Relevant bibliographies by topics / Tsc1, Tsc2

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tsc1, Tsc2'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Tsc1, Tsc2"

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Kwiatkowski, David. "Cancer Genetics: TSC1, TSC2, TSC3? or mosaicism?" European Journal of Human Genetics 13, no. 6 (2005): 695–96. http://dx.doi.org/10.1038/sj.ejhg.5201412.

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Goncharova, Elena, Dmitry Goncharov, Daniel Noonan, and Vera P. Krymskaya. "TSC2 modulates actin cytoskeleton and focal adhesion through TSC1-binding domain and the Rac1 GTPase." Journal of Cell Biology 167, no. 6 (2004): 1171–82. http://dx.doi.org/10.1083/jcb.200405130.

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Tuberous sclerosis complex (TSC) 1 and TSC2 are thought to be involved in protein translational regulation and cell growth, and loss of their function is a cause of TSC and lymphangioleiomyomatosis (LAM). However, TSC1 also activates Rho and regulates cell adhesion. We found that TSC2 modulates actin dynamics and cell adhesion and the TSC1-binding domain (TSC2-HBD) is essential for this function of TSC2. Expression of TSC2 or TSC2-HBD in TSC2−/− cells promoted Rac1 activation, inhibition of Rho, stress fiber disassembly, and focal adhesion remodeling. The down-regulation of TSC1 with TSC1 siRN
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Wang, Yanye, Song Xu, Shikang Zhao, et al. "Clinical and molecular characteristics of TSC1/2 mutant lung cancer." Journal of Clinical Oncology 38, no. 15_suppl (2020): e21647-e21647. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e21647.

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e21647 Background: Tumor suppressor genes TSC1 and TSC2 inhibit cell growth through inactivation the function of mTORC1. Previous studies have demonstrated that loss of function mutation of either TSC1 or TSC2 gene result in formation of neoplasm in multiple tissues. However, the clinical significance of TSC1 and TSC2 in non-small-cell lung cancer (NSCLC) remains unknown. This study aimed to investigate the clinical and molecular characteristics of TSC1 and TSC2 mutation in NSCLC patients. Methods: We retrieved the clinical and genomic information of 1144 NSCLC from the Pan-Lung cancer dataset
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Hoogeveen-Westerveld, Marianne, Leontine van Unen, Ans van den Ouweland, Dicky Halley, Andre Hoogeveen, and Mark Nellist. "The TSC1-TSC2 complex consists of multiple TSC1 and TSC2 subunits." BMC Biochemistry 13, no. 1 (2012): 18. http://dx.doi.org/10.1186/1471-2091-13-18.

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Gan, Boyi, Zara K. Melkoumian, Xiaoyang Wu, Kun-Liang Guan, and Jun-Lin Guan. "Identification of FIP200 interaction with the TSC1–TSC2 complex and its role in regulation of cell size control." Journal of Cell Biology 170, no. 3 (2005): 379–89. http://dx.doi.org/10.1083/jcb.200411106.

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FIP200 (focal adhesion kinase [FAK] family interacting protein of 200 kD) is a newly identified protein that binds to the kinase domain of FAK and inhibits its kinase activity and associated cellular functions. Here, we identify an interaction between FIP200 and the TSC1–TSC2 complex through FIP200 binding to TSC1. We found that association of FIP200 with the TSC1–TSC2 complex correlated with its ability to increase cell size and up-regulate S6 kinase phosphorylation but was not involved in the regulation of cell cycle progression. Conversely, knockdown of endogenous FIP200 by RNA interference
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Huang, Jingxiang, and Brendan D. Manning. "A complex interplay between Akt, TSC2 and the two mTOR complexes." Biochemical Society Transactions 37, no. 1 (2009): 217–22. http://dx.doi.org/10.1042/bst0370217.

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Akt/PKB (protein kinase B) both regulates and is regulated by the TSC (tuberous sclerosis complex) 1–TSC2 complex. Downstream of PI3K (phosphoinositide 3-kinase), Akt phosphorylates TSC2 directly on multiple sites. Although the molecular mechanism is not well understood, these phosphorylation events relieve the inhibitory effects of the TSC1–TSC2 complex on Rheb and mTORC1 [mTOR (mammalian target of rapamycin) complex] 1, thereby activating mTORC1 in response to growth factors. Through negative-feedback mechanisms, mTORC1 activity inhibits growth factor stimulation of PI3K. This is particularl
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Huang, Jingxiang, Christian C. Dibble, Mika Matsuzaki, and Brendan D. Manning. "The TSC1-TSC2 Complex Is Required for Proper Activation of mTOR Complex 2." Molecular and Cellular Biology 28, no. 12 (2008): 4104–15. http://dx.doi.org/10.1128/mcb.00289-08.

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ABSTRACT The mammalian target of rapamycin (mTOR) is a protein kinase that forms two functionally distinct complexes important for nutrient and growth factor signaling. Both complexes phosphorylate a hydrophobic motif on downstream protein kinases, which contributes to the activation of these kinases. mTOR complex 1 (mTORC1) phosphorylates S6K1, while mTORC2 phosphorylates Akt. The TSC1-TSC2 complex is a critical negative regulator of mTORC1. However, how mTORC2 is regulated and whether the TSC1-TSC2 complex is involved are unknown. We find that mTORC2 isolated from a variety of cells lacking
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Bilanges, Benoit, Rhoda Argonza-Barrett, Marina Kolesnichenko, et al. "Tuberous Sclerosis Complex Proteins 1 and 2 Control Serum-Dependent Translation in a TOP-Dependent and -Independent Manner." Molecular and Cellular Biology 27, no. 16 (2007): 5746–64. http://dx.doi.org/10.1128/mcb.02136-06.

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ABSTRACT The tuberous sclerosis complex (TSC) proteins TSC1 and TSC2 regulate protein translation by inhibiting the serine/threonine kinase mTORC1 (for mammalian target of rapamycin complex 1). However, how TSC1 and TSC2 control overall protein synthesis and the translation of specific mRNAs in response to different mitogenic and nutritional stimuli is largely unknown. We show here that serum withdrawal inhibits mTORC1 signaling, causes disassembly of translation initiation complexes, and causes mRNA redistribution from polysomes to subpolysomes in wild-type mouse embryo fibroblasts (MEFs). In
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Li, Yong, Ken Inoki, and Kun-Liang Guan. "Biochemical and Functional Characterizations of Small GTPase Rheb and TSC2 GAP Activity." Molecular and Cellular Biology 24, no. 18 (2004): 7965–75. http://dx.doi.org/10.1128/mcb.24.18.7965-7975.2004.

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ABSTRACT Tuberous sclerosis complex (TSC) is a genetic disease caused by a mutation in either the tsc1 or tsc2 tumor suppressor gene. Recent studies have demonstrated that TSC2 displays GAP (GTPase-activating protein) activity specifically towards the small G protein Rheb and inhibits its ability to stimulate the mTOR signaling pathway. Rheb and TSC2 comprise a unique pair of GTPase and GAP, because Rheb has high basal GTP levels and TSC2 does not have the catalytic arginine finger found in Ras-GAP. To investigate the function of TSC2 and Rheb in mTOR signaling, we analyzed the TSC2-stimulated
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Matsumoto, Sanae, Amitabha Bandyopadhyay, David J. Kwiatkowski, Umadas Maitra, and Tomohiro Matsumoto. "Role of the Tsc1-Tsc2 Complex in Signaling and Transport Across the Cell Membrane in the Fission Yeast Schizosaccharomyces pombe." Genetics 161, no. 3 (2002): 1053–63. http://dx.doi.org/10.1093/genetics/161.3.1053.

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Abstract Heterozygous inactivation of either human TSC1 or TSC2 causes tuberous sclerosis (TSC), in which development of benign tumors, hamartomas, occurs via a two-hit mechanism. In this study, fission yeast genes homologous to TSC1 and TSC2 were identified, and their protein products were shown to physically interact like the human gene products. Strains lacking tsc1+ or tsc2+ were defective in uptake of nutrients from the environment. An amino acid permease, which is normally positioned on the plasma membrane, aggregated in the cytoplasm or was confined in vacuole-like structures in Δtsc1 a
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Dissertations / Theses on the topic "Tsc1, Tsc2"

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Azzi-Nogueira, Deborah. "Os produtos dos genes Tsc1 e Tsc2 em processos neurodegenerativos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-09122016-154805/.

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O complexo da esclerose tuberosa (TSC) é uma doença genética que pode afetar órgãos específicos de qualquer sistema do organismo humano. Em geral, as lesões surgem pela inativação bialélica de um dos genes supressores tumorais Tuberous Sclerosis Complex 1 (TSC1) ou 2 (TSC2). Por outro lado, nas regiões corticais e subcorticais do cérebro, as lesões decorrentes de falhas de migração neuronal e sua arborização podem ser explicadas pela haploinsuficiência de TSC1 ou TSC2. As lesões do córtex cerebral apresentam-se comumente com epilepsia refratária, a qual, por sua vez, pode se associar a deficiê
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Khatri, Shikha. "FOXO3a Regulates Glycolysis via Transcriptional Control of Tumor Suppressor TSC1." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1282570293.

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Marín, Alexandra Belén Saona. "Capacidade proliferativa in vitro de precursores neuro-gliais, telencefálicos e expressão dos genes 1 e 2 do Complexo da Esclerose Tuberosa (TSC1 e TSC2)." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-08032013-105224/.

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O complexo da esclerose tuberosa (TSC) é um transtorno clínico, com expressividade variável, caracterizado por hamartomas que podem ocorrer em diferentes órgãos. Tem herança autossômica dominante e é devido a mutações em um de dois genes supressores de tumor, TSC1 ou TSC2. Estes codificam para as proteínas hamartina e tuberina, respectivamente, que se associam formando um complexo macromolecular que regula funções como proliferação, diferenciação, crescimento e migração celular. As lesões cerebrais podem ser muito graves em pacientes com TSC e caracterizam-se por nódulos subependimários (SEN),
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Schmid, Maria [Verfasser], and Joachim-Ulrich [Akademischer Betreuer] Walther. "Genotyp-Phänotyp-Korrelation beim Tuberöse-Sklerose-Komplex : Auswertung der Mutationsanalyse von TSC1 und TSC2 aus der Diagnostik von TSC-Patienten und Vergleich unterschiedlicher Techniken / Maria Schmid ; Betreuer: Joachim-Ulrich Walther." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1127527851/34.

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Schmid, Maria Anna Katharina [Verfasser], and Joachim-Ulrich [Akademischer Betreuer] Walther. "Genotyp-Phänotyp-Korrelation beim Tuberöse-Sklerose-Komplex : Auswertung der Mutationsanalyse von TSC1 und TSC2 aus der Diagnostik von TSC-Patienten und Vergleich unterschiedlicher Techniken / Maria Schmid ; Betreuer: Joachim-Ulrich Walther." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1127527851/34.

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Alzhrani, Jasser Ali S. "Na+/K+ Pump and Cl--coupled Na+ and K+ co-transporters in Mouse Embryonic Fibroblasts lacking the Tuberous Sclerosis Complex TSC1 and TSC2 genes." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1440683830.

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Zügge, Karin Louise. "Molecular genetic investigation of the variability of the GTPase activating protein- (GAP-) related domain of the tuberous sclerosis-2 (TSC2) gene in TSC patients and healthy subjects." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972115366.

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Wilson, Catherine. "Molecular analysis of a Tsc1-deficient mouse." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/54274/.

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Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by mutation in either the TSC1 or TSC2 genes and characterised by the development of benign hamartomatous growths in multiple organ systems. We have inactivated Tsd in the mouse germ line by gene targeting in ES cells and confirmed that the mutant allele (Tsc1) has a recessive embryonic lethal phenotype. Tsc1+, mice developed macroscopically visible renal lesions as early as 3-6 months. Renal lesions progressed from cysts through cystadenomas to solid carcinomas. Eighty percent of Tsc1+/ mice on a Balb/c background exhib
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Hien, Annie. "Regulation of Translation and Synaptic Plasticity by TSC2." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1097.

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Mutations in TSC2 cause the disorder tuberous sclerosis (TSC), which has a high incidence of autism and intellectual disability. TSC2 regulates mRNA translation required for group 1 metabotropic glutamate receptor-dependent synaptic long-term depression (mGluR-LTD), but the identity of mRNAs responsive to mGluR-LTD signaling in the normal and TSC brain is largely unknown. We generated Tsc2+/- mice to model TSC autism and performed ribosome profiling to identify differentially expressed genes following mGluR-LTD in the normal and Tsc2+/- hippocampus. Ribosome profiling reveals that in Tsc2+/-mi
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Virdi, Simerjot Kaur. "Roles of the TSN1 and TSC2 Genes in Conferring Susceptibility of Durum Wheat to Tan Spot and Septoria Nodorum Blotch." Thesis, North Dakota State University, 2015. https://hdl.handle.net/10365/27628.

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Tan spot is an important disease caused by the necrotrophic fungus Pyrenophora triticirepentis. Two common necrotrophic effectors produced by this fungus are Ptr ToxA and Ptr ToxB, which recognize host sensitivity genes Tsn1 and Tsc2, respectively. In this research, a tetraploid recombinant inbred line population was evaluated for reaction to the Ptr ToxA and Ptr ToxB-producing isolates 86-124 (race 2) and DW5 (race 5). The results indicated that a compatible Tsc2-Ptr ToxB interaction accounted for 26% of the disease variation, which states that this interaction plays a significant role
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Books on the topic "Tsc1, Tsc2"

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Chrismon, Randolph L. The TSCA compliance handbook. Executive Enterprises Publications Co., 1989.

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Griffin, Ginger L. The TSCA compliance handbook. Executive Enterprises, 1994.

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Woodyard, John P. PCB management under TSCA. Executive Enterprises Publications Co., 1989.

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The TSCA compliance handbook. 3rd ed. J. Wiley & Sons, 1996.

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Alfonso, Armada. TSC: Diario da noite. Edicións Xerais de Galicia, 2009.

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TSC: Diario da noite. Edicións Xerais de Galicia, 2009.

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Tume ya Utumishi wa Walimu (Tanzania). Ijue Tume ya Utumishi wa Walimu (TSC). 2nd ed. Jamhuri ya Muungano wa Tanzania, Tume ya Utumishi wa Walimu, 2002.

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1950-, Thunder James M., ed. Federal chemical regulation: TSCA, EPCRA and the Pollution Prevention Act. Bureau of National Affairs, 1997.

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Fritz, Donald J. Nusa Tenggara Timur transport system consultancy project (TSCP): Final report. Direktorat Tata Kota dan Tata Daerah, Direktorat Jenderal Cipta Karya, Departemen Pekerjaan Umum, 1989.

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Wagner, Travis. The complete guide to the hazardous waste regulations: RCRA, TSCA, HMTA, OSHA, and Superfund. 3rd ed. J. Wiley, 1999.

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Book chapters on the topic "Tsc1, Tsc2"

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Kajino, K., and O. Hino. "TSC1 and TSC2 Gene Mutations in Human Kidney Tumors." In Contributions to Nephrology. KARGER, 1999. http://dx.doi.org/10.1159/000059974.

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Fischer, R. X., and W. H. Baur. "TSC." In Zeolite-Type Crystal Structures and their Chemistry. Framework Type Codes STO to ZON. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-32372-0_11.

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Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, et al. "TSC." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7534.

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Gooch, Jan W. "TSC." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_12187.

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Harris, P. C. "The TSC2/PKD1 Contiguous Gene Syndrome." In Hereditary Kidney Diseases. KARGER, 1997. http://dx.doi.org/10.1159/000059872.

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Campbell, Daniel, Corey Ray-Subramanian, Winifred Schultz-Krohn, et al. "TSC Tuberous Sclerosis." In Encyclopedia of Autism Spectrum Disorders. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_101486.

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Donnelly, Shawn. "The TSCG and EMU reform." In Power Politics, Banking Union and EMU. Routledge, 2018. http://dx.doi.org/10.4324/9780203702130-3.

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Giassi, Lisa J., and John L. Gainer. "TSC and Hemorrhagic Shock." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-6125-2_9.

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Jellinek, Steven D. "Information needs for TSCA and FIFRA." In Chemical Information. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-75165-3_10.

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Arand, M., E. Harwig, M. Schultheiß, and L. Kinzl. "Verlaufsbeurteilung nach operativer Therapie der traumatischen Spondylolisthesis C2 (TSC2)." In Hefte zur Zeitschrift „Der Unfallchirurg“. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60913-8_83.

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Conference papers on the topic "Tsc1, Tsc2"

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Goncharova, Elena A., Dmitry A. Goncharov, and Vera P. Krymskaya. "TSC1 And TSC2 Differentially Modulate Actin Cytoskeleton And Motility." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2092.

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Goncharova, Elena A., Dmitry A. Goncharov, Irene Khavin, Okio Hino, and Vera P. Krymskaya. "Pulmonary Lymphangioleiomyomatosis (LAM): TSC1/TSC2 Modulates E-Cadherin Localization Through Small GTPase Rac1." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2091.

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Palma, Norma A., Juliann Chmielecki, Garrett Frampton, et al. "Abstract P2-03-06: FoundationOne profiling of TSC1 and TSC2-mutated advanced breast cancers." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p2-03-06.

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Kang, Ju-Yeon, Youn-Young Jang, Nam-Su Huh, Ki-Seok Kim, and Woo-Yeon Cho. "Limit Strains of X70 Pipes With a Semi-Elliptical Crack Based on Initiation and Ductile Tearing Criteria." In ASME 2018 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/pvp2018-84641.

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Crack-tip opening displacement (CTOD) and J-integral have been used for elastic-plastic fracture parameters as a crack driving force (CDF) and crack resistance curve to evaluate tensile strain capacity (TSC) of cracked pipelines based on strain-based design (SBD). The TSC can be determined by using two kinds of failure criteria. One is based on the limit state corresponding to an onset of stable crack growth and the other is tangency approach which determines an onset of unstable crack growth by comparing crack driving force and resistance curve. For this reason, the accurate calculation of cr
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Moon, Ji-Hee, Nam-Su Huh, and Ki-Seok Kim. "Investigation Into Applications of Local Failure Criterion for X70 Pipeline With Corrosion Defect." In ASME 2018 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/pvp2018-84566.

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In this paper, the local failure criterion using stress modified critical strain method based on annex B of API 579 is applied to evaluate the ductile failure of API X70 pipelines with a volumetric corrosion defect. Ductile failure is quantified in terms of strain, representing the tensile strain capacity (TSC) which is commonly used in strain-based assessment for fitness-for-service of pipelines installed in frozen area where large-scale ground movement can arise due to earthquakes, freezing and thawing. Based on the local failure criterion suggested for API X70 steel material, the TSCs of th
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Lafont, J., J. H. Catherine, M. Lejeune, U. Ordioni, R. Lan, and F. Campana. "Manifestations buccales de la sclérose tubéreuse de Bourneville." In 66ème Congrès de la SFCO. EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603014.

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L’objectif de ce travail est de faire le point sur les manifestations buccales de la sclérose tubéreuse de Bourneville (STB) à travers le cas d’un jeune patient. Un jeune homme de 15 ans était adressée pour la mise en place de minivis orthodontique afin de fermer des espaces d’agénésies de 35 et 45. L’interrogatoire retrouvait une STB dont les manifestations épileptiques étaient traitées par de la lamotrigine 75mg/j et de la carbamazépine LP 200mg/j. L’examen clinique exo-buccal retrouvait des macules hypochromiques sur le membre inférieur droit, des angiofibromes faciaux et une malformation v
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Liu, Ming, Yong-Yi Wang, David Horsley, and Steve Nanney. "Multi-Tier Tensile Strain Models for Strain-Based Design: Part 3 — Model Evaluation Against Experimental Data." In 2012 9th International Pipeline Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/ipc2012-90660.

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This is the third paper in a three-paper series related to the development of tensile strain models. The fundamental basis [1] and formulation [2] of the models are presented in two companion papers. This paper covers the evaluation of the models against large-scale experimental data which include a total of 24 full-scale pipe tests with and without internal pressure [3,4] and 30 curved wide plate (CWP) tests [5,6]. The 24 full-scale pipe specimens are nominally X65 grade (12.75″ OD and 12.7-mm wall thickness) and made by two manufacturers. The actual yield strength of the two pipes differs by
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Hahm, Oliver, Cédric Adjih, Emmanuel Baccelli, Thomas C. Schmidt, and Matthias Wählisch. "ICN over TSCH." In ICN'16: 3rd International Conference on Information-Centric Networking. ACM, 2016. http://dx.doi.org/10.1145/2984356.2985226.

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van der Lee, Tim, Antonio Liotta, and Georgios Exarchakos. "TSCH schedules assessment." In 2017 IEEE 14th International Conference on Networking, Sensing and Control (ICNSC). IEEE, 2017. http://dx.doi.org/10.1109/icnsc.2017.8000175.

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Zorbas, Dimitrios, Panayiotis Kotzanikolaou, and Christos Douligeris. "R-TSCH: Proactive Jamming Attack Protection for IEEE 802.15.4-TSCH Networks." In 2018 IEEE Symposium on Computers and Communications (ISCC). IEEE, 2018. http://dx.doi.org/10.1109/iscc.2018.8538705.

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Reports on the topic "Tsc1, Tsc2"

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Nellist, Mark, Marianne Hoogeveen-Westerveld, and Dicky Halley. Biochemical Characterisation of TSC1 and TSC2 Variants Identifiedd in Patients with Tuberous sclerosis Complex. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada622174.

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Nellist, Mark, Marianne Hoogeveen-Westerveld, and Dicky Halley. Biochemical Characterisation of TSC1 and TSC2 Variants Identified in Patients with Tuberous Sclerosis Complex. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada624706.

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Guan, Kun-Liang. Regulation of TS1/TSC2 Stability and Rheb GTP Level by Herc1. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada470087.

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Ess, Kevin. Neural Development in tsc2-Deficient Zebrafish. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada590191.

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Walker, Cheryl. TSC2 Happloinsufficiency Leads to a Mutator Phenotype. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada481229.

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Smith, L. L. Technical evaluation of the TSCA Ambient Air Monitoring Program. [Toxic Substances Control Act (TSCA)]. Office of Scientific and Technical Information (OSTI), 1992. http://dx.doi.org/10.2172/5122074.

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D. L. Layton. Toxic Substances Control Act (TSCA) Polychlorinate. Office of Scientific and Technical Information (OSTI), 2013. http://dx.doi.org/10.2172/1084682.

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Wang, Lizhong. Synergistic Action of FOXP3 and TSC1 Pathways During Tumor Progression. Defense Technical Information Center, 2015. http://dx.doi.org/10.21236/ada625959.

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Zervas, Mark. Temporal Loss of Tsc1: Neural Development and Brain Disease in Tuberous Sclerosis. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada609442.

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Zervas, Mark. Temporal Loss of Tsc1: Neural Development and Brain Disease in Tuberous Sclerosis. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada584730.

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