Relevant bibliographies by topics / RagC

Academic literature on the topic 'RagC'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "RagC"

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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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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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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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Meng, Jin, and Shawn M. Ferguson. "GATOR1-dependent recruitment of FLCN–FNIP to lysosomes coordinates Rag GTPase heterodimer nucleotide status in response to amino acids." Journal of Cell Biology 217, no. 8 (May 30, 2018): 2765–76. http://dx.doi.org/10.1083/jcb.201712177.

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Folliculin (FLCN) is a tumor suppressor that coordinates cellular responses to changes in amino acid availability via regulation of the Rag guanosine triphosphatases. FLCN is recruited to lysosomes during amino acid starvation, where it interacts with RagA/B as a heterodimeric complex with FLCN-interacting proteins (FNIPs). The FLCN–FNIP heterodimer also has GTPase-activating protein (GAP) activity toward RagC/D. These properties raised two important questions. First, how is amino acid availability sensed to regulate lysosomal abundance of FLCN? Second, what is the relationship between FLCN lysosome localization, RagA/B interactions, and RagC/D GAP activity? In this study, we show that RagA/B nucleotide status determines the FLCN–FNIP1 recruitment to lysosomes. Starvation-induced FLCN–FNIP lysosome localization requires GAP activity toward Rags 1 (GATOR1), the GAP that converts RagA/B to the guanosine diphosphate (GDP)-bound state. This places FLCN–FNIP recruitment to lysosomes under the control of amino acid sensors that act upstream of GATOR1. By binding to RagA/BGDP and acting on RagC/D, FLCN–FNIP can coordinate nucleotide status between Rag heterodimer subunits in response to changes in amino acid 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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Lypaczewski, Patrick, Wen-Wei Zhang, and Greg Matlashewski. "Evidence that a naturally occurring single nucleotide polymorphism in the RagC gene of Leishmania donovani contributes to reduced virulence." PLOS Neglected Tropical Diseases 15, no. 2 (February 23, 2021): e0009079. http://dx.doi.org/10.1371/journal.pntd.0009079.

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Leishmaniasis is a widespread neglected tropical disease transmitted by infected sand flies resulting in either benign cutaneous infection or fatal visceral disease. Leishmania donovani is the principal species responsible for visceral leishmaniasis, yet an atypical L. donovani has become attenuated in several countries including Sri Lanka and causes cutaneous leishmaniasis. Previous studies have identified 91 genes altered in the atypical cutaneous L. donovani compared to typical visceral disease associated L. donovani including mutations in the RagC and Raptor genes that are part of the eukaryotic conserved TOR pathway and its upstream sensing pathway. In the present study, we investigate whether the RagC R231C mutation present in atypical cutaneous L. donovani introduced into the virulent L. donovani 1S2D chromosome by CRISPR gene editing could affect virulence for survival in visceral organs. Through bioinformatic analysis, we further investigated the presence of sensing pathway components upstream of TOR in L. donovani including RagC complexing proteins, RagA and Raptor. L. donovani 1S2D edited to express mutant RagC R231C were viable in promastigote but had reduced visceral parasitemia in infected BALB/c mice. The RagC R231C mutant retained the ability to interact with RagA and gene knockout experiments revealed that although the RagA gene was essential, the RagC gene was not essential under promastigote culture conditions but was essential for survival in the liver of experimentally infected mice. These results provide evidence that the TOR associated sensing pathway plays a prominent role in L. donovani visceral disease and the RagC R231C mutation contributed to the atypical pathology of cutaneous L. donovani in Sri Lanka.
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Anandapadamanaban, Madhanagopal, Glenn R. Masson, Olga Perisic, Alex Berndt, Jonathan Kaufman, Chris M. Johnson, Balaji Santhanam, Kacper B. Rogala, David M. Sabatini, and Roger L. Williams. "Architecture of human Rag GTPase heterodimers and their complex with mTORC1." Science 366, no. 6462 (October 10, 2019): 203–10. http://dx.doi.org/10.1126/science.aax3939.

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The Rag guanosine triphosphatases (GTPases) recruit the master kinase mTORC1 to lysosomes to regulate cell growth and proliferation in response to amino acid availability. The nucleotide state of Rag heterodimers is critical for their association with mTORC1. Our cryo–electron microscopy structure of RagA/RagC in complex with mTORC1 shows the details of RagA/RagC binding to the RAPTOR subunit of mTORC1 and explains why only the RagAGTP/RagCGDP nucleotide state binds mTORC1. Previous kinetic studies suggested that GTP binding to one Rag locks the heterodimer to prevent GTP binding to the other. Our crystal structures and dynamics of RagA/RagC show the mechanism for this locking and explain how oncogenic hotspot mutations disrupt this process. In contrast to allosteric activation by RHEB, Rag heterodimer binding does not change mTORC1 conformation and activates mTORC1 by targeting it to lysosomes.
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Li, Kristina, Shogo Wada, Bridget S. Gosis, Chelsea Thorsheim, Paige Loose, and Zolt Arany. "Folliculin promotes substrate-selective mTORC1 activity by activating RagC to recruit TFE3." PLOS Biology 20, no. 3 (March 31, 2022): e3001594. http://dx.doi.org/10.1371/journal.pbio.3001594.

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Mechanistic target of rapamycin complex I (mTORC1) is central to cellular metabolic regulation. mTORC1 phosphorylates a myriad of substrates, but how different substrate specificity is conferred on mTORC1 by different conditions remains poorly defined. Here, we show how loss of the mTORC1 regulator folliculin (FLCN) renders mTORC1 specifically incompetent to phosphorylate TFE3, a master regulator of lysosome biogenesis, without affecting phosphorylation of other canonical mTORC1 substrates, such as S6 kinase. FLCN is a GTPase-activating protein (GAP) for RagC, a component of the mTORC1 amino acid (AA) sensing pathway, and we show that active RagC is necessary and sufficient to recruit TFE3 onto the lysosomal surface, allowing subsequent phosphorylation of TFE3 by mTORC1. Active mutants of RagC, but not of RagA, rescue both phosphorylation and lysosomal recruitment of TFE3 in the absence of FLCN. These data thus advance the paradigm that mTORC1 substrate specificity is in part conferred by direct recruitment of substrates to the subcellular compartments where mTORC1 resides and identify potential targets for specific modulation of specific branches of the mTOR pathway.
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Rogala, Kacper B., Xin Gu, Jibril F. Kedir, Monther Abu-Remaileh, Laura F. Bianchi, Alexia M. S. Bottino, Rikke Dueholm, et al. "Structural basis for the docking of mTORC1 on the lysosomal surface." Science 366, no. 6464 (October 10, 2019): 468–75. http://dx.doi.org/10.1126/science.aay0166.

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The mTORC1 (mechanistic target of rapamycin complex 1) protein kinase regulates growth in response to nutrients and growth factors. Nutrients promote its translocation to the lysosomal surface, where its Raptor subunit interacts with the Rag guanosine triphosphatase (GTPase)–Ragulator complex. Nutrients switch the heterodimeric Rag GTPases among four different nucleotide-binding states, only one of which (RagA/B•GTP–RagC/D•GDP) permits mTORC1 association. We used cryo–electron microscopy to determine the structure of the supercomplex of Raptor with Rag-Ragulator at a resolution of 3.2 angstroms. Our findings indicate that the Raptor α-solenoid directly detects the nucleotide state of RagA while the Raptor “claw” threads between the GTPase domains to detect that of RagC. Mutations that disrupted Rag-Raptor binding inhibited mTORC1 lysosomal localization and signaling. By comparison with a structure of mTORC1 bound to its activator Rheb, we developed a model of active mTORC1 docked on the lysosome.
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Alhazmi, Hatem, Syyed Shah, and Atif Mahmood. "Sustainable Development of Innovative Green Construction Materials: A Study for Economical Eco-Friendly Recycled Aggregate Based Geopolymer Concrete." Materials 13, no. 21 (October 30, 2020): 4881. http://dx.doi.org/10.3390/ma13214881.

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Green revolution and high carbon footprint concepts have attracted the development of a green and sustainable environment. This work endeavors to investigate the behavior of recycled aggregate geopolymer concrete (RAGC) developed with four different types of effluents to develop sustainability in the construction industry and to produce an eco-friendly environment. Each of the types of effluents was used by completely replacing the freshwater in RAGC to examine its influence on compressive strength (CS), chloride ion migration (CIM), split tensile strength (STS), and resistance to the sulfuric acid attack of RAGC at various testing ages. The test outputs portray that the effluent obtained from the textile mill performed well for the CS (25% higher than the control mix) and STS (17% higher than the control mix) of RAGC. Similarly, the highest mass loss of RAGC due to the acid attack (41% higher than control mix) and the highest CIM (29% higher than control mix) were represented by the RAGC mix made with effluent obtained from fertilizer mill. The statistical analysis indicated no significant influence of using textile mill effluent (TE), fertilizer mill effluent (FE), and sugar mill effluent (SE) on the STS, CIM, and mass loss due to acid attack while it presented a significant influence on the CS of various mixes. Therefore, this investigation solidly substantiates the acceptability of studied types of effluents for the fabrication of eco-friendly green materials.
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Dissertations / Theses on the topic "RagC"

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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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Lalk, Michael [Verfasser]. "Tumorregionen-abhängige Expression der Aminosäure-Sensoren MAP4K3, RagC und VPS34 in Glioblastomen / Michael Lalk." Magdeburg : Universitätsbibliothek, 2018. http://d-nb.info/1174626593/34.

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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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PRETRE, PHILIPPE. "Rage et voyages." Besançon, 1991. http://www.theses.fr/1991BESA3052.

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Mengual, Nathalie. "Epidémiologie et prophylaxie de la rage en Afrique : stratégies de lutte." Paris 5, 1989. http://www.theses.fr/1989PA05P192.

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Tanner, Anne. "Human Herpesvirus 6A Infection and Immunopathogenesis in Humanized Rag2-/-γc-/- Mice and Relevance to HIV/AIDS and Autoimmunity." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6078.

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Human herpesvirus 6A (HHV-6A) has yet to be definitively linked to a specific disease. This is due in part to the ubiquitous nature of the virus. Humanized Rag2-/-γc-/- (Rag-hu) mice were tested to determine if these were a suitable animal model to study the virus. Both cell-free and cell-associated virus was used for infection and both were found to be efficient at infecting the mice. Viral DNA was found in the plasma and cellular blood fractions, bone marrow, lymph node, and thymus, indicating successful infection and propagation of the virus in vivo. The CD3+CD4- population was depleted, while the CD3-CD4+ was increased in infected animals. The CD3-CD4+CD8- and CD3+CD4+CD8- populations were depleted and the CD3+CD4+CD8+ population increased when analysis was gated upon CD4+ cells. The CD3-CD4+CD8+ population expanded and the CD3-CD4+CD8- population was reduced when analysis was gated on the CD3- population. Additional flow cytometry analysis revealed increases in CD4+CD8+ double positive cells in the peripheral blood of cell-free infected mice, which could indicate improper T cell selection and a premature departure of these cells from the thymus, possibly contributing to autoimmunity. Previous research has shown that HIV and HHV-6A may have a synergistic effect on one another and that HHV-6A may act as a cofactor in the progression to AIDS. After determining the Rag-hu mouse model was suitable for studying HHV-6A infection, a coinfection of HHV-6A and HIV-1 was performed. Coinfected mice had fewer thymocytes when compared with the HIV-1 only, mock-infected, and to a lesser extent HHV-6A only groups which could indicate increased cell death in the coinfected group as well as possible disruptions in migration of cells, either causing cells to be sequestered in the bone marrow and unable to migrate to the thymus, or causing premature egress of the cells in the thymus due in part to premature upregulation of CCR7, both of which would explain the smaller cellular populations found in the coinfected mouse thymi. Additional studies were performed to determine if a preferential targeting existed between HHV-6A and HIV-1 as these viruses are found simultaneously coinfecting the same cell. Preferential targeting was not observed by cell-associated migration assay, but increased migration of HHV-6A-infected cells was observed in a CCL21 dependent manner. These studies have provided useful information about HHV-6A and its relevance to HIV/AIDS as well as a possible mechanism of the involvement of HHV-6A in multiple sclerosis (MS) and other autoimmune diseases.
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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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Books on the topic "RagC"

1

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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Copyright Paperback Collection (Library of Congress), ed. Rage. New York City: Leisure Books, 2004.

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Smith, Wilbur A. Rage. London: Pan Books, 1988.

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Book chapters on the topic "RagC"

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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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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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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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Simpson, Terry. "Beyond Rage." In Speaking Our Minds, 215–16. London: Macmillan Education UK, 1996. http://dx.doi.org/10.1007/978-1-349-25159-9_55.

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Lamy, Philip. "Millennium Rage." In Millennium Rage, 1–30. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-6076-4_1.

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Datta, Asoke Kumar, Sandeep Singh Solanki, Ranjan Sengupta, Soubhik Chakraborty, Kartik Mahto, and Anirban Patranabis. "Raga Identification." In Signals and Communication Technology, 101–24. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3959-1_6.

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Conference papers on the topic "RagC"

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Guo, Zhijun, Shaoping Wu, Julissa Molina-Vega, Rafael Castillo, Jaime Barrera, Veronica Johnson, Carol Lange, and David Potter. "Abstract LB-023: CYP monooxygenases regulate nuclear localization of ERá and mTORC1 component RagC in ER+HER2- breast cancer cells." In 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-lb-023.

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Guo, Zhijun, Shaoping Wu, Julissa Molina-Vega, Rafael Castillo, Jaime Barrera, Veronica Johnson, Carol Lange, and David Potter. "Abstract LB-023: CYP monooxygenases regulate nuclear localization of ERá and mTORC1 component RagC in ER+HER2- breast cancer cells." In 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-lb-023.

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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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Choi, Yongsuk, Yeongseong Park, Jongmoo Choi, Seong-je Cho, and Hwansoo Han. "RAMC." In the 7th International Conference. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2448556.2448623.

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Nanda, Saurav, and Thomas J. Hacker. "RACC." In HPDC '18: The 27th International Symposium on High-Performance Parallel and Distributed Computing. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3217871.3217876.

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Khalil, Rami A., and Naranker Dulay. "RANC." In SAC '22: The 37th ACM/SIGAPP Symposium on Applied Computing. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3477314.3507056.

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Masucci, Michael. "Rage to know." In SIGGRAPH07: Special Interest Group on Computer Graphics and Interactive Techniques Conference. New York, NY, USA: ACM, 2007. http://dx.doi.org/10.1145/1280120.1280143.

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Papadopoulos, Panos, Thanasis Loukopoulos, Ioannis Anagnostopoulos, Nikolaos Tziritas, and Michael Vassilakopoulos. "RAC." In PCI '15: 19th Panhellenic Conference on Informatics. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2801948.2801978.

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Reports on the topic "RagC"

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Attaya, H. Input instructions for RACC-P. Office of Scientific and Technical Information (OSTI), September 1994. http://dx.doi.org/10.2172/10196555.

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Novak, Mark E., Dirk T. Bussey, and Edward J. Daniszewski. RADC Cathode Life Test Facility. Fort Belvoir, VA: Defense Technical Information Center, February 1991. http://dx.doi.org/10.21236/ada234309.

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Topiwala, P. T. Rate-Adaptive Video Coding (RAVC). Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada482958.

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Duvall, Lorraine M. RADC Software Acquisition Management and Analysis. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada208526.

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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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Kezunovic, Mladen, Shmuel Oren, Kory Hedman, Erick Moreno Centeno, Garng Huang, and Alex Sprintson. Robust Adaptive Topology Control Project (RATC). Office of Scientific and Technical Information (OSTI), July 2015. http://dx.doi.org/10.2172/1209678.

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Buluc, Aydin, Tamara Kolda, Stefan Wild, Mihai Anitescu, Anthony Degennaro, John Jakeman, Chandrika Kamath, et al. Randomized Algorithms for Scientific Computing (RASC). Office of Scientific and Technical Information (OSTI), April 2021. http://dx.doi.org/10.2172/1807223.

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Tardelli, J. D., J. LeBlanc, and P. D. Gatewood. RADC/EEV Diagnostic Rhyme Test System Improvements. Fort Belvoir, VA: Defense Technical Information Center, November 1989. http://dx.doi.org/10.21236/ada223187.

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Teegarden, Kenneth J. RADC (Rome Air Development Center) Photonics Center Support. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada206607.

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Landon, Mark D., and Carrie Yeager. Rapid Aero-Shape Generator (RAGE). SBIR Phase 2. Fort Belvoir, VA: Defense Technical Information Center, August 1993. http://dx.doi.org/10.21236/ada295635.

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