Literatura académica sobre el tema "HIPPO-PATHWAY-YAP"
Crea una cita precisa en los estilos APA, MLA, Chicago, Harvard y otros
Consulte las listas temáticas de artículos, libros, tesis, actas de conferencias y otras fuentes académicas sobre el tema "HIPPO-PATHWAY-YAP".
Junto a cada fuente en la lista de referencias hay un botón "Agregar a la bibliografía". Pulsa este botón, y generaremos automáticamente la referencia bibliográfica para la obra elegida en el estilo de cita que necesites: APA, MLA, Harvard, Vancouver, Chicago, etc.
También puede descargar el texto completo de la publicación académica en formato pdf y leer en línea su resumen siempre que esté disponible en los metadatos.
Artículos de revistas sobre el tema "HIPPO-PATHWAY-YAP"
Matthaios, Dimitrios, Maria Tolia, Davide Mauri, Konstantinos Kamposioras y Michalis Karamouzis. "YAP/Hippo Pathway and Cancer Immunity: It Takes Two to Tango". Biomedicines 9, n.º 12 (20 de diciembre de 2021): 1949. http://dx.doi.org/10.3390/biomedicines9121949.
Texto completoSalem y Hansen. "The Hippo Pathway in Prostate Cancer". Cells 8, n.º 4 (23 de abril de 2019): 370. http://dx.doi.org/10.3390/cells8040370.
Texto completoAgarinis, C., V. Orsini, P. Megel, Y. Abraham, H. Yang, C. Mickanin, V. Myer, T. Bouwmeester, J. S. Tchorz y C. N. Parker. "Activation of Yap-Directed Transcription by Knockdown of Conserved Cellular Functions". Journal of Biomolecular Screening 21, n.º 3 (2 de diciembre de 2015): 269–76. http://dx.doi.org/10.1177/1087057115617906.
Texto completoGrijalva, James L., Megan Huizenga, Kaly Mueller, Steven Rodriguez, Joseph Brazzo, Fernando Camargo, Ghazaleh Sadri-Vakili y Khashayar Vakili. "Dynamic alterations in Hippo signaling pathway and YAP activation during liver regeneration". American Journal of Physiology-Gastrointestinal and Liver Physiology 307, n.º 2 (15 de julio de 2014): G196—G204. http://dx.doi.org/10.1152/ajpgi.00077.2014.
Texto completoYang, Haitang, Sean R. R. Hall, Beibei Sun, Liang Zhao, Yanyun Gao, Ralph A. Schmid, Swee T. Tan, Ren-Wang Peng y Feng Yao. "NF2 and Canonical Hippo-YAP Pathway Define Distinct Tumor Subsets Characterized by Different Immune Deficiency and Treatment Implications in Human Pleural Mesothelioma". Cancers 13, n.º 7 (29 de marzo de 2021): 1561. http://dx.doi.org/10.3390/cancers13071561.
Texto completoHuang, Shiyuan, Xiaona Wang, Xinmei Wu, Jiale Yu, JinJing Li, Xiaoyuan Huang, Chunfang Zhu y Hongshan Ge. "Yap regulates mitochondrial structural remodeling during myoblast differentiation". American Journal of Physiology-Cell Physiology 315, n.º 4 (1 de octubre de 2018): C474—C484. http://dx.doi.org/10.1152/ajpcell.00112.2018.
Texto completoJagannathan, Radhika, Gregory V. Schimizzi, Kun Zhang, Andrew J. Loza, Norikazu Yabuta, Hitoshi Nojima y Gregory D. Longmore. "AJUBA LIM Proteins Limit Hippo Activity in Proliferating Cells by Sequestering the Hippo Core Kinase Complex in the Cytosol". Molecular and Cellular Biology 36, n.º 20 (25 de julio de 2016): 2526–42. http://dx.doi.org/10.1128/mcb.00136-16.
Texto completoHöffken, Verena, Anke Hermann, Hermann Pavenstädt y Joachim Kremerskothen. "WWC Proteins: Important Regulators of Hippo Signaling in Cancer". Cancers 13, n.º 2 (15 de enero de 2021): 306. http://dx.doi.org/10.3390/cancers13020306.
Texto completoThaventhiran, James, Anja Hoffmann y Douglas Fearon. "CTLA-4 activates the hippo pathway to regulate terminal differentiation of the CD8+ T cell. (46.17)". Journal of Immunology 186, n.º 1_Supplement (1 de abril de 2011): 46.17. http://dx.doi.org/10.4049/jimmunol.186.supp.46.17.
Texto completoCasati, G., L. Giunti, A. Iorio, A. Marturano y I. Sardi. "P04.20 The role of YAP in Glioblastoma cell lines". Neuro-Oncology 23, Supplement_2 (1 de septiembre de 2021): ii22—ii23. http://dx.doi.org/10.1093/neuonc/noab180.074.
Texto completoTesis sobre el tema "HIPPO-PATHWAY-YAP"
Bui, Duyen Amy. "The Hippo Pathway Effector YAP Regulates Cytokinesis". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467231.
Texto completoMedical Sciences
Moleirinho, Susana. "Mammalian upstream Hippo signalling pathway proteins activate core pathway kinases and functionally antagonize oncogenic YAP". Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/3662.
Texto completoToloczko, Aleksandra. "Deubiquitination and control of the Hippo pathway". Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/deubiquitination-and-control-of-the-hippo-pathway(8afdf3df-8635-4116-99c8-57fbe423501e).html.
Texto completoSidor, C. M. "Mask proteins are co-factors of Yorkie/YAP in the Hippo signaling pathway". Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1352451/.
Texto completoAstone, Matteo. "A novel Yap/Taz zebrafish reporter reveals a role of Hippo pathway transducers in angiogenesis". Doctoral thesis, Università degli studi di Padova, 2015. http://hdl.handle.net/11577/3424650.
Texto completoYAP e TAZ, orchestrando la proliferazione, la morte e il differenziamento cellulari, rappresentano elementi chiave di una complessa rete di vie di segnalazione che agiscono durante lo sviluppo. L’alterazione della segnalazione YAP/TAZ causa una crescita fuori controllo degli organi durante l’organogenesi, che si traduce nella perdita dell’omeostasi tissutale nell’adulto e conseguente sviluppo tumorale. YAP/TAZ sono co-attivatori trascrizionali che interagiscono con i fattori di trascrizione TEAD per promuovere la proliferazione e la sopravvivenza cellulari. La loro attività trascrizionale è regolata dal trasporto nucleo-citoplasmatico e dall’accumulo nucleare, che sono controllati dalla cascata chinasica della via di Hippo, ma anche dagli stimoli meccanici percepiti dalla cellula e da altre vie. Fra queste, la via di Wnt/β-catenina assume una particolare rilevanza, dal momento che è stato recentemente dimostrato che essa regola l’attività di YAP/TAZ attraverso il loro sequestro nel complesso di degradazione della β-catenina mediato da AXIN. In questa tesi vengono descritte la generazione, la validazione e la caratterizzazione di un nuovo zebrafish biosensore che riporta l’attività di Yap/Taz. Esso esprime le proteine mCherry nucleare, eGFP o la proteina verde fluorescente destabilizzata VenusPEST sotto il controllo di un frammento promotoriale del gene umano CTGF target di YAP/TAZ, contenente 3 siti di legame per TEAD. Sono stati identificati diversi pesci fondatori indipendenti in grado di trasmettere il transgene alla linea germinale, i quali sono stati utilizzati per instaurare le linee reporter stabili. Tutti i pesci transgenici condividevano un pattern di espressione similare, mantenuto nelle generazioni successive. Per validare il reporter sono stati usati approcci di downregolazione e overespressione. La co-iniezione di due morfolini diretti contro i pre-mRNA di Yap e Taz ha ridotto il segnale reporter, mentre l’iniezione di mRNA codificanti per una forma costitutivamente attiva di Yap, Taz o Tead (YAP-5SA, TAZ-4SA, TEAD-VP16) lo ha aumentato. Le linee transgeniche basate sul gene CTGF rappresentano perciò bona fide dei reporter dell’attività di Yap/Taz. Durante lo sviluppo, un forte segnale reporter è visibile principalmente nella lente, la vescicola otica, gli archi faringei, il cuore, la pinna pettorale e la rete vascolare, ma l’espressione della proteina reporter è rilevabile in molti altri tessuti e organi. L’attivazione quasi ubiquitaria di Yap/Taz osservata durante l’embriogenesi precoce, consistente con il ruolo generale di YAP/TAZ nel promuovere la proliferazione cellulare e la crescita degli organi, è ampiamente silenziata nel pesce adulto, dove il segnale reporter è ristretto a lente, ovario, cuore e intera rete vascolare. Lo zebrafish biosensore è anche in grado di riportare l’attivazione di Yap/Taz durante la rigenerazione della coda nella larva e nell’adulto, come atteso dal ruolo che riveste la segnalazione YAP/TAZ nei processi rigenerativi. Lo zebrafish reporter basato sul gene CTGF ha permesso di mostrare in un organismo vivente durante lo sviluppo la regolazione che la via di Wnt/β-catenina esercita sull’attività di Yap/Taz. I nostri risultati in termini di variazione del segnale reporter, in seguito alla modulazione genetica e farmacologica dell’attività della via di Wnt, sono in linea con il modello disegnato di recente in vitro. L’attività generale e sostenuta del reporter nell’endotelio durante l’embriogenesi ha suggerito un coinvolgimento funzionale della segnalazione Yap/Taz nell’angiogenesi precoce. La downregolazione di Yap/Taz è risultata in una compromissione della crescita dei vasi intersegmentali (ISVs), mentre l’attivazione spinta della trascrizione mediata da Yap/Taz ha causato un ramificarsi anomalo degli ISVs. La capacità di Yap/Taz di promuovere tale ramificazione vascolare è “cell-autonomous”, dal momento che lo stesso fenomeno è stato osservato esprimendo TAZ-4SA sotto il controllo di un promotore endotelio-specifico. Lo zebrafish reporter sviluppato è un nuovo potente strumento per studiare in vivo l’attivazione della via di Yap/Taz, con possibili applicazioni nello screening farmacologico e nella biologia della rigenerazione e del cancro. Ha permesso di confermare in vivo durante lo sviluppo l’interazione fra le vie di Wnt/β-catenina e Yap/Taz e di scoprire un nuovo ruolo di Yap/Taz nella ramificazione vascolare, suggerendo una funzione pro-angiogenica dell’attività trascrizionale di YAP/TAZ.
Meléndez, García Rodrigo. "YAP as a Regulator of DNA Replication Timing". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL014.
Texto completoStemness could be defined as a state in which a cell is able to self-renew and/or to differentiate after cell division. Before this happens, exhaustive duplication of the genome free of errors must occur in order to avoid deleterious mutations, a hallmark of cancer. Thus, DNA replication is particularly important to stem cells because of their continuous division capacities. Regarding DNA replication in eukaryotes, it was discovered that segments of chromosomes close in space, replicate in a coordinated manner during S phase, a process called replication timing. Moreover, major changes in replication timing correlate with cell differentiation, 3D chromatin architecture and transcription. However, the molecules that govern its regulation are poorly understood. Previously, my laboratory found that YAP, the downstream effector of the Hippo pathway, regulates S phase progression of retinal stem cells in Xenopus laevis. To test YAP function in the direct control of replication timing, we took advantage of the powerful in vitro DNA replication system of X. laevis egg extracts. Briefly, we discovered that YAP is recruited to replicating chromatin dependently of origin licensing. In addition, YAP depleted extracts showed increased DNA synthesis and origin activation; revealing that YAP normal function is to slow-down replication by limiting origin firing. Interestingly, we found Rif1, a major regulator of replication timing, as a novel partner of YAP. In vivo, Rif1 expression overlaps that of Yap within the stem cell compartment of the Xenopus retina. Knockdown of Rif1 leaded to a small-eye phenotype and alterations in replication foci of retinal stem cells, resembling the effect observed in YAP deficient cells. Finally, early-embryonic depletion of both molecules resulted in a strikingly acceleration of cell division.Altogether, our findings unveil YAP implication in the regulation of replication dynamis and show Rif1 as a novel partner. Further investigation to analyze this interaction would help us to understand the biological relevance in the control of replication timing and whether it could be used as a target in regenerative medicine
Cherrett, Claire. "Structural and functional studies of proteins from the Hippo signalling pathway". Thesis, University of Bath, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548103.
Texto completoGarcía-García, Diana. "Müller Cells and Retinal Regeneration : The Role of the Hippo/YAP Signaling Pathway Yap Haploinsufficiency Leads to Müller Cell Dysfunction and Late-Onset Cone Dystrophy Linking YAP to Müller Glia Quiescence Exit in the Degenerative Retina". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL068.
Texto completoDegenerative diseases of the retina are one of the main causes of blindness. Among the various therapeutic strategies currently being studied, our team is focusing on the regenerative potential of the retina. One cellular source of interest are Müller cells, the main type of glial cells in the retina capable of reactivating in case of degeneration, a process called reactive gliosis, and in some species adopting certain characteristics of stem cells. If such a process sustains powerful regeneration abilities in teleosts, it is however largely inefficient in mammals. Hence, increasing our knowledge of the molecular mechanisms underlying the behaviour of these cells under pathological conditions may help turning their regenerative properties into new therapeutic strategies. In this context, my laboratory focused on the terminal effector of the Hippo pathway, the co-transcriptional factor YAP, which has been shown to stimulate regeneration of several injured organs. In the retina, YAP is specifically expressed in Müller cells and upregulated in case of damage. However, its function in retinal homeostasis, and its role in retinal regeneration remained unknown.The first part of my PhD aimed at deciphering YAP function in mouse Müller cells in both physiological and pathological conditions. In essence, we revealed a central role of YAP in Müller cell-dependent retinal homeostasis and as such, as a key player for cone survival during aging. In case of retinal damage, we showed that YAP upregulation is critical for cell-cycle gene reactivation that normally accompanies reactive gliosis. In this context, we also found a functional interaction between YAP and the EGFR signaling pathway, supporting a function of YAP as a hub within the complex signaling network of key regenerative signaling pathways. I also found that YAP overactivation is sufficient to induce mouse Müller cell reprogramming into highly proliferative cells, mimicking a fish or amphibian condition, when Müller cells spontaneously proliferate upon injury. As a whole, this work highlights the critical role of YAP in driving mammalian Müller cells to exit quiescence and thus reveals a potential target for regenerative medicine.The second part of my PhD project stemmed from the emerging discoveries highlighting inflammatory pathways as regulators of the regenerative process. Although inflammation is considered to hamper retinal regeneration in mammals, there are no studies regarding the influence of inflammation on mouse Müller cell-dependent regenerative process. In addition, recent discoveries on the role of YAP in the regulation of the inflammatory process lead to the hypothesis that it could play a role in the relationship between inflammation and retinal regeneration. I thus aimed at investigating the role played by the injury-induced inflammation on mouse Müller cell behavior and how YAP fits in this interplay. I unexpectedly discovered that a microglial-dependent pro-inflammatory context stimulates mouse Müller cell proliferation in retinal explants. Importantly, my results showed that this mitogenic effect occurs in a YAP-dependent manner. Moreover, I uncovered that the effect of YAP overexpression on Müller cell proliferation can be potentiated by a pro-inflammatory environment, and abolished upon microglia depletion. Finally, we found that, in turn, YAP regulates key inflammatory cytokines. Altogether, this part of my project not only deepen our knowledge regarding the impact of inflammation on mouse Müller cell behavior, it also highlights YAP as a key player in the crosstalk between inflammation and retinal regeneration
Kimura, Masahiro. "Homeobox A4 Suppresses Vascular Remodeling as a Novel Regulator of YAP/TEAD Transcriptional Activity". Kyoto University, 2020. http://hdl.handle.net/2433/253486.
Texto completoRuggeri, Naomi. "REGULATION OF YAP BY GLUCOCORTICOIDS". Doctoral thesis, Università degli studi di Trieste, 2015. http://hdl.handle.net/10077/11122.
Texto completoThe Hippo signalling pathway is tumour suppressor cascade with a central role in the regulation of fundamental cellular biological processes, such as cell proliferation, apoptosis, organ size control and stem cell functions. The Hippo pathway transduces external signals that come to the cell into the nucleus, where it can control the expression of specific target genes, mainly involved in cell proliferation and differentiation. The Hippo pathway is an inhibitory pathway that control by phosphorylation and inhibition Yes-associated protein (YAP) coactivator, one of the two nuclear effectors of this signalling, involved in the regulation of proliferation and organ size. As consequence, deregulation of Hippo tumor suppressor pathway or hyperactivation of its downstream effectors is often associated with formation, development and tumour dissemination. Consistently, YAP is often over-expressed in a broad range of different tumours and it has aberrant activity in breast cancer as well as in several other human carcinomas. Up-regulation of YAP activity increases stem cell self-renewal in normal and cancer stem cells. In this work we describe the identification of a new hormonal-dependent layer for YAP regulation in breast cancer by the glucocorticoids and we analyze the mechanisms through which this regulation occurs. We found that Glucocorticoid Receptor (GR) binds directly the YAP promoter and induces the transcription of YAP mRNA after GC stimulation in cancer cells. Moreover, GC lead to efficient YAP de-phosphorylation and transcriptional activation, in a transcription-independent manner, by inducing actin cytoskeleton reorganization. Importantly, inhibition of the GR by means of RU486 (GR competitive antagonist) strongly blunted the expansion of the cancer stem cell pool in breast cancer cells by blunting the GR/YAP axis.
XXVII Ciclo
1987
Capítulos de libros sobre el tema "HIPPO-PATHWAY-YAP"
Reuven, Nina y Yosef Shaul. "The c-Abl/YAP/p73 Apoptotic Module and the HIPPO Pathway". En The Hippo Signaling Pathway and Cancer, 173–95. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_9.
Texto completoYi, Chunling y Joseph Kissil. "Merlin and Angiomotin in Hippo-Yap Signaling". En The Hippo Signaling Pathway and Cancer, 11–25. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_2.
Texto completoYu, Fa-Xing, Bin Zhao y Kun-Liang Guan. "Regulation of YAP and TAZ Transcription Co-activators". En The Hippo Signaling Pathway and Cancer, 71–87. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_5.
Texto completoPiccolo, Stefano y Michelangelo Cordenonsi. "Regulation of YAP and TAZ by Epithelial Plasticity". En The Hippo Signaling Pathway and Cancer, 89–113. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_6.
Texto completoDonzelli, Sara, Sabrina Strano y Giovanni Blandino. "YAP and p73: A Matter of Mutual Specificity in Tumor Suppression". En The Hippo Signaling Pathway and Cancer, 147–72. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6220-0_8.
Texto completoNazir, Aqsa, Muhammad Aqib y Muhammad Usman. "Liver Cancer-Genesis, Progression and Metastasis". En Liver Cancer - Genesis, Progression and Metastasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106020.
Texto completoActas de conferencias sobre el tema "HIPPO-PATHWAY-YAP"
Schönbeck, K., A. Winkler, MJ Witthauer, A. Szymansky, J. Toedling, A. Schramm, F. Hertwig, A. Eggert y JH Schulte. "Hippo-YAP pathway activation favors neuroblastoma progression". En 31. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645011.
Texto completoTang, Tracy T., Andrei W. Konradi, Ying Feng, Xiao Peng, Sofie Qiao y Leonard Post. "Abstract PR07: Targeting the Hippo-YAP pathway with small-molecule compounds". En 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-pr07.
Texto completoKulkarni, A., J. Vissers y K. Harvey. "PO-100 Targeting YAP and TAZ to treat hippo pathway mutant malignant mesotheliomas". En Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.141.
Texto completoIsago, Hideaki, Akihisa Mitani, Shiho Kohno, Hiroyuki Nagoshi, Taro Ishimori, Minako Saito, Hiroyuki Tamiya et al. "The Hippo pathway effectors TAZ and YAP are sequentially required in lung development". En ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa3604.
Texto completoTang, Tracy T., Andrei W. Konradi, Ying Feng, Xiao Peng, Sofie Qiao y Leonard Post. "Abstract 2693: Targeting the Hippo-YAP pathway with novel small-molecule inhibitors of the YAP-TEAD transcription activity". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2693.
Texto completoTang, Tracy T., Andrei W. Konradi, Ying Feng, Xiao Peng, Sofie Qiao y Leonard Post. "Abstract 2693: Targeting the Hippo-YAP pathway with novel small-molecule inhibitors of the YAP-TEAD transcription activity". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2693.
Texto completoLiu, K., M. Tóth, T. Guo, F. Rose, SME Weiler, S. Wan, M. Heikenwälder, P. Schirmacher, T. Longerich y K. Breuhahn. "Hippo pathway effectors YAP and TAZ are opponents in the regulation of hepatic fibrosis". En 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402120.
Texto completoIsfort, Ilka, Sandra Elges, Magdalene Cyra, Danielle Brandes, Ruth Berthold, Marcus Renner, Gunhild Mechtersheimer et al. "Abstract 2139: Hippo pathway transcriptional coactivators YAP/TAZ in soft tissue and bone tumors". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2139.
Texto completoIsfort, Ilka, Sandra Elges, Magdalene Cyra, Danielle Brandes, Ruth Berthold, Marcus Renner, Gunhild Mechtersheimer et al. "Abstract 2139: Hippo pathway transcriptional coactivators YAP/TAZ in soft tissue and bone tumors". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2139.
Texto completoKim, Ji Su, Ei Yong Ahn y Young Nyun Park. "Abstract C87: Regulation of stemness by Hippo-YAP pathway under hypoxia in hepatocellular carcinoma". En Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c87.
Texto completo