, forming a ternary complex that is independent of c-diGMP. These results allow us to propose possible mechanisms by which PilZ and FimX control T4P biogenesis. Other results obtained during this period include the resolution of the crystal structure of the SufE protein from Xac using the molecular replacement technique. We show that SufE induces a 10-fold increase in the cysteine desulfurase activity of SufS, similar to that observed for the SufE-SufS complex from E. coli. Several proteins involved in quorum sensing and c-di-GMP signaling were cloned, expressed and submitted to crystallization trials. Crystals of the HPT (histidine phophotransferase) domain) of the RpfC sensor histidine kinase were obtained

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Книги з теми "YAE1"

Cócora: La historia de Yael. Panamá, República de Panamá: Puello's Books, 2015.

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editor, Yoneda Yūsuke 1936, ed. Yae no zanka. Tōkyō: Chūō Kōron Bijutsu Shuppan, 2018.

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Yura, Yayoi. Niijima Yae to Ishin: Aizu ni saita yae no sakura. Tōkyō: Bungeisha, 2013.

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Yae, Kurō. Yae Kurō no denshō. Sapporo-shi: Hokkaidō Kyōiku Iinkai, 1993.

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Asano, Yae. Asano Yae yusai, 1955-nen-1982-nen =: Yae Asano paintings, 1955-1982. Nagoya: Sakura Gallery, 1985.

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Yael and the party of the year. New York: Simon & Schuster, 2018.

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The Geneva option: A Yael Azoulay novel. New York, NY: HarperCollins Publishers, 2013.

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Dōsōkai, Dōshisha. Niijima Yae: Hansamu na joketsu no shōgai = The life history of Yae Neesima. Kyōto-shi: Tankōsha, 2012.

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Tah zamā ṭolah shāʻirī yae! Peṣhawar: Dānish Khparandūyah Ṭolanah, 2013.

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Yae-san, onorini narimasu ka. Kyōto-shi: Shibunkaku Shuppan, 2012.

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Leavy, Patricia, and Victoria Scotti. "Yael." In Low-Fat Love Stories, 105–10. Rotterdam: SensePublishers, 2017. http://dx.doi.org/10.1007/978-94-6300-818-1_14.

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Molos, Dimitrios. "Tamir, Yael." In Encyclopedia of Global Justice, 1057–58. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-1-4020-9160-5_131.

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Wilmer, S. E. "Yael Ronen." In Dramaturgies of Interweaving, 176–96. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003187233-17.

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Koch, Roberta Maria. "Wie innovative Start-ups zu Kapital kommen." In Die Wirtschaft im Wandel, 59–63. Wiesbaden: Springer Fachmedien Wiesbaden, 2021. http://dx.doi.org/10.1007/978-3-658-31735-5_10.

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ZusammenfassungInnovative Jungunternehmen brauchen dringend Risikokapital. Die Kreditgeber sind zurückhaltend, verlangen Sicherheiten und wollen verlässliche Hinweise auf gute Erfolgsaussichten sehen. Aber das Risiko ist hoch und der Erfolg auf dem Markt ungewiss. Wie können innovative Start-ups zu Kapital kommen? Verwertbare Patente dienen als Sicherheit and schaffen Zugang zu Kredit. Erfahrene Wagnisfinanziers können besser als andere die Erfolgschancen beurteilen und sind eher bereit, sich zu engagieren. Darauf können auch andere Kreditgeber vertrauen. Wagniskapital hilft gleich zweimal. Die Wagniskapitalisten geben selber Beteiligungskapital. Sie geben auch anderen Kapitalgebern das notwendige Vertrauen, damit diese weitere Finanzierung bereitstellen. Deshalb ist ein aktiver Markt für Wagniskapital in einer innovativen Wirtschaft so wichtig.Hochberg, Yael, Carlos Serrano and Rosemarie H. Ziedonis (2018), Patent Collateral, Investor Commitment, and the Market for Venture Lending, Journal of Financial Economics 130, 74–94.

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Assis, Elie. "“THE HAND OF A WOMAN”: DEBORAH AND YAEL (JUDGES 4)." In Perspectives on Hebrew Scriptures II, 363–70. Piscataway, NJ, USA: Gorgias Press, 2007. http://dx.doi.org/10.31826/9781463212834-025.

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Sudol, Marius, Irwin H. Gelman, and Jianmin Zhang. "YAP1 Uses Its Modular Protein Domains and Conserved Sequence Motifs to Orchestrate Diverse Repertoires of Signaling." In The Hippo Signaling Pathway and Cancer, 53–70. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_4.

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Hutchison, Yvette. "Women Playwrights in Post-Apartheid South Africa: Yael Farber, Lara Foot-Newton, and the Call for Ubuntu." In Contemporary Women Playwrights, 148–63. London: Macmillan Education UK, 2013. http://dx.doi.org/10.1007/978-1-137-27080-1_10.

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"YAP1." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 2123. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_18310.

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Garrett, S. "Yak1." In The Protein Kinase FactsBook, 254–55. Elsevier, 1995. http://dx.doi.org/10.1016/b978-012324719-3/50076-5.

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"54 Yael." In Jews in East Norse Literature, 1109–10. De Gruyter, 2022. http://dx.doi.org/10.1515/9783110775747-066.

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Тези доповідей конференцій з теми "YAE1"

Bölöni, Ladislau, and Damla Turgut. "YAES." In the 8th ACM international symposium. New York, New York, USA: ACM Press, 2005. http://dx.doi.org/10.1145/1089444.1089473.

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Douze, Matthijs, and Hervé Jégou. "The Yael Library." In MM '14: 2014 ACM Multimedia Conference. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2647868.2654892.

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Botelho Paz, Giovanni Scataglia, and Solange Wagner Locatelli. "METACOGNITIVE INCIDENTS MANIFESTED BY STUDENTS OF YOUTH AND ADULT EDUCATION IN AN INVESTIGATIVE ACTIVITY." In 3rd International Baltic Symposium on Science and Technology Education (BalticSTE2019). Scientia Socialis Ltd., 2019. http://dx.doi.org/10.33225/balticste/2019.158.

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Practices that take into account youth and adult education (YAE) are still rare in the literature. The present work applied an investigative activity with YAE students from the last year of middle education, in the discipline of sciences, about the methods of construction of science and tests of variables. From the categorization of metacognitive incidents used, it was verified that the stimulus to the argumentation that the investigative activity potentiated was fundamental for the students to conclude the activity successfully. Keywords: adult education, investigative activities, youth education, metacognitive incidents.

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Calvet, Loreley, Odette Dos Santos, Véronique Jean-Baptiste, Emmanuel Spanakis, Yvette Ruffin, Isabelle Sanchez, Jessica Mestadier, et al. "Abstract 4858: Oncogenic HIPPO-YAP1:in vivotarget validation of YAP1 in malignant mesothelioma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4858.

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Zhu, Ming, Ruiqing Peng, Xin Liang, Zhengdao Lan, Meng Tang, Pingping Hou, Jian H. Song, et al. "Yap1 Hydroxylation Suppress Prostate Cancer Metastasis." In Leading Edge of Cancer Research Symposium. The University of Texas at MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00102.

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"Session YA1: Signal Processing 3." In 2005 IEEE Instrumentationand Measurement Technology Conference Proceedings. IEEE, 2005. http://dx.doi.org/10.1109/imtc.2005.1604434.

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Marino, Gloria, Shuai Ye, Koreana Pak, Jennifer Shah, Jason Godfrey, Susan Chor, Shaun Egolf, and T. S. Karin Eisinger-Mathason. "Abstract 3531: YAP1-mediated circadian oscillation in sarcoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3531.

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Marino, Gloria, Shaun Egolf, Shuai Ye, Koreana Pak, Jenn Shah, Adrian Rivera-Reyes, Susan Chor, and T. S. Karin Eisinger-Mathason. "Abstract B21: YAP1-mediated circadian oscillation in sarcoma." In Abstracts: Advances in Sarcomas: From Basic Science to Clinical Translation; May 16-19, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.sarcomas17-b21.

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Liu, Ying, Gabrielle Ciotti, and T. S. Karin Eisinger-Mathason. "Abstract A02: YAP1 opposes differentiation in mesenchymal tumors." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-a02.

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Biagioni, Francesca, Ottavio Croci, Elisa Donato, Silvia Sberna, Serena De Fazio, Arianna Sabò, Bruno Amati, and Stefano Campaner. "Abstract B37: Genomic view of YAP1 dependent transcription." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-b37.

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Звіти організацій з теми "YAE1"

Camargo, Fernando, and Betty Diamond. Yap1 as a New Therapeutic Target in Neurofibromatosis Type 2. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada606101.

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Camargo, Fernando. Yap1 as a New Therapeutic Target in Neurofibromatosis Type 2. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada611708.

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Is infant empathy linked with later externalizing problems? ACAMH, November 2020. http://dx.doi.org/10.13056/acamh.13959.

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Until recently, it has been assumed that young infants cannot feel empathy for others.1 However, emerging data suggest that this might not actually be the case.2 Now, Yael Paz and colleagues have examined empathy development during the first years of life, analysing data from 165 infants involved in a longitudinal, prospective study.

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