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Academic literature on the topic 'RagD'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "RagD"

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Lee, Minji, Jong Hyun Kim, Ina Yoon, Chulho Lee, Mohammad Fallahi Sichani, Jong Soon Kang, Jeonghyun Kang, et al. "Coordination of the leucine-sensing Rag GTPase cycle by leucyl-tRNA synthetase in the mTORC1 signaling pathway." Proceedings of the National Academy of Sciences 115, no. 23 (May 21, 2018): E5279—E5288. http://dx.doi.org/10.1073/pnas.1801287115.

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A protein synthesis enzyme, leucyl-tRNA synthetase (LRS), serves as a leucine sensor for the mechanistic target of rapamycin complex 1 (mTORC1), which is a central effector for protein synthesis, metabolism, autophagy, and cell growth. However, its significance in mTORC1 signaling and cancer growth and its functional relationship with other suggested leucine signal mediators are not well-understood. Here we show the kinetics of the Rag GTPase cycle during leucine signaling and that LRS serves as an initiating “ON” switch via GTP hydrolysis of RagD that drives the entire Rag GTPase cycle, whereas Sestrin2 functions as an “OFF” switch by controlling GTP hydrolysis of RagB in the Rag GTPase–mTORC1 axis. The LRS–RagD axis showed a positive correlation with mTORC1 activity in cancer tissues and cells. The GTP–GDP cycle of the RagD–RagB pair, rather than the RagC–RagA pair, is critical for leucine-induced mTORC1 activation. The active RagD–RagB pair can overcome the absence of the RagC–RagA pair, but the opposite is not the case. This work suggests that the GTPase cycle of RagD–RagB coordinated by LRS and Sestrin2 is critical for controlling mTORC1 activation, and thus will extend the current understanding of the amino acid-sensing mechanism.
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Gollwitzer, Peter, Nina Grützmacher, Sabine Wilhelm, Daniel Kümmel, and Constantinos Demetriades. "A Rag GTPase dimer code defines the regulation of mTORC1 by amino acids." Nature Cell Biology 24, no. 9 (September 2022): 1394–406. http://dx.doi.org/10.1038/s41556-022-00976-y.

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AbstractAmino acid availability controls mTORC1 activity via a heterodimeric Rag GTPase complex that functions as a scaffold at the lysosomal surface, bringing together mTORC1 with its activators and effectors. Mammalian cells express four Rag proteins (RagA–D) that form dimers composed of RagA/B bound to RagC/D. Traditionally, the Rag paralogue pairs (RagA/B and RagC/D) are referred to as functionally redundant, with the four dimer combinations used interchangeably in most studies. Here, by using genetically modified cell lines that express single Rag heterodimers, we uncover a Rag dimer code that determines how amino acids regulate mTORC1. First, RagC/D differentially define the substrate specificity downstream of mTORC1, with RagD promoting phosphorylation of its lysosomal substrates TFEB/TFE3, while both Rags are involved in the phosphorylation of non-lysosomal substrates such as S6K. Mechanistically, RagD recruits mTORC1 more potently to lysosomes through increased affinity to the anchoring LAMTOR complex. Furthermore, RagA/B specify the signalling response to amino acid removal, with RagB-expressing cells maintaining lysosomal and active mTORC1 even upon starvation. Overall, our findings reveal key qualitative differences between Rag paralogues in the regulation of mTORC1, and underscore Rag gene duplication and diversification as a potentially impactful event in mammalian evolution.
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Figlia, Gianluca, Sandra Müller, Anna M. Hagenston, Susanne Kleber, Mykola Roiuk, Jan-Philipp Quast, Nora ten Bosch, et al. "Brain-enriched RagB isoforms regulate the dynamics of mTORC1 activity through GATOR1 inhibition." Nature Cell Biology 24, no. 9 (September 2022): 1407–21. http://dx.doi.org/10.1038/s41556-022-00977-x.

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AbstractMechanistic target of rapamycin complex 1 (mTORC1) senses nutrient availability to appropriately regulate cellular anabolism and catabolism. During nutrient restriction, different organs in an animal do not respond equally, with vital organs being relatively spared. This raises the possibility that mTORC1 is differentially regulated in different cell types, yet little is known about this mechanistically. The Rag GTPases, RagA or RagB bound to RagC or RagD, tether mTORC1 in a nutrient-dependent manner to lysosomes where mTORC1 becomes activated. Although the RagA and B paralogues were assumed to be functionally equivalent, we find here that the RagB isoforms, which are highly expressed in neurons, impart mTORC1 with resistance to nutrient starvation by inhibiting the RagA/B GTPase-activating protein GATOR1. We further show that high expression of RagB isoforms is observed in some tumours, revealing an alternative strategy by which cancer cells can retain elevated mTORC1 upon low nutrient availability.
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Shen, Kuang, and David M. Sabatini. "Ragulator and SLC38A9 activate the Rag GTPases through noncanonical GEF mechanisms." Proceedings of the National Academy of Sciences 115, no. 38 (September 4, 2018): 9545–50. http://dx.doi.org/10.1073/pnas.1811727115.

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The mechanistic target of rapamycin complex 1 (mTORC1) growth pathway detects nutrients through a variety of sensors and regulators that converge on the Rag GTPases, which form heterodimers consisting of RagA or RagB tightly bound to RagC or RagD and control the subcellular localization of mTORC1. The Rag heterodimer uses a unique “locking” mechanism to stabilize its active (GTPRagA–RagCGDP) or inactive (GDPRagA–RagCGTP) nucleotide states. The Ragulator complex tethers the Rag heterodimer to the lysosomal surface, and the SLC38A9 transmembrane protein is a lysosomal arginine sensor that upon activation stimulates mTORC1 activity through the Rag GTPases. How Ragulator and SLC38A9 control the nucleotide loading state of the Rag GTPases remains incompletely understood. Here we find that Ragulator and SLC38A9 are each unique guanine exchange factors (GEFs) that collectively push the Rag GTPases toward the active state. Ragulator triggers GTP release from RagC, thus resolving the locked inactivated state of the Rag GTPases. Upon arginine binding, SLC38A9 converts RagA from the GDP- to the GTP-loaded state, and therefore activates the Rag GTPase heterodimer. Altogether, Ragulator and SLC38A9 act on the Rag GTPases to activate the mTORC1 pathway in response to nutrient sufficiency.
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Mu, Ying, Dongmei Zheng, Cong Wang, Wei Yu, and Xiaonan Zhang. "RagD regulates amino acid mediated-casein synthesis and cell proliferation via mTOR signalling in cow mammary epithelial cells." Journal of Dairy Research 85, no. 2 (May 2018): 204–11. http://dx.doi.org/10.1017/s0022029918000146.

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This research paper addresses the hypothesis that RagD is a key signalling factor that regulates amino acid (AA) mediated-casein synthesis and cell proliferation in cow mammary epithelial cells (CMECs). The expression of RagD was analysed at different times during pregnancy and lactation in bovine mammary tissue from dairy cows. We showed that expression of RagD at lactation period was higher (P < 0·05) than that at pregnancy period. When CMECs were treated with methionine (Met) or lysine (Lys), expression of RagD, β-casein (CSN2), mTOR and p-mTOR, and cell proliferation were increased. Further, when CMECs were treated to overexpress RagD, expression of CSN2, mTOR and p-mTOR, and cell proliferation were up-regulated. Furthermore, the increase in expression of CSN2, mTOR and p-mTOR, and cell proliferation in response to Met or Lys supply was inhibited by inhibiting RagD, and those effects were reversed in the overexpression model. When CMECs were treated with RagD overexpression together with mTOR inhibition or conversely with RagD inhibition together with mTOR overexpression, results showed that the increase in expression of CSN2 and cell proliferation in response to RagD overexpression was prevented by inhibiting mTOR, and those effects were reversed by overexpressing mTOR. The interaction of RagD with subunit proteins of mTORC1 was analysed, and the result showed that RagD interacted with Raptor. CMECs were treated with Raptor inhibition, and the result showed that the increase in expression of mTOR and p-mTOR in response to RagD overexpression was inhibited by inhibiting Raptor.In conclusion, our study showed that RagD is an important activation factor of mTORC1 in CMECs, activating AA-mediated casein synthesis and cell proliferation, potentially acting via Raptor.
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Zhang, Yiwen, Hongrong Hu, Weiwei Liu, Shu-Mei Yan, Yuzhuang Li, Likai Tan, Yingshi Chen, et al. "Amino acids and RagD potentiate mTORC1 activation in CD8+ T cells to confer antitumor immunity." Journal for ImmunoTherapy of Cancer 9, no. 4 (April 2021): e002137. http://dx.doi.org/10.1136/jitc-2020-002137.

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BackgroundIn the tumor microenvironment, tumor cells are able to suppress antitumor immunity by competing for essential nutrients, including amino acids. However, whether amino acid depletion modulates the activity of CD8+ tumor-infiltrating lymphocytes (TILs) is unclear.MethodIn this study, we evaluated the roles of amino acids and the Rag complex in regulating mammalian target of rapamycin complex 1 (mTORC1) signaling in CD8+ TILs.ResultsWe discovered that the Rag complex, particularly RagD, was crucial for CD8+ T-cell antitumor immunity. RagD expression was positively correlated with the antitumor response of CD8+ TILs in both murine syngeneic tumor xenografts and clinical human colon cancer samples. On RagD deficiency, CD8+ T cells were rendered more dysfunctional, as demonstrated by attenuation of mTORC1 signaling and reductions in proliferation and cytokine secretion. Amino acids maintained RagD-mediated mTORC1 translocation to the lysosome, thereby achieving maximal mTORC1 activity in CD8+ T cells. Moreover, the limited T-cell access to leucine (LEU), overshadowed by tumor cell amino acid consumption, led to impaired RagD-dependent mTORC1 activity. Finally, combined with antiprogrammed cell death protein 1 antibody, LEU supplementation improved T-cell immunity in MC38 tumor-bearing mice in vivo.ConclusionOur results revealed that robust signaling of amino acids by RagD and downstream mTORC1 signaling were crucial for T-cell receptor-initiated antitumor immunity. The characterization the role of RagD and LEU in nutrient mTORC1 signaling in TILs might suggest potential therapeutic strategies based on the manipulation of RagD and its upstream pathway.
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Prior, C., P. Mamessier, H. Fukuhara, X. J. Chen, and M. Wesolowski-Louvel. "The hexokinase gene is required for transcriptional regulation of the glucose transporter gene RAG1 in Kluyveromyces lactis." Molecular and Cellular Biology 13, no. 7 (July 1993): 3882–89. http://dx.doi.org/10.1128/mcb.13.7.3882-3889.1993.

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The RAG1 gene of Kluyveromyces lactis encodes a low-affinity glucose/fructose transporter. Its transcription is induced by glucose, fructose, and several other sugars. The RAG4, RAG5, and RAG8 genes are trans-acting genes controlling the expression of the RAG1 gene. We report here the characterization of one of these genes, RAG5. The nucleotide sequence of the cloned RAG5 gene indicated that it encodes a protein that is homologous to hexokinases of Saccharomyces cerevisiae. rag5 mutants showed no detectable hexokinase or glucokinase activity, suggesting that the sugar kinase activity encoded by this gene is the only hexokinase in K. lactis. Both high- and low-affinity transport systems of glucose were affected in rag5 mutants. The defect of the low-affinity component was found to be due to a block of transcription of the RAG1 gene by the hexokinase mutation. In vivo complementation of the rag5 mutation by the HXK2 gene of S. cerevisiae and complementation of hxk1 hxk2 mutations of S. cerevisiae by the RAG5 gene showed that RAG5 and HXK2 were equivalent for sugar-phosphorylating activity but that RAG5 could not restore glucose repression in the S. cerevisiae hexokinase mutants.
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Prior, C., P. Mamessier, H. Fukuhara, X. J. Chen, and M. Wesolowski-Louvel. "The hexokinase gene is required for transcriptional regulation of the glucose transporter gene RAG1 in Kluyveromyces lactis." Molecular and Cellular Biology 13, no. 7 (July 1993): 3882–89. http://dx.doi.org/10.1128/mcb.13.7.3882.

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The RAG1 gene of Kluyveromyces lactis encodes a low-affinity glucose/fructose transporter. Its transcription is induced by glucose, fructose, and several other sugars. The RAG4, RAG5, and RAG8 genes are trans-acting genes controlling the expression of the RAG1 gene. We report here the characterization of one of these genes, RAG5. The nucleotide sequence of the cloned RAG5 gene indicated that it encodes a protein that is homologous to hexokinases of Saccharomyces cerevisiae. rag5 mutants showed no detectable hexokinase or glucokinase activity, suggesting that the sugar kinase activity encoded by this gene is the only hexokinase in K. lactis. Both high- and low-affinity transport systems of glucose were affected in rag5 mutants. The defect of the low-affinity component was found to be due to a block of transcription of the RAG1 gene by the hexokinase mutation. In vivo complementation of the rag5 mutation by the HXK2 gene of S. cerevisiae and complementation of hxk1 hxk2 mutations of S. cerevisiae by the RAG5 gene showed that RAG5 and HXK2 were equivalent for sugar-phosphorylating activity but that RAG5 could not restore glucose repression in the S. cerevisiae hexokinase mutants.
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Kim, Chanwoo, Jinjoo Jung, Truong T. Tung, and Seung Bum Park. "β-Turn mimetic-based stabilizers of protein–protein interactions for the study of the non-canonical roles of leucyl-tRNA synthetase." Chemical Science 7, no. 4 (2016): 2753–61. http://dx.doi.org/10.1039/c5sc03493k.

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For the systematic perturbation of protein–protein interactions, we designed and synthesized tetra-substituted hexahydro-4H-pyrazino[2,1-c][1,2,4]triazine-4,7(6H)-diones as β-turn mimetics.5c{3,9}stabilizes the direct interaction between LRS and RagD and activates mTORC1 in living cells.
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Suryawan, Agus, Marko Rudar, Marta L. Fiorotto, and Teresa A. Davis. "Differential regulation of mTORC1 activation by leucine and β-hydroxy-β-methylbutyrate in skeletal muscle of neonatal pigs." Journal of Applied Physiology 128, no. 2 (February 1, 2020): 286–95. http://dx.doi.org/10.1152/japplphysiol.00332.2019.

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Leucine (Leu) and its metabolite β-hydroxy-β-methylbutyrate (HMB) stimulate mechanistic target of rapamycin (mTOR) complex 1 (mTORC1)-dependent protein synthesis in the skeletal muscle of neonatal pigs. This study aimed to determine whether HMB and Leu utilize common nutrient-sensing mechanisms to activate mTORC1. In study 1, neonatal pigs were fed one of five diets for 24 h: low protein (LP), high protein (HP), or LP supplemented with 4 (LP+HMB4), 40 (LP+HMB40), or 80 (LP+HMB80) μmol HMB·kg body wt−1·day−1. In study 2, neonatal pigs were fed for 24 h: LP, LP supplemented with Leu (LP+Leu), or HP diets delivering 9, 18, and 18 mmol Leu·kg body wt−1·day−1, respectively. The upstream signaling molecules that regulate mTORC1 activity were analyzed. mTOR phosphorylation on Ser2448 and Ser2481 was greater in LP+HMB40, LP+HMB80, and LP+Leu than in LP and greater in HP than in HMB-supplemented groups ( P < 0.05), whereas HP and LP+Leu were similar. Rheb-mTOR complex formation was lower in LP than in HP ( P < 0.05), with no enhancement by HMB or Leu supplementation. The Sestrin2-GATOR2 complex was more abundant in LP than in HP and was reduced by Leu ( P < 0.05) but not HMB supplementation. RagA-mTOR and RagC-mTOR complexes were higher in LP+Leu and HP than in LP and HMB groups ( P < 0.05). There were no treatment differences in RagB-SH3BP4, Vps34-LRS, and RagD-LRS complex abundances. Phosphorylation of Erk1/2 and TSC2, but not AMPK, was lower in LP than HP ( P < 0.05) and unaffected by HMB or Leu supplementation. Our results demonstrate that HMB stimulates mTORC1 activation in neonatal muscle independent of the leucine-sensing pathway mediated by Sestrin2 and the Rag proteins. NEW & NOTEWORTHY Dietary supplementation with either leucine or its metabolite β-hydroxy-β-methylbutyrate (HMB) stimulates protein synthesis in skeletal muscle of the neonatal pig. Our results demonstrate that both leucine and HMB stimulate mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) phosphorylation in neonatal muscle. This leucine-stimulated process involves dissociation of the Sestrin2-GATOR2 complex and increased binding of Rag A/C to mTOR. However, HMB’s activation of mTORC1 is independent of this leucine-sensing pathway.
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Dissertations / Theses on the topic "RagD"

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ESPOSITO, ALESSANDRA. "DIVERSITY IN MTORC1 SUBSTRATE RECRUITMENT ENABLES SPECIFICITY OF METABOLIC RESPONSES TO NUTRITIONAL CUES." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/793428.

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The mechanistic target of rapamycin kinase complex 1 (mTORC1) is a key signaling hub that acts as a central regulator of several cellular processes, including cell growth and metabolism. The activation of mTORC1 occurs at the lysosomal surface via a two-step mechanism that requires a) its amino acid-dependent recruitment to the lysosome via the Rag GTPases and b) its growth factor-dependent activation by Rheb. mTORC1 senses and integrates multiple upstream signals to phosphorylate a broad number of substrates and modulate the crucial balance between cell anabolism and catabolism. However, whether mTORC1 can differentially regulate specific proteins to selectively respond to such a variety of intracellular and environmental cues is poorly understood. Here we show that Transcription Factor EB (TFEB), a master modulator of lysosomal biogenesis and autophagy, is modulated by mTORC1 via a specific substrate recruitment mechanism that is mediated by Rag GTPases. Differently from the well-characterized mTORC1 substrates S6K and 4E-BP1, which are recruited by mTORC1 via binding to the regulatory subunit Raptor, TFEB interaction with mTORC1 relies on its physical association with active Rag C/D. Owing to this mechanism, TFEB phosphorylation is insensitive to growth factor-mediated activation of Rheb but highly sensitive to amino acid-mediated activation of Rag GTPases. Strikingly, substituting the region of TFEB responsible for its recruitment to mTORC1 with the one of S6K, inverted TFEB phosphorylation behaviour and made it similar to S6K/4E-BP1. Thus, our findings reveal that diversity in mTORC1 substrate recruitment mechanisms enables mTORC1 to induce selective responses to specific nutritional cues.
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Zarrin, Ali Akbar. "Characterization of the human recombination activating gene 1 (RAG1) and RAG2 promoter regions." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0024/NQ49915.pdf.

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Zheng, Xiuzhong. "Definition of Ku-interacting domains in RAG1 and RAG2 proteins in V(D)J recombination." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27102.

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V(D)J recombination is a process that generates the diversity of the immune repertoire against foreign antigens. During B and T cell development, genes encoding immunoglobulins (Ig) and T cell receptors (TCR) variable region are somatically assembled by selective V (variable), D (diversity) and J (joining) segments pre-existing in the germline. Recombination-activating genes 1 and 2 (RAG1/RAG2), the lymphocyte-specific factors, initiate V(D)J recombination by nicking at the border the heptamer sequence of RSS (recombination signal sequence) and generate four DNA double stranded breaks (DSB) in the cleavage step. After cleavage, RAG1/RAG2 complex are still bound to the DNA ends. In the joining step, DNA breaks are processed and rejoined by non-homologous end joining apparatus, which includes Ku70/Ku80, DNA-PKcs, Artemis, XRCC4 and DNA ligase IV. However, how the cleavage step is linked to the joining step is not yet known. My results suggest that a physical interaction between RAG1/2 and Ku antigen may help coordinate the cleavage stage of V(D)J with the non homologous DNA end rejoining of the mature sequences. (Abstract shortened by UMI.)
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Corneo, Barbara. "Physiopathologie de la recombinaison v(d)j : structure et fonction des proteines rag1 et rag2." Paris 5, 2001. http://www.theses.fr/2001PA05N025.

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Cayuela, Jean-Michel. "La recombinaison V-(D)-J : étude de l'expression des gènes RAG1 et RAG2 dans les cellules lymphoi͏̈des malignes humaines." Paris 5, 1991. http://www.theses.fr/1991PA05P177.

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Muppalaneni, Nitin. "Adaptive Hierarchial RAID." Thesis, Indian Institute of Science, 1998. http://hdl.handle.net/2005/50.

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Redundant Arrays of Inexpensive Disks or RAID is a popular method of improving the reliability and performance of disk storage. Of various levels of RAID, mirrored or RAID1 and rotating parity or RAID5 configurations have become moat popular. Mirrored or RAID1 provides best overall performance and is easier to configure, but has 100 percent storage overhead for the redundancy. Rotating parity or RAID5, on the other hand, is quite inexpensive for the redundancy it provides, shorn impressive performance for reads and full-stripe writes in normal mode, but the small write performance is poor due to the read-modify-write cycle involved. The performance drops drastically when one of the disks fails and the system enters degraded mode. Also RAID5 is relatively difficult to configure. Typical non-scientific system disk access patterns exhibit very high locality of reference. This thesis presents the design and implementation of an Adaptive Hierarchical RAID array to exploit this high locality. Frequently accessed data is migrated towards the top of the hierarchy and not so frequently acee88ed data is moved down the hierarchy, thus adaptively rearranging itself to the access patterns. Previous work on Adaptive Hierarchical RAID such as HP AutoRAID has explored one part of the design space, namely design of configurable storage at the SGSI level with no interaction with higher level layers like volume manager. This thesis explores a different design point: namely, one that is centered at the volume manager layer. This is important also for the reason that with fibre channel disks and SCSI-3, Storage Area Networks (SAN) no longer need a conventional controller but a modified version of a controller that is more close to a volume manager.
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PRETRE, PHILIPPE. "Rage et voyages." Besançon, 1991. http://www.theses.fr/1991BESA3052.

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Li, Yan. "Scalability of RAID systems." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/3382.

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RAID systems (Redundant Arrays of Inexpensive Disks) have dominated backend storage systems for more than two decades and have grown continuously in size and complexity. Currently they face unprecedented challenges from data intensive applications such as image processing, transaction processing and data warehousing. As the size of RAID systems increases, designers are faced with both performance and reliability challenges. These challenges include limited back-end network bandwidth, physical interconnect failures, correlated disk failures and long disk reconstruction time. This thesis studies the scalability of RAID systems in terms of both performance and reliability through simulation, using a discrete event driven simulator for RAID systems (SIMRAID) developed as part of this project. SIMRAID incorporates two benchmark workload generators, based on the SPC-1 and Iometer benchmark specifications. Each component of SIMRAID is highly parameterised, enabling it to explore a large design space. To improve the simulation speed, SIMRAID develops a set of abstraction techniques to extract the behaviour of the interconnection protocol without losing accuracy. Finally, to meet the technology trend toward heterogeneous storage architectures, SIMRAID develops a framework that allows easy modelling of different types of device and interconnection technique.Simulation experiments were first carried out on performance aspects of scalability. They were designed to answer two questions: (1) given a number of disks, which factors affect back-end network bandwidth requirements; (2) given an interconnection network, how many disks can be connected to the system. The results show that the bandwidth requirement per disk is primarily determined by workload features and stripe unit size (a smaller stripe unit size has better scalability than a larger one), with cache size and RAID algorithm having very little effect on this value. The maximum number of disks is limited, as would be expected, by the back-end network bandwidth. Studies of reliability have led to three proposals to improve the reliability and scalability of RAID systems. Firstly, a novel data layout called PCDSDF is proposed. PCDSDF combines the advantages of orthogonal data layouts and parity declustering data layouts, so that it can not only survivemultiple disk failures caused by physical interconnect failures or correlated disk failures, but also has a good degraded and rebuild performance. The generating process of PCDSDF is deterministic and time-efficient. The number of stripes per rotation (namely the number of stripes to achieve rebuild workload balance) is small. Analysis shows that the PCDSDF data layout can significantly improve the system reliability. Simulations performed on SIMRAID confirm the good performance of PCDSDF, which is comparable to other parity declustering data layouts, such as RELPR. Secondly, a system architecture and rebuilding mechanism have been designed, aimed at fast disk reconstruction. This architecture is based on parity declustering data layouts and a disk-oriented reconstruction algorithm. It uses stripe groups instead of stripes as the basic distribution unit so that it can make use of the sequential nature of the rebuilding workload. The design space of system factors such as parity declustering ratio, chunk size, private buffer size of surviving disks and free buffer size are explored to provide guidelines for storage system design. Thirdly, an efficient distributed hot spare allocation and assignment algorithm for general parity declustering data layouts has been developed. This algorithm avoids conflict problems in the process of assigning distributed spare space for the units on the failed disk. Simulation results show that it effectively solves the write bottleneck problem and, at the same time, there is only a small increase in the average response time to user requests.
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Herwig, Nadine. "Der RAGE-Ligand S100A4." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-214035.

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Das maligne Melanom zählt zu den aggressivsten und behandlungsresistentesten aller Krebsarten. In den letzten 20 Jahren hat sich die Rate der Melanom-Erkrankungen innerhalb der weißen Bevölkerung verdreifacht. Mittlerweile liegen eine Reihe von Untersuchungen zu den molekularbiologischen Mechanismen der Entwicklung und Progression des malignen Melanoms vor. Aktuelle Forschungsvorhaben beschäftigen sich vor allem mit der Identifizierung Melanom-spezifischer Biomarker, die diagnostische und prognostische Informationen liefern sowie die Entwicklung einer zielgerichteten, kombinierten und individualisierten Therapie des metastasierenden Melanoms ermöglichen. In diesem Kontext soll die vorliegende Arbeit einen weiteren Beitrag zum Verständnis der Metastasierungskaskade und der daran beteiligten Proteine leisten. Aufgrund der Überexpression in einer Reihe von Tumoren und seiner geringen Molmasse von lediglich 11,5 kDa bietet sich das S100A4-Protein als Marker mit hoher prognostischer Signifikanz für verschiedene Tumorentitäten an. Jedoch ist die Beteiligung von S100A4 bei der Ausbildung des invasiven Tumorphänotyps noch nicht vollständig aufgeklärt. S100A4 besitzt zahlreiche intra- und extrazelluläre Bindungspartner, wobei die Metastasierung scheinbar ausschließlich durch das extrazelluläre Protein beeinflusst wird. S100A4 wechselwirkt extrazellulär beispielsweise mit dem Rezeptor für fortgeschrittene Glykierungsendprodukte (RAGE). Ziel dieser Arbeit war es, speziell die Bedeutung von S100A4 und seiner Interaktion mit RAGE für das prometastatische Verhalten von Melanomzellen in vitro und in vivo näher zu charakterisieren. Darüber hinaus sollte die Beteiligung von S100A4 bei der Gehirn-Metastasierung untersucht werden, wobei insbesondere die Regulierung der Endothelzell-Permeabilität und der transendothelialen Migration der Melanomzellen im Vordergrund stand. Im Rahmen dieser Arbeit wurde gezeigt, dass S100A4 und die Interaktion mit RAGE die prometastatischen Eigenschaften der A375-Melanomzellen förderte. Zudem verringerte extrazelluläres S100A4 die Zell-Integrität von Gehirn-Endothelzellen und erleichterte somit die Durchdringung der Blut-Hirn-Schranke. Diese Erkenntnis lässt sich möglicherweise auf andere Blut-Gewebe-Schranken übertragen. Die In-vivo-Orientierungsstudie zeigte, dass S100A4- und RAGE-überexprimierende Zellen zu einer verstärkten disseminierten Metastasierung führten, wobei sich zwei unterschiedliche Verteilungsmuster ergaben. Darüber hinaus führten beide Zelllinien vereinzelt zur Bildung von Gehirnmetastasen, wodurch sich die intrakardiale Injektion durchaus als Modell für weitere Therapiestudien mit dem Augenmerk der S100A4-RAGE-stimulierten Metastasierung eignet. Die genauere Kenntnis regulativer Mechanismen bei der Synthese und Sekretion von S100A4 sowie die pathophysiologische Differenzierung der S100A4-Interaktion mit RAGE eröffnen neue Wege, die S100A4-vermittelten Effekte therapeutisch zu beeinflussen. Daraus lassen sich möglicherweise neue zielgerichtete Radionuklid-basierte Therapieansätze für das metastasierende Melanom ableiten.
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LO, LINE MEI FRANCOIS. "La rage en afrique." Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20044.

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Books on the topic "RagD"

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Grey, Nyxia. Rad Rag: Your Flow Is Fly. Salem, MA: the author, 2015.

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Ulateig, Egil. Raud krigar, raud spion. Oslo: Norske Samlaget, 1989.

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Bomba, Bernard. Rags and again rags: Poems. Westfield, NJ: Town Book Press, 2000.

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Tanasukharāma, Gupta. Raga raga Hindū merā paricaya. Dillī: Sūrya Bhāratī Prakāśana, 2002.

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Kellerman, Jonathan. Rage. New York: Random House Publishing Group, 2005.

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Smith, Wilbur A. Rage. London: Pan, 1997.

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Smith, Wilbur A. Rage. London: BCA, 1987.

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Rage. Middletown, Conn: Wesleyan University Press, 2002.

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Smith, Wilbur A. Rage. London: Mandarin, 1995.

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Rage. Boston: Graphia, 2011.

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Book chapters on the topic "RagD"

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Wassholm, Johanna, and Anna Sundelin. "Rag Collectors: Mobility and Barter in a Circular Flow of Goods." In Encounters and Practices of Petty Trade in Northern Europe, 1820–1960, 69–94. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98080-1_4.

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AbstractThis chapter traces a forgotten, yet important itinerant means of livelihood, namely rag collecting. Rags played an essential role as raw material for the paper and textile industries in the nineteenth century. The chapter identifies a business logic based on the idea that material perceived by one individual as worthless could be turned into something of economic value. As rags were commodified, they acquired new value in a different context. By analyzing newspapers, periodical articles and responses to ethnographic questionnaires, the authors follow a group of rag collectors from the Karelian Isthmus, who utilized their favorable geographic location to gain a livelihood from a circular flow of goods. The chapter demonstrates how an earthenware pot could be bartered for a discarded garment, which in turn became a piece of the puzzle in the process that kept industry and economic growth going.
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Petit, Jean-Pierre. "Rand auf Rand." In Die Abenteuer des Anselm Wüßtegern Das Topologikon, 23–25. Wiesbaden: Vieweg+Teubner Verlag, 1995. http://dx.doi.org/10.1007/978-3-322-83125-5_6.

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Reutlinger, Christian. "Rand." In Raumwissenschaftliche Basics, 211–20. Wiesbaden: VS Verlag für Sozialwissenschaften, 2010. http://dx.doi.org/10.1007/978-3-531-92619-3_21.

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Burger, Alissa. "Rage." In Teaching Stephen King, 73–85. New York: Palgrave Macmillan US, 2016. http://dx.doi.org/10.1057/9781137483911_6.

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Mercado, Gustavo. "rage." In The Filmmaker's Eye: The Language of the Lens, 72–73. London; New York: Routledge, 2019.: Routledge, 2019. http://dx.doi.org/10.4324/9780429446894-14.

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DiGiuseppe, Raymond A., and Kristine McKiernan. "Rage." In Encyclopedia of Personality and Individual Differences, 4258–60. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_548.

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DiGiuseppe, Raymond A., and Kristine McKiernan. "Rage." In Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_548-1.

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Moore, Frances H. "Rage." In Growing Through the Erotic Transference, 53–55. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003326700-15.

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Murnane, Ben. "Rand Noir vs. Rand Incorporated." In Ayn Rand and the Posthuman, 93–131. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90853-3_4.

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Whitaker, Ashley. "Existential Rage." In Encyclopedia of Personality and Individual Differences, 1476–79. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_2343.

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Conference papers on the topic "RagD"

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Zeljko, Ivan, Miodrag Spasic, and Damir Sekulic. "Predicting futsal specific change of direction speed and reactive agility; analysis of specific correlates in top-level players." In 12th International Conference on Kinanthropology. Brno: Masaryk University Press, 2020. http://dx.doi.org/10.5817/cz.muni.p210-9631-2020-18.

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Purpose: Change of direction speed (CODS) and reactive agility (RAG) are important qual-ities in futsal, but studies rarely examined the predictors of these conditioning capacities in players of advanced level. This study aimed to evaluate predictive validity of certain an-thropometric and conditioning capacities in evaluation of futsal specific CODS and RAG in top-level players. Methods: The sample comprised 54 male players from Croatia and Bosnia and Herzegovina, members of teams competing at the highest national rank, including national champions for the 2017–2018 competitive season in both countries. The variables comprised set of pre-dictors (body mass, body height, triceps skinfold, reactive strength index [RSI], sprint 10 m [S10M], and broad jump [BJ]; and four criteria: futsal specific CODS and RAG, performed with and without dribbling (CODS_D, CODS_WD, RAG_D, RAG_WD). To identify the asso-ciation between variables Pearson’s correlation and multiple regressions were calculated. Results: Observed predictors explained statistically significant (p < 0.05) percentage of vari-ance for all four criteria (Rsq: 0.28, 0.30, 0.23 and 0.25, for CODS_WD, CODS_D, RAG_WD, RAG_D, respectively). Body mass was significant predictor for all criteria (Beta: 0.35–0.51), with poorer performances in heavier players. In both performances which involved dribbling, significant predictors was RSI (Beta: −0.27 and −0.31 for CODS_D and RAG_D, respective-ly), with superior performances in players with better RSI. The S10M and BJ were not identi-fied as being significantly correlated to studied RAG and CODS performances. Conclusion: Study confirmed specific influence of studied predictors of futsal specific CODS and RAG with consistent negative influence of body mass on studied performances. Almost certainly this can be explained by specifics of RAG and CODS execution. Specifically, tests are performed over relatively small distances, with several changes of direction, which clear-ly mimic the futsal specific performances. Although sprint performance is often observed as important determinant of CODS and RAG, herein we did not confirm its predictive validity in explanation of futsal specific CODS and RAG. Future studies should evaluate other poten-tially important predictors of these capacities in futsal.
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Liu, Hudan, Yumi Yashiro-Ohtani, Anthony W. S. Chi, and Warren S. Pear. "Abstract 3075: NOTCH1 dimerization directly activates Rag1 and Rag2 in murine T-cell leukemia." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3075.

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Ru, Heng, Melissa G. Chambers, Tian-Min Fu, Alexander B. Tong, Maofu Liao, and Hao Wu. "Abstract B122: Molecular mechanism of V(D)J recombination from synaptic RAG1-RAG2 complex structures." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b122.

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Wiarda, Shaylyn L., Walter R. Fehr, and Matthew E. O'Neal. "Influence of the Rag1 and Rag2 genes on aphid resistance and agronomic performance of soybean lines." In Proceedings of the 21st Annual Integrated Crop Management Conference. Iowa State University, Digital Press, 2010. http://dx.doi.org/10.31274/icm-180809-41.

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Bhargava, Bharat, John Dilley, and John Riedl. "RAID." In the 2nd workshop. New York, New York, USA: ACM Press, 1986. http://dx.doi.org/10.1145/503956.503965.

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Uehara, Minoru. "Combining N-ary RAID to RAID MP." In 2009 International Conference on Network-Based Information Systems (NBIS). IEEE, 2009. http://dx.doi.org/10.1109/nbis.2009.27.

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Tobagi, Fouad A., Joseph Pang, Randall Baird, and Mark Gang. "Streaming RAID." In the first ACM international conference. New York, New York, USA: ACM Press, 1993. http://dx.doi.org/10.1145/166266.168435.

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Demmler, Daniel, Amir Herzberg, and Thomas Schneider. "RAID-PIR." In CCS'14: 2014 ACM SIGSAC Conference on Computer and Communications Security. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2664168.2664181.

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Wang, Mingyang, and Yiming Hu. "i-RAID." In SAC 2016: Symposium on Applied Computing. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2851613.2851735.

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Balakrishnan, Mahesh, Asim Kadav, Vijayan Prabhakaran, and Dahlia Malkhi. "Differential RAID." In the 5th European conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1755913.1755916.

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Reports on the topic "RagD"

1

Blais, A. Copper Rand Mine. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1991. http://dx.doi.org/10.4095/132280.

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Christmas, James D. The Raid on Trenton. Fort Belvoir, VA: Defense Technical Information Center, January 2002. http://dx.doi.org/10.21236/ada403700.

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Thiemann-Linden, Jörg, and Wolfgang Aichinger. Kommunikationskampagnen pro Rad. Deutsches Institut für Urbanistik (Difu), 2012. http://dx.doi.org/10.26128/2022.86.

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Zee, Nicolaas J. van der. The Roots of Muslim Rage Revisited. Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada590272.

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Eckerman, Keith F., and Andrea L. Sjoreen. Rad Toolbox User's Guide. Office of Scientific and Technical Information (OSTI), May 2013. http://dx.doi.org/10.2172/1201298.

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Thiemann-Linden, Jörg, and Tobias Mettenberger. Unfallrisiken beim Rad fahren. Deutsches Institut für Urbanistik (Difu), 2012. http://dx.doi.org/10.26128/2022.72.

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Mead, Steve. The impact of RAID on disk imaging. Gaithersburg, MD: National Institute of Standards and Technology, 2005. http://dx.doi.org/10.6028/nist.ir.7276.

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Chiaro, PJ. RAD/COMM Cricket Test Report. Office of Scientific and Technical Information (OSTI), August 2003. http://dx.doi.org/10.2172/885856.

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Chiaro, P. J. RAD/COMM ''Cricket'' Test Report. Office of Scientific and Technical Information (OSTI), May 2002. http://dx.doi.org/10.2172/814478.

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Grigsby, Stan, and Donna W. Blake. Assessing Uncertainties in the Probability of Raid Annihilation. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada444529.

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