Relevant bibliographies by topics / TRAF

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Academic literature on the topic 'TRAF'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "TRAF"

1

Devergne, O., E. Hatzivassiliou, K. M. Izumi, K. M. Kaye, M. F. Kleijnen, E. Kieff, and G. Mosialos. "Association of TRAF1, TRAF2, and TRAF3 with an Epstein-Barr virus LMP1 domain important for B-lymphocyte transformation: role in NF-kappaB activation." Molecular and Cellular Biology 16, no. 12 (December 1996): 7098–108. http://dx.doi.org/10.1128/mcb.16.12.7098.

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The Epstein-Barr virus (EBV) transforming protein LMP1 appears to be a constitutively activated tumor necrosis factor receptor (TNFR) on the basis of an intrinsic ability to aggregate in the plasma membrane and an association of its cytoplasmic carboxyl terminus (CT) with TNFR-associated factors (TRAFs). We now show that in EBV-transformed B lymphocytes most of TRAF1 or TRAF3 and 5% of TRAF2 are associated with LMP1 and that most of LMP1 is associated with TRAF1 or TRAF3. TRAF1, TRAF2, and TRAF3 bind to a single site in the LMP1 CT corresponding to amino acids (aa) 199 to 214, within a domain which is important for B-lymphocyte growth transformation (aa 187 to 231). Further deletional and alanine mutagenesis analyses and comparison with TRAF binding sequences in CD40, in CD30, and in the LMP1 of other lymphycryptoviruses provide the first evidence that PXQXT/S is a core TRAF binding motif. The negative effects of point mutations in the LMP1(1-231) core TRAF binding motif on TRAF binding and NF-kappaB activation genetically link the TRAFs to LMP1(1-231)-mediated NF-kappaB activation. NF-kappaB activation by LMP1(1-231) is likely to be mediated by TRAF1/TRAF2 heteroaggregates since TRAF1 is unique among the TRAFs in coactivating NF-kappaB with LMP1(1-231), a TRAF2 dominant-negative mutant can block LMP1(1-231)-mediated NF-kappaB activation as well as TRAF1 coactivation, and 30% of TRAF2 is associated with TRAF1 in EBV-transformed B cells. TRAF3 is a negative modulator of LMP1(1-231)-mediated NF-kappaB activation. Surprisingly, TRAF1, -2, or -3 does not interact with the terminal LMP1 CT aa 333 to 386 which can independently mediate NF-kappaB activation. The constitutive association of TRAFs with LMP1 through the aa 187 to 231 domain which is important in NF-kappaB activation and primary B-lymphocyte growth transformation implicates TRAF aggregation in LMP1 signaling.
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Chin, Arnold I.-Dah, Junyan Shu, Chong Shan Shi, Zhengbin Yao, John H. Kehrl, and Genhong Cheng. "TANK Potentiates Tumor Necrosis Factor Receptor-Associated Factor-Mediated c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase Activation through the Germinal Center Kinase Pathway." Molecular and Cellular Biology 19, no. 10 (October 1, 1999): 6665–72. http://dx.doi.org/10.1128/mcb.19.10.6665.

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ABSTRACT Tumor necrosis factor (TNF) receptor-associated factors (TRAFs) are mediators of many members of the TNF receptor superfamily and can activate both the nuclear factor κB (NF-κB) and stress-activated protein kinase (SAPK; also known as c-Jun N-terminal kinase) signal transduction pathways. We previously described the involvement of a TRAF-interacting molecule, TRAF-associated NF-κB activator (TANK), in TRAF2-mediated NF-κB activation. Here we show that TANK synergized with TRAF2, TRAF5, and TRAF6 but not with TRAF3 in SAPK activation. TRAF2 and TANK individually formed weak interactions with germinal center kinase (GCK)-related kinase (GCKR). However, when coexpressed, they formed a strong complex with GCKR, thereby providing a potential mechanism for TRAF and TANK synergy in GCKR-mediated SAPK activation, which is important in TNF family receptor signaling. Our results also suggest that TANK can form potential intermolecular as well as intramolecular interactions between its amino terminus and carboxyl terminus. This study suggests that TANK is a regulatory molecule controlling the threshold of NF-κB and SAPK activities in response to activation of TNF receptors. In addition, CD40 activated endogenous GCKR in primary B cells, implicating GCK family proteins in CD40-mediated B-cell functions.
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Miller, William E., Jeanette L. Cheshire, and Nancy Raab-Traub. "Interaction of Tumor Necrosis Factor Receptor-Associated Factor Signaling Proteins with the Latent Membrane Protein 1 PXQXT Motif Is Essential for Induction of Epidermal Growth Factor Receptor Expression." Molecular and Cellular Biology 18, no. 5 (May 1, 1998): 2835–44. http://dx.doi.org/10.1128/mcb.18.5.2835.

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ABSTRACT The Epstein-Barr virus latent membrane protein 1 (LMP1) oncoprotein causes multiple cellular changes, including induction of epidermal growth factor receptor (EGFR) expression and activation of the NF-κB transcription factor. LMP1 and the cellular protein CD40, which also induces EGFR expression, interact with the tumor necrosis factor receptor-associated factor (TRAF) proteins. The LMP1 carboxy-terminal activation region 1 signaling domain interacts specifically with the TRAFs and is essential for EGFR induction through a mechanism independent of NF-κB alone. LMP1 and CD40 share a common TRAF binding motif, PXQXT. In this study, the PXQXT motifs in both LMP1 and CD40 were altered and mutant proteins were analyzed for induction of EGFR expression. Replacement of the T residue with A in CD40 completely blocked induction of the EGFR, while the same mutation in LMP1 did not affect EGFR induction. Replacement of both P and Q residues with A’s in LMP1 reduced EGFR induction by >75%, while deletion of PXQXT blocked EGFR induction. These results genetically link EGFR induction by LMP1 to the TRAF signaling pathway. Overexpression of TRAF2 potently activates NF-κB, although TRAF2 did not induce expression of the EGFR either alone or in combination with TRAF1 and TRAF3. In vivo analyses of the interaction of the TRAFs with LMP1 variants mutated in the PXQXT domain indicate that high-level induction of EGFR expression requires interaction with TRAF1, -2, and -3. However, exogenous expression of TRAF3 decreased EGFR induction mediated by either LMP1 or CD40. These data suggest that TRAF-mediated activation of EGFR expression requires assembly of a complex containing the appropriate stoichiometry of TRAF proteins clustered at the cell membrane with LMP1.
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Conti, Alfredo, M'Hammed Aguennouz, Domenico La Torre, Salvatore Cardali, Filippo Flavio Angileri, Catia Buemi, Chiara Tomasello, et al. "Expression of the tumor necrosis factor receptor—associated factors 1 and 2 and regulation of the nuclear factor—kB antiapoptotic activity in human gliomas." Journal of Neurosurgery 103, no. 5 (November 2005): 873–81. http://dx.doi.org/10.3171/jns.2005.103.5.0873.

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Object. Tumor necrosis factor receptor (TNFR)—associated factors (TRAFs) are a recently established group of proteins involved in the intracellular signaling of the TNFR superfamily members. The TRAFs have been implicated in promoting cell survival through the activation of transcription factor nuclear factor (NF)—κB. The authors investigated the expression of NF-κB, caspase 3, TRAF1, TRAF2, and TRAF-associated NF-κB activator/TRAF—interacting protein (TANK/I-TRAF), a regulator of TRAF activity, in human gliomas. Methods. Tumor samples were obtained in 27 adult patients harboring seven low-grade gliomas, nine anaplastic astrocytomas, and 11 glioblastomas multiforme. The NF-κB activation was analyzed using the electrophoresis mobility shift assay; TRAF1, TRAF2, TANK/I-TRAF, and caspase 3 expression were studied using Western blot analysis. Upregulated NF-κB DNA—binding activity, compared with that in normal brain tissue, was detected in all tumor samples (p = 0.002). The level of NF-κB activity showed some correlation with World Health Organization tumor grades (p = 0.01), even though variable activity levels were demonstrated in relation to tissue heterogeneity, which resulted in a substantial number of outliers in the quantitative analysis. Increased levels of TRAF1, TRAF2, and TANK/I-TRAF were expressed in astrocytomas compared with levels in normal brain tissue (p = 0.02, 0.006, and 0.01, respectively). Conclusions. Data in this study confirm the upregulation of NF-κB in gliomas and reveal a correlation between levels of this transcription factor and tumor grade. A constitutive expression of TRAF1, TRAF2, and TANK/I-TRAF in human gliomas was documented. These proteins are involved in the intracellular signal transduction of the TNFR superfamily and in the control of NF-κB expression and its antiapoptotic activity.
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Miyazaki, Ryo, Yoshiyuki Ohtsubo, Yuji Nagata, and Masataka Tsuda. "Characterization of the traD Operon of Naphthalene-Catabolic Plasmid NAH7: a Host-Range Modifier in Conjugative Transfer." Journal of Bacteriology 190, no. 19 (August 1, 2008): 6281–89. http://dx.doi.org/10.1128/jb.00709-08.

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ABSTRACT Pseudomonas putida G7 carries a naphthalene-catabolic and self-transmissible plasmid, NAH7, which belongs to the IncP-9 incompatibility group. Adjacent to the putative origin of conjugative transfer (oriT) of NAH7 are three genes, traD, traE, and traF, whose functions and roles in conjugation were previously unclear. These three genes were transcribed monocistronically and thus were designated the traD operon. Mutation of the three genes in the traD operon resulted in 10- to 105-fold decreases in the transfer frequencies of the plasmids from Pseudomonas to Pseudomonas and Escherichia coli and from E. coli to E. coli. On the other hand, the traD operon was essential for the transfer of NAH7 from E. coli to Pseudomonas strains. These results indicated that the traD operon is a host-range modifier in the conjugative transfer of NAH7. The TraD, TraE, and TraF proteins were localized in the cytoplasm, periplasm, and membrane, respectively, in strain G7 cells. Our use of a bacterial two-hybrid assay system showed that TraE interacted in vivo with other essential components for conjugative transfer, including TraB (coupling protein), TraC (relaxase), and MpfH (a channel subunit in the mating pair formation system).
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Bhat, Eijaz, Chang Kim, Sunghwan Kim, and Hyun Park. "In Vitro Inhibitory Mechanism Effect of TRAIP on the Function of TRAF2 Revealed by Characterization of Interaction Domains." International Journal of Molecular Sciences 19, no. 8 (August 20, 2018): 2457. http://dx.doi.org/10.3390/ijms19082457.

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TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development. Although the critical function of TRAIP in NF-κB signaling is well-known, the molecular inhibitory mechanism of TRAIP remains unclear. We found that the TRAIP coiled-coil domain altered its stoichiometry between dimer and trimer in a concentration-dependent manner. Additionally, the TRAIP RING domain induced even higher-ordered assembly, which was necessary for interacting with the TRAF-N domain of TRAF2 but not TRAF1. Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling.
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Eliopoulos, Aristides G., Elyse R. Waites, Sarah M. S. Blake, Clare Davies, Paul Murray, and Lawrence S. Young. "TRAF1 Is a Critical Regulator of JNK Signaling by the TRAF-Binding Domain of the Epstein-Barr Virus-Encoded Latent Infection Membrane Protein 1 but Not CD40." Journal of Virology 77, no. 2 (January 15, 2003): 1316–28. http://dx.doi.org/10.1128/jvi.77.2.1316-1328.2003.

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ABSTRACT The oncogenic Epstein-Barr virus (EBV)-encoded latent infection membrane protein 1 (LMP1) mimics a constitutive active tumor necrosis factor (TNF) family receptor in its ability to recruit TNF receptor-associated factors (TRAFs) and TNF receptor-associated death domain protein (TRADD) in a ligand-independent manner. As a result, LMP1 constitutively engages signaling pathways, such as the JNK and p38 mitogen-activated protein kinases (MAPK), the transcription factor NF-κB, and the JAK/STAT cascade, and these activities may explain many of its pleiotropic effects on cell phenotype, growth, and transformation. In this study we demonstrate the ability of the TRAF-binding domain of LMP1 to signal on the JNK/AP-1 axis in a cell type- dependent manner that critically involves TRAF1 and TRAF2. Thus, expression of this LMP1 domain in TRAF1-positive lymphoma cells promotes significant JNK activation, which is blocked by dominant-negative TRAF2 but not TRAF5. However, TRAF1 is absent in many established epithelial cell lines and primary nasopharyngeal carcinoma (NPC) biopsy specimens. In these cells, JNK activation by the TRAF-binding domain of LMP1 depends on the reconstitution of TRAF1 expression. The critical role of TRAF1 in the regulation of TRAF2-dependent JNK signaling is particular to the TRAF-binding domain of LMP1, since a homologous region in the cytoplasmic tail of CD40 or the TRADD-interacting domain of LMP1 signal on the JNK axis independently of TRAF1 status. These data further dissect the signaling components used by LMP1 and identify a novel role for TRAF1 as a modulator of oncogenic signals.
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Graham, John P., and Gail A. Bishop. "The role of the TRAF2/3 binding site in LMP1 and CD40 signaling (44.6)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 44.6. http://dx.doi.org/10.4049/jimmunol.182.supp.44.6.

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Abstract The Epstein-Barr virus protein, LMP1, is a mimic of the cellular receptor CD40. However, LMP1 signals to B lymphocytes in an amplified and sustained manner compared to CD40. LMP1 contributes to the development of B lymphoma in HIV patients or in immunosuppressed transplant recipients. LMP1 binds the signaling adaptor TRAF2 with lower affinity than CD40, and TRAF2 is needed for inducing CD40-mediated degradation of TRAFs 2 and 3. LMP1 doesn't induce TRAF degradation, and employs TRAF3 as a positive mediator of cell signaling, whereas CD40 signals are inhibited by TRAF3. We thus tested the hypothesis that relative affinity for TRAF2 and/or, distinct sequence differences in the TRAF2/3 binding sites (TBS) of CD40 vs. LMP1, controls the disparate ways in which CD40 and LMP1 use TRAFs 2 and 3, and their distinct signaling characteristics. We examined CD40 and LMP1 mutants in which the TBS sequences were swapped, testing TRAF binding and degradation, and induction of B cell activation. Results revealed that TRAF binding affinity and TBS sequence dictate some, but not all CD40 vs. LMP1 signaling properties. Examination of TRAF binding, degradation, cytokine production, IgM secretion, and the activation of c-Jun kinase and NF-kB revealed that some events are dictated by TBS sequences, others partially regulated, and still others appear independent of the TBS sequence. NIH grant CA099997
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Duckett, C. S., R. W. Gedrich, M. C. Gilfillan, and C. B. Thompson. "Induction of nuclear factor kappaB by the CD30 receptor is mediated by TRAF1 and TRAF2." Molecular and Cellular Biology 17, no. 3 (March 1997): 1535–42. http://dx.doi.org/10.1128/mcb.17.3.1535.

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CD30 is a lymphoid cell-specific surface receptor which was originally identified as an antigen expressed on Hodgkin's lymphoma cells. Activation of CD30 induces the nuclear factor kappaB (NF-kappaB) transcription factor. In this study, we define the domains in CD30 which are required for NF-kappaB activation. Two separate elements of the cytoplasmic domain which were capable of inducing NF-kappaB independently of one another were identified. The first domain (domain 1) mapped to a approximately 120-amino-acid sequence in the membrane-proximal region of the CD30 cytoplasmic tail, between residues 410 and 531. A second, more carboxy-terminal region (domain 2) was identified between residues 553 and 595. Domain 2 contains two 5- to 10-amino-acid elements which can mediate the binding of CD30 to members of the tumor necrosis factor receptor-associated factor (TRAF) family of signal transducing proteins. Coexpression of CD30 with TRAF1 or TRAF2 but not TRAF3 augmented NF-kappaB activation through domain 2 but not domain 1. NF-kappaB induction through domain 2 was inhibited by coexpression of either full-length TRAF3 or dominant negative forms of TRAF1 or TRAF2. In contrast, NF-kappaB induction by domain 1 was not affected by alterations in TRAF protein levels. Together, these data support a model in which CD30 can induce NF-kappaB by both TRAF-dependent and -independent mechanisms. TRAF-dependent induction of NF-kappaB appears to be regulated by the relative levels of individual TRAF proteins in the cell.
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Chen, Haiming, Richard A. Campbell, Daocheng Zhu, Sonia Guangxu Li, Christine Pan James, Janice Santos, Cathy S. Wang, Benjamin Bonavida, and James R. Berenson. "Inhibition of Multiple Myeloma Cell Proliferation and Increase of Apoptosis through Regulation of the NF-κB and JNK Pathways by Silencing TRAF6 C-Domain mRNA." Blood 104, no. 11 (November 16, 2004): 3355. http://dx.doi.org/10.1182/blood.v104.11.3355.3355.

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Abstract Several members of the tumor necrosis factor receptor-associated factor (TRAF) family, including TRAF2, TRAF5, and TRAF6 have been implicated in regulating signal transduction from various TRAF family members. However, the unique biological function of TRAF6 is largely determined by its TRAF-C domain, which does not interact with peptide motifs that are recognized by TRAF1, -2, -3 or -5. Based on TRAF6, CD40, and RANKL sequences and crystal structures, we targeted the TRAF6 C-domain residues from 420 to 440 because the TRAF6 interaction domain with CD40 or RANKL resides in residues 333 to 508. We found that silencing TRAF6 mRNA with the C-terminal domain siRNA significantly inhibited MM cell proliferation maximally at 72 hours whereas effects on inducing MM cell apoptosis were most prominent at 48 hours. The decrease in cell proliferation and increase in cell apoptosis occurred in a concentration (of siRNA)-dependent fashion. Furthermore, NF-κB mRNA expression and protein levels were also reduced using siRNA of the TRAF6 C-domain. We also examined the effect of TRAF6 siRNA on the JNK pathway since this signaling pathway is also associated with cell cycle effects in myeloma. We measured JUN kinase kinase (JNKK), which activates the MAP kinase homologues SAPK and JNK in response to IL-1 receptor stimulation. The results showed that the phosphorylation of JNKK is clearly reduced after knockdown of TRAF6 gene expression by siRNA. Furthermore, we examined c-Jun, a component of the transcription factor complex AP-1, which binds and activates transcription at TRE/AP-1 elements. The transcription activity of c-Jun is regulated by SAPK/JNK binding to c-Jun and phosphorylation of c-Jun at Ser63/73. We found that total endogenous c-Jun is reduced after silencing TRAF6 mRNA in the RPMI8226 MM cell line. In contrast, our data demonstrated that TRAF6 C-domain does not affect TRAF5 or TRAF2 gene expression. In addition, introduction of siRNA derived from the Zn-finger sequence into RPMI8226 MM cells failed to inhibit TRAF6 production. These studies suggest that the TRAF6 C-Domain may be an excellent target to block myeloma cell signaling important for the survival and proliferation of MM cells.
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Dissertations / Theses on the topic "TRAF"

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Brittain, George C. IV. "A Novel Role for the TRAFs as Co-Activators and Co-Repressors of Transcriptional Activity." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/451.

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The tumor necrosis factor (TNF) receptor-associated factors (TRAFs) were initially discovered as proteins that inducibly interact with the intracellular region of TNF receptors (TNFRs). Because the TNFRs lack intrinsic catalytic activity, the TRAFs are hypothesized to orchestrate signaling activation downstream of the TNFR superfamily, however their mechanism of activation remains unclear (Inoue et al., 2000; Bishop, 2004). Originally, the TRAFs were compared to the signal transducers and activators of transcription (STAT) protein family, due to their sequence homology, and the presence of multiple RING- and zinc-finger domains, suggesting that their function may be to regulate transcriptional activity (Rothe et al., 1994; Hu et al., 1994; Sato et al. 1995; Cheng et al., 1995). However, subsequent research focused predominantly on their cytoplasmic functions, and more recently on their function as E3 ubiquitin ligases (Pineda et al., 2007). In my research, I analyzed the subcellular localizations of the TRAFs following CD40 ligand (CD40L)-stimulation, and found that TRAF2 and 3 rapidly translocate into the nucleus of primary neurons and Neuro2a cells. Interestingly, similar analysis conducted in pre-B lymphocytes (Daudi cells) revealed a different response to CD40L-stimulation, with TRAF2 and 3 being rapidly degraded within 5-minutes of stimulation. These findings are significant because they demonstrate for the first time that the TRAFs translocate into the nucleus and suggest that they may function within the nucleus in a cell-specific manner. I next analyzed the ability of TRAF2 and 3 to bind to DNA, and found that they both bind to chromatin and the NF-kappaB consensus element in Neuro2a cells, following CD40L-stimulation. Similar analyses of the chromatin binding of TRAF2 and 3 in Daudi cells revealed that they were rapidly degraded, similar to the results from my analysis of their subcellular localization. These findings show for the first time that the TRAFs interact with DNA, and therefore support the hypothesis that the TRAFs may function within the nucleus as transcriptional regulators. Finally, I analyzed the ability of the TRAFs to regulate transcriptional activity by luciferase assay. Previous studies showed that overexpression of TRAF2 and 6 could induce NF-kappaB transcriptional activity; however researchers have not been able to determine the mechanism by which they do so. In my studies, I found that every TRAF can directly regulate transcriptional activity either as co-activators or co-repressors of transcription, in a cell- and target protein-specific manner. Additionally, I found that TRAF2 can act as a transcriptional activator, and that its ability to regulate transcription is largely dependent upon the presence of its RING-finger domain. In conclusion, these studies have revealed an entirely novel function for the TRAFs as immediate-early transcriptional regulators. Future research into the genes that are regulated by the specific TRAF complexes will further elucidate how the TRAFs regulate TNFR signaling, as well as whether dysfunctions in TRAF signaling may be associated with known disorders. If specific TRAF complexes are found to regulate specific genes, then pharmacological targeting of the individual TRAF complexes may allow for the highly specific inhibition of signaling events downstream of the TNFRs, without compromising overall receptor signaling, transcription factor pathways, or cellular systems.
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Gardam, Sandra Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Regulation of lymphocyte development and function by TRAF2 and TRAF3." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/42104.

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Tumour necrosis factor receptor (TNFR) family members are widely expressed in cells of the immune system and are essential for the development and function of many immune cell types. The TNFR associated factor (TRAF) family are signal adapter molecules that are recruited to various members of the TNFR family and are important for the transduction of signals downstream of these receptors. In these studies, gene targeting was used to create a mouse capable of undergoing conditional inactivation of the Traf3 gene. These mice were studied alongside previously generated mice that were similarly genetically modified with respect to the Traf2 gene. The mice produced lacked expression of either TRAF2 or TRAF3 in either B or T cells. In resting B cells TRAF2 and TRAF3 were shown to cooperate to negatively regulate the signalling of B cell activating factor of the TNF family (BAFF) and its receptor (BAFF-R), the TNF ligand and receptor pair that provide obligate survival signals to B cells. Thus, TRAF2- and TRAF3-deficient B cells displayed hyperactive NF-kB2 signalling, an increased ability to survive, and almost identical gene expression profiles, emphasizing the cooperative nature of their roles in resting B cells. Importantly, the survival of these B cells was completely independent of BAFF. In normal B cells, BAFF signalling was shown to lift the negative regulation of survival mediated by TRAF2 and TRAF3, by depleting TRAF3 from the cell. This process was shown to require TRAF2. T cells deficient in TRAF2 or TRAF3 also displayed hyperactivity of the NF-kB2 pathway, but they did not accumulate in vivo or show extended survival in vitro. Mice lacking TRAF2 or TRAF3 in their T cells did however display a decrease in the number of memory phenotype CD8+ T cells. These studies indicate that some of the roles of TRAF2 and TRAF3 are common between B and T cells. However, the consequences of loss of TRAF2 or TRAF3 in B and T cells differs considerably, presumably due to the differential TNFR expression and usage by each cell type.
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Graham, John. "CD40-Induced TRAF degradation in immune regulation." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/808.

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CD40 is a TNF receptor superfamily (TNFRSF) member central to the development of many aspects of the adaptive immune response. CD40 signaling promotes adaptive immunity in part by inducing the expression of cytokines, chemokines, and various adhesion and co-stimulatory molecules. The family of cytoplasmic adapter proteins, the TNFR-associated factors (TRAFs), serve as major mediators of TNFRSF pathways. CD40 regulates itself in part via the signaling induced degradation of TRAF2 and TRAF3. However, the effect of CD40-induced TRAF degradation on other TRAF dependent pathways is unknown. Here I provide evidence that CD40-mediated degradation of TRAFs 2 and 3 also influences the responsiveness of immune cells to CD40-independent, TRAF2- and 3-dependent pathways. LMP1 is a functional mimic of CD40, but signals to B lymphocytes in an amplified and sustained manner. LMP1 contributes to the development of B cell lymphoma in immunosuppressed patients, and may exacerbate flares of certain autoimmune diseases. The cytoplasmic (CY) domain of LMP1 binds TRAF2 with lower avidity than the CY domain of CD40, and TRAF2 is needed for CD40-mediated degradation of TRAFs 2 and 3. LMP1 doesn't induce TRAF degradation, and employs TRAF3 as a positive mediator of cell signaling, whereas CD40 signals are inhibited by TRAF3. Here, I tested the hypothesis that relative affinity for TRAF2, and/or distinct sequence differences in the TRAF2/3 binding sites of CD40 vs. LMP1, controls the disparate ways in which CD40 and LMP1 use TRAFs 2 and 3. The results revealed that TRAF binding affinity and TRAF binding site sequence dictate a distinct subset of CD40 vs. LMP1 signaling properties. The E3 ubiquitin ligases, cIAP1 and cIAP2, have been reported to play a crucial role in CD40 signaling. Because LMP1 is a mimic of CD40 signals, I hypothesized that LMP1 requires the cIAPs for signaling. To elucidate the role of the cIAPs in CD40 and LMP1 signaling, I specifically depleted the cIAPs and found that the cIAPs are differentially utilized in CD40 and LMP1 signaling. I also sought to further the understanding of the molecular underpinnings of how CD40, but not LMP1 signaling induces TRAF2 and TRAF3 degradation upon signaling. To do this, I investigated the ability of various CD40 and LMP1 mutants to induce TRAF degradation in distinct TRAF or cIAP deficient models. I found that neither a high TRAF2 binding potential nor the presence of the cIAP molecules are required for this process. Thus, this work reveals important insights into the molecular mechanisms of and role of CD40-mediated TRAF degradation in the immune system.
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Hauer, Julia. "Signaltransduktion durch TRAF-bindende Mitglieder der TNF-Rezeptor-Superfamilie (TNFR-SF)." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57662.

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Anto, Michel Nathaly [Verfasser], Andreas [Akademischer Betreuer] Zirlik, and Rudolf [Akademischer Betreuer] Grosschedl. "The role of tumor necrosis associated factor (TRAF)-1 in cardio-metabolic disease." Freiburg : Universität, 2017. http://d-nb.info/1173086897/34.

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Foight, Glenna Wink. "Determinants of protein-peptide interaction specificity in the Bcl-2 and TRAF families." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/101350.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, September 2015.
Cataloged from PDF version of thesis. "September 2015."
Includes bibliographical references.
Protein-peptide interactions have important roles in the majority of cellular processes. There are many families of peptide recognition domains in which homologous members display differential binding preferences for peptide sequence features. Peptide binding specificity is critical for the functional roles played by each family member, which can be overlapping or distinct. The two peptide recognition domain families discussed in this work, Bcl-2 and TRAF proteins, have roles in cellular processes including apoptosis, inflammation, and immunity. Aberrant function of these proteins has been linked to a variety of diseases. There is great interest in understanding the mechanistic basis of protein-peptide binding specificity in these families and others. An improved understanding will enable models of binding preferences for interactome prediction and design of specific peptide reagents for the inhibition and study of protein-peptide interactions. The anti-apoptotic Bcl-2 family members bind [alpha]-helical Bcl-2-homology 3 (BH3) motifs in pro-apoptotic Bcl-2 family members to prevent apoptosis. Kaposi Sarcoma herpesvirus and Epstein Barr herpesvirus express viral homologs of the anti-apoptotic Bcl-2 proteins, KSBcl-2 and BHRF 1, respectively, during viral replication to prevent host cell death. Because human Bel- 2 proteins are important in preventing apoptosis in cancers, there is interest in targeting the viral homologs, as they may also have a role in herpesvirus-associated malignancies. I designed and screened libraries of BH3 peptide variants for binding specificity to KSBcl-2 and BHRF 1. From library screening and additional rational mutagenesis, I developed peptides that showed specific binding to KSBcl-2, BHRF 1, or the human homolog Ml- 1, and displayed large margins of specificity over the other human Bel-2 homologs. TRAF proteins bind sequences in the unstructured regions of cell surface receptors and other adapter proteins in order to mediate downstream signaling events. TRAF-peptide binding preferences are relatively uncharacterized. I adapted a bacterial surface display system for screening peptides for TRAF binding. Using this system, I explored the binding preferences of TRAFs 2, 3, and 5 to single and double mutant libraries of two peptide interaction partners from CD40 and TANK. Comparison of the enriched peptide sequences reveals a surprising degree of difference between these three close TRAF homologs, yielding hypotheses relevant to TRAF function and inhibition.
by Glenna Wink Foight.
Ph. D.
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Bani, Younes Maram Younis Saleh. "Efficient Traffic Control Protocols for Vehicular Ad-Hoc Networks." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32060.

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Traffic efficiency applications over road networks have been investigated recently using VANETs. This area of research is primarily concerned with increasing the traffic fluency over road networks. In this thesis, we first propose an efficient and accurate protocol to detect congested road segments in a downtown area using VANETs. We refer to this protocol as the Efficient COngestion DEtection (ECODE) protocol. ECODE evaluates three different traffic characteristics of each road segment including traffic speed, traffic density, and the time required to travel the segment. Moreover, ECODE evaluates traffic characteristics and detects the congestion level in each direction of the road segment. In addition, we propose an intelligent, dynamic, distributed, and real-time path recommendations protocol. We refer to this protocol as Intelligent path reCOmenDation (ICOD) protocol. ICOD is the first path recommendation protocol that does not rely on a central database of gathered traffic data for each area of interest. Eliminating centralized behavior resolves bottleneck as well as single point of failure problems, which in turn minimizes congestion and collision problems in VANETs. Furthermore, ICOD selects the path towards each destination in a hop-by-hop manner, which makes the turn decision at each road intersection more accurate and real-time. Different variants of ICOD are introduced that consider travel time, travel distance, fuel consumption, gas emissions, and context-awareness of each road segment parameters. Moreover, two traffic balancing mechanisms are proposed in this thesis to distribute traffic over the road network evenly, namely Bal-Traf and Abs-Bal. These mechanisms eliminate the highly congested road segment scenarios that are caused by the path recommendation protocol. Bal-Traf detects and eliminates the highly congested output road segment at each road intersection. However, Abs-Bal aims to keep the traffic density balanced among all output road segments at each road intersection. Finally, we propose an Intelligent Traffic Light Controlling (ITLC) algorithm to schedule the phases of each traffic light at isolated road intersections. This algorithm aims to decrease the queuing delay time of competing traffic flows and to increase the throughput of each signalized road intersection. ITLC has also been adapted in this thesis to the Arterial Traffic Lights (ATLs) algorithm for arterial road network scenarios. In ATLs the expected platoons on the arterial street are considered in the scheduling algorithm of each traffic light located on the arterial street coordinates. Transmitting packets among these traffic lights report the main characteristics of each predicted platoon.
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CAZZANIGA, FEDERICO ANGELO. "IL RUOLO DEL PATHWAY SOCS-1/TRAF-6 NELL'INCREMENTO DELL'OSTEOCLASTOGENESI IN PAZIENTI HIV+ IN CART." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/548313.

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Up to 30% of cART treated HIV-infected patients show an early onset osteopenia/osteoporosis, leading to a significant increase in the risk of fractures. The pathogenic molecular mechanisms remain poorly understood. However, it has been shown that, in HIV transgenic rats model, osteoclasts (OCs) express high levels of suppressor of cytokine signaling-1 (SOCS-1) and tumor necrosis factor receptor-associated factor-6 (TRAF-6), inducing an increased osteoclastogenesis through IFN-γ pathway inhibition. Given these premises, our study aims to investigate osteoclastogenesis and SOCS-1/TRAF-6 pathways in human peripheral blood-derived-OCs of HIV positive cART-treated patients with and without reduced BMD (Bone Mineral Density). Material and Methods. We consecutively enrolled 40 HIV+ patients on virally-effective cART (HIV-RNA <40cp/ml) matched for viro-immunologic/demographic features: 16 resulted with normal BMD (nBMD) by dual x-ray absorptiometry (osteopenia, z-score -1/-2.5; osteoporosis, z-score <-2.5), 24 with reduced BMD (rBMD, including osteopenic and osteoporotic patients). We enrolled 15 HIV-negative as healthy controls (HIV-). Circulating OC precursors (OCPs; CD14+CD11b+CD51/61+ and C14+/CD16++) were studied by flow-cytometry. OCs were differentiated from peripheral blood-purified CD14+ supplemented with M-CFS and RANKL (8 days). OCs differentiation/maturation was evaluated by: TRAP staining and dentin resorption. RANK, SOCS-1, TRAF6, MMP-9 and CTSK expression of OCs ex vivo differentiated were analyzed by Real-Time PCR and Western-Blot with and without IFN-γ stimulation (100 U, 2 h). Kruskal-Wallis, Mann–Whitney and ANCOVA were used. Results. Higher levels of OCPs (CD14+CD11b+CD51/61+ and C14+/CD16++) were observed in HIV+ rBMD group compared to HIV+ nBMD (respectively, p=.0001; p=.0068). CD14+ cultures from HIV+ rBMD were enriched in large multinucleated TRAP+ OCs versus nBMD and HIV- (p=.012; p=.023), as confirmed by TRAP quantification (p=.038; p=.04). Interestingly, OCs from HIV+ rBMD expressed significantly higher SOCS-1 and TRAF-6: > 2.14, >1.65 fold vs HIV-, respectively, significantly higher than nBMD (p=.027; p=.014). IFN-γ challenge resulted in an up-regulation of SOCS-1 in HIV+ rBMD/nBMD OCs and HIV- OCs, respectively (p=.0022; p=.0057; p=.0013). Despite this, only in HIV+ rBMD we detected an increasing in TRAF-6 (p=.024). No difference was found in MMP-9, on the contrary we observed an increasing trend of CTSK mRNA expression in HIV+ rBMD OCs. Interestingly, ANCOVA test demonstrated an interaction between SOCS-1/ TRAF-6 upregulation, HIV infection and bone impairment (p=.003, p=.025). Conclusion. HIV+ rBMD patients show increased circulating OCPs and OCs ex-vivo differentiation, indicating heightened osteoclastogenesis in treated HIV+ osteopenic/osteoporotic patients. Relevantly, we show that OCs from HIV+ rBMD express high SOCS-1/TRAF-6 levels, that are further upregulated upon IFN-γ challenge. Together, these findings identify deregulated SOCS-1/TRAF-6 as molecular pro-osteoclastogenesis pathway that might be sustained by abnormal interferon-mediated inflammation in successfully-treated HIV.
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Cartier, Jessy. "Influence de clAP1 sur la prolifération cellulaire." Thesis, Dijon, 2010. http://www.theses.fr/2010DIJOS016.

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La protéine cIAP1 (cellular Inhibitor of Apoptosis Protein-1) de la famille des IAP (Inhibitor of Apoptosis Protein) est une E3 ubiquitine ligase qui présente des propriétés oncogéniques. Notre équipe s’intéresse aux processus permettant la différenciation des monocytes en macrophages. Au cours de la différenciation de nombreux modèles cellulaires (macrophages, cellules dendritiques, cellules épithéliales du colon, cellules souches hématopoïetiques, cardiomyocytes), cIAP1 sort du noyau pour se relocaliser dans le cytoplasme. La plupart des fonctions connues de cIAP1 sont liées à sa localisation cytoplasmique où elle est un régulateur important des voies de signalisation des récepteurs du TNFα et de NF-κB. Lors de la différenciation macrophagique, nous avons montré que cIAP1, une fois dans le cytoplasme, induit la dégradation de TRAF-2, un adaptateur moléculaire impliqué dans la transduction du signal des voies des récepteurs du TNFα et de NF-κB. Cette dégradation bloque la voie canonique de NF-κB et est essentielle à la différenciation terminale des monocytes en macrophages qui nécessite une activation transitoire de cette voie de signalisation. Cependant, cIAP1 est principalement exprimée dans le noyau de différents types cellulaires ce qui n’est pas en accord avec son rôle dans la signalisation cellulaire. Mon objectif a donc consisté à identifier les fonctions nucléaires de cIAP1 dans des cellules prolifératives ou lors de la différenciation macrophagique. Mon travail de thèse a permis d’identifier un rôle de cIAP1 dans la prolifération cellulaire. cIAP1 interagit avec le facteur de transcription E2F1 et favorise son recrutement sur les promoteurs des Cycline E et A impliquées dans les transitions G1/S et G2 du cycle cellulaire, ce qui augmente l’expression des transcrits et des protéines de ces deux cibles. Il semblerait que par cette activité, cIAP1 régule la prolifération des cellules et soit important dans l’équilibre entre la prolifération et la différenciation, deux mécanismes cellulaires étroitement liés
The inhibitor of apoptosis protein cIAP1 (cellular inhibitor of apoptosis protein-1) from the IAP family (Inhibitor of Apoptosis Protein) is an E3 ubiquitin ligase that displays oncogenic properties. Our team is interested in the mecanisms that allow macrophagic differentiation from monocytes. cIAP1 is relocalised from the nucleus to the cytoplasm during the differentiation of many kind of cellular models (macrophages, dendritic cells, colon epithelial cells, hematopoietic stem cells, cardiomyocytes). The well-known functions of cIAP1 are associated with its cytoplasmic localisation, where it regulates the TNFα receptors and NF-κB signalling pathways. During macrophage differentiation, we show that cIAP1, once it is in cytoplasm, induces TRAF-2 degradation, a molecular adaptator of the TNFα receptors family and NF-κB signalling pathways. This degradation blocks the canonical pathway of NF-κB and is essential for the terminal differentiation into macrophages that needs a transitory activation of this pathway. However, cIAP1 is mainly expressed in the nucleus on many cell types which is not in accordance with its cell signalling activity. My objective was to investigate the nuclear function of cIAP1 in proliferative cells or during macrophage differentiation. My work identifies a function of cIAP1 in proliferation regulation. cIAP1 interacts with E2F1 transcription factor and favors its recruitment on Cyclins E and A promoters, both involved in G1/S and G2 phases of the cell cycle, which leads to high level of transcript and protein expression of these two targets. It seems that cIAP1 regulates the cellular proliferation and is important for the balance between proliferation and differentiation, two mechanisms tightly connected in cells
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Silva, Rodrigo Borsatto Sommer da. "Projeto destinos indutores: avanços e desafios do TRAF - Turismo Rural na Agricultura Familiar em Rancho Queimado (SC)." Universidade do Estado de Santa Catarina, 2010. http://tede.udesc.br/handle/handle/1408.

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O Projeto Destinos Indutores é uma proposta do MTur - Ministério do Turismo para estruturar 65 destinos indutores com qualidade turística internacional. Deste projeto reservou-se 10 destinos para atender a estruturação de segmentos turísticos. Entre esses está o TRAF - Turismo Rural na Agricultura Familiar que deve ser organizado e estruturado por quatro municípios de Santa Catarina, entre eles Rancho Queimado. O TRAF é um segmento turístico realizado no espaço rural, que busca por meio da aproximação entre turistas e agricultores familiares, a valorização do patrimônio cultural e do meio ambiente local. Certamente a organização, planejamento e a presença do GTTuR Grupo Técnico de Turismo Rural e da Associação de Agroturismo Acolhida na Colônia foram fatores determinantes na escolha de Santa Catarina como referência do TRAF no Brasil. O diálogo sobre esse segmento está voltado a entender como o TRAF pode ser utilizado como ferramenta de estímulo a participação popular no planejamento e organização do turismo municipal. Para isso, se utilizou as ideias de desenvolvimento socioespacial e autonomia para auxiliar a compreensão das dinâmicas sociais ocorridas no município de Rancho Queimado. Por conta disso, essa pesquisa busca analisar a contribuição do Projeto Destinos Indutores para a participação comunitária no planejamento e organização do turismo rural na agricultura familiar de Rancho Queimado (SC). Através desses objetivos pretende-se entender: como o Projeto Destinos Indutores pode incentivar a participação comunitária na organização do turismo rural na agricultura familiar em Rancho Queimado? Essa pesquisa caracteriza-se quanto à abordagem do problema como qualitativa e de cunho exploratório. O método de procedimento é o estudo de caso
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Books on the topic "TRAF"

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Watts, G. R. Traf fic induced vibrations in buildings. Crowthorne: Vehicles and Environment Division, Vehicles Group, Transportand Road Research Laboratory, 1990.

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Grabowski, Wojciech. Archi-traf: Opowieści o architekturze Śląska i Zagłębia. Katowice: Wydawnictwo "Śląsk", 2015.

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Lehti, Martti. Traf ficking in human beings, illegal immigration and Finland. Helsinki, Finland: HEUNI, European Institute for Crime Prevention and Control, affiliated with the United Nations, 2002.

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Čabaravdić-Kamber, Emina. Der Schänder: Nach Jahren traf sie ihn wieder ... : eine Erzählung. Hundorf: Edition Nordwindpress, 1998.

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National Highway Institute (U.S.), ed. TRAF-CORFLO training course: Participant workbook : NHI course no. 13367. [Washington, D.C.?]: U.S. Dept. of Transportation, Federal Highway Administration, National Highway Institute, 1994.

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Paluch, Andrea. Der Tag, an dem ich meinen toten Mann traf: Roman. München: Piper, 2005.

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National Highway Institute (U.S.), ed. TRAF-CORFLO training course: Participant workbook : NHI course no. 13367. [Washington, D.C.?]: U.S. Dept. of Transportation, Federal Highway Administration, National Highway Institute, 1994.

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Buch, Hans Christoph. Wie Karl May Adolf Hitler traf und andere wahre Geschichten. Berlin: Eichborn, 2003.

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Golz, Jochen, Klaus-Martin Bresgott, and Volker G. Probst. "In Güstrow traf ich-- ": Von Runge bis Barlach - Goethe und Mecklenburg. Güstrow: Graphikkabinett, Ernst Barlach Stiftung, 2004.

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Jacobson, Eldon L. Evaluation of the TRAF family of models: Testing of the CORFLO and FRESIM models : final report, Research Project GC 8286, Task 17, TRAF Software for I-405 Lane Construction. [Olympia, Wash.?]: Washington State Dept. of Transportation, Washington State Transportation Commission, Transit, Research, and Intermodal Planning (TRIP) Division, in cooperation with U.S. Dept. of Transportation, Federal Highway Administration, 1992.

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Book chapters on the topic "TRAF"

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Roser, Traugott, and Margit Gratz. "Und dann traf es mich selbst …" In Wie viel Tod verträgt das Team?, 126–36. Göttingen: Vandenhoeck & Ruprecht, 2014. http://dx.doi.org/10.13109/9783666403415.126.

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Wajant, H., and P. Scheurich. "Analogies Between Drosophila and Mammalian TRAF Pathways." In Invertebrate Cytokines and the Phylogeny of Immunity, 47–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-18670-7_3.

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Reichardt, Anna D., Jose Pindado, Shivam A. Zaver, and Genhong Cheng. "TRAF Protein Function in Noncanonical NF-κB Signaling." In Methods in Molecular Biology, 247–68. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2422-6_14.

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Samsonowicz, Henryk. "Wer traf die Entscheidungen in den selbstverwalteten Städten des mittelalterlichen Polen?" In Rechtsstadtgründungen im mittelalterlichen Polen, 373–84. Köln: Böhlau Verlag, 2011. http://dx.doi.org/10.7788/boehlau.9783412213848.373.

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Kawabata, Hideyuki, Yuta Tanaka, Mai Kimura, and Tetsuo Hironaka. "Traf: A Graphical Proof Tree Viewer Cooperating with Coq Through Proof General." In Programming Languages and Systems, 157–65. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02768-1_9.

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Wong, Shui-Ying. "Capacity and level of service by simulation – A case study of TRAF-NETSIM." In Highway Capacity and Level of Service, 467–83. London: Routledge, 2021. http://dx.doi.org/10.1201/9780203751916-48.

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Schäffner, Christina. "Translation studies." In Handbook of Pragmatics, 1412–26. Amsterdam: John Benjamins Publishing Company, 2022. http://dx.doi.org/10.1075/hop.m2.tra1.

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O’Connell, Daniel C., and Sabine Kowal. "Transcription systems for spoken discourse." In Handbook of Pragmatics, 1839–51. Amsterdam: John Benjamins Publishing Company, 2022. http://dx.doi.org/10.1075/hop.m2.tra2.

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Holmen, Anne. "Translanguaging pedagogy." In Handbook of Pragmatics, 1404–11. Amsterdam: John Benjamins Publishing Company, 2022. http://dx.doi.org/10.1075/hop.m2.tra3.

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Schäffner, Christina. "Translation studies." In Handbook of Pragmatics, 1–21. Amsterdam: John Benjamins Publishing Company, 2011. http://dx.doi.org/10.1075/hop.15.tra1.

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Conference papers on the topic "TRAF"

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Qi, Jiayin, Hongli Zhang, Zhenzhou Ji, and Liu Yun. "Analyzing BitTorrent Traf?c Across Large Network." In 2008 International Conference on Cyberworlds (CW). IEEE, 2008. http://dx.doi.org/10.1109/cw.2008.150.

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Guo, Rong, Tong Wu, and Xiaochen Wu. "Characteristics of Spatial Connection Based on Intercity Passenger Traffic Flow in Harbin-Changchun Urban Agglomeration, China." In Post-Oil City Planning for Urban Green Deals Virtual Congress. ISOCARP, 2020. http://dx.doi.org/10.47472/vhps3943.

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With the continuous improvement of transportation facilities and information networks, the obstruction of distance in geographic space has gradually weakened, and the hotspots of urban geography research have gradually changed from the previous city hierarchy to the characteristics of urban connections and networks. As the main carrier and manifestation of elements, mobility such as people and material, traf ic flow is of great significance for understanding the characteristics of spatial connection. In this paper, Harbin-Changchun agglomeration proposed by China's New Urbanization Plan (2014-2020) is taken as a research object. With the data of intercity passenger traf ic flow including highway and railway passenger trips between 73 county-level spatial units in the research area, a traf ic flow model is constructed to measure the intensity of spatial connection. Using social network analysis method, the characteristics of spatial connection of Harbin-Changchun urban agglomeration are analyzed, and the results are visualized with ArcGIS technique. The results show that the spatial connection of the Harbin-Changchun urban agglomeration based on traf ic flow presents a distance attenuation ef ect that weakens in the directions of "Harbin-Daqing-Qiqihar-Mudanjiang" and "Changchun-Jilin-Tumen", and the connection strength of Harbin or Changchun districts and other spatial units is the strongest, follow by Daqing, Qiqihar or Jilin districts and other spatial units; the network is highly centralized, the core city has the dominant role on the whole network, and the connection between network nodes is not balanced; the connection nodes present a dual- core-edge hierarchical distribution; the network based on railway shift of Harbin-Changchun urban agglomeration can be divided into four subgroups,showing block distribution characteristic in Harbin-Changchun urban agglomeration. The research can provide support for the proposal of regionally coordinated sustainable development strategies of Harbin-Changchun urban agglomeration.
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Xuemei Zhu and Zucheng Liu. "Estimation of traf efficiencies in a distillation column sfstem." In 2nd International Conference on Computer and Automation Engineering (ICCAE 2010). IEEE, 2010. http://dx.doi.org/10.1109/iccae.2010.5451335.

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Feng, Shibing, Jian Tang, Ming Zhao, Zhen Zhang, and Hengchang Liu. "Traf: A Camera based System for Traffic Flow Analysis." In 2017 International Conference on Mechanical, Electronic, Control and Automation Engineering (MECAE 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/mecae-17.2017.64.

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Wang, Xiaoming, and David J. Parish. "Optimised TCP Traf“c Classi“cation with multiple statistical algorithms." In 2010 International Conference on Information, Networking and Automation (ICINA 2010). IEEE, 2010. http://dx.doi.org/10.1109/icina.2010.5636393.

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Eittenberger, Philipp M., and Udo R. Krieger. "Atheris: A First Step Towards a Uni?ed Peer-to-Peer Traf?c Measurement Framework." In 2011 19th Euromicro International Conference on Parallel, Distributed and Network-Based Processing (PDP). IEEE, 2011. http://dx.doi.org/10.1109/pdp.2011.34.

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Poli, Francesco, Michele Marconcini, Roberto Pacciani, Donato Magarielli, Ennio Spano, and Andrea Arnone. "Exploiting GPU-Based HPC Architectures to Accelerate an Unsteady CFD Solver for Turbomachinery Applications." In ASME Turbo Expo 2022: Turbomachinery Technical Conference and Exposition. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/gt2022-82569.

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Abstract Aircraft engine designers are nowadays facing more and more challenges: they strive to reduce fuel consumption, obtain better engine performance, and create quieter, safer, and environmentally friendlier products. One of the key factors to achieve these goals is the availability of numerical simulation tools able to accurately predict engine behavior and of hardware/software platforms where the tools can successfully run. However, accurate numerical simulations, particularly unsteady Computational Fluid Dynamics (CFD) ones based on sophisticated solvers, are time-consuming and demanding in terms of hardware resources. This may limit the industrial applicability of these methods. A possible strategy to overcome this problem is the acceleration of numerical solvers on advanced High Performance Computing (HPC) architectures, in order to reduce the execution time down to values compatible with industrial needs. Traf is a CFD solver for steady/unsteady three-dimensional Reynolds-averaged Navier-Stokes equations. It is developed at the University of Florence, with a special focus on turbomachinery applications. The current production release is a parallel code that runs on CPU-based platforms. A new version of Traf has been ported to and optimized for GPU-based HPC architectures, in order to dramatically accelerate CFD analyses. The code has been tested on an industrial-grade use case concerning a low-pressure turbine module for aeronautical applications in the context of the EU H2020 funded project LEXIS (Large-Scale Execution for Industry & Society, GA 825532), comparing its performance with the CPU-based release and obtaining promising results. To this aim, the speedup weighted to account for the different hardware cost is selected as a meaningful Key Performance Indicator (KPI).
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Lioris, Jennie, Pravin Varaiya, and Alexander Kurzhanskiy. "Performance Evaluation of Alternative Traf?c Signal Control Schemes for an Arterial Network by DES Approach-Overview." In Proceedings of The 9th EUROSIM Congress on Modelling and Simulation, EUROSIM 2016, The 57th SIMS Conference on Simulation and Modelling SIMS 2016. Linköping University Electronic Press, 2018. http://dx.doi.org/10.3384/ecp17142265.

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Liu-Mares, Wen, Jennifer J. Hu, Ioanna Konidari, Glenn O. Allen, Peter E. Clark, M. Craig Hall, Chuanhui Dong, J. Sunil Rao, and William K. Scott. "Abstract 2771: Genetic variation in interleukin, TLR, TNF and TRAF genes of NF-κB activation pathway and risk of prostate cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2771.

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Agnolucci, Andrea, Michele Marconcini, Andrea Arnone, Lorenzo Toni, Angelo Grimaldi, and Marco Giachi. "Centrifugal Compressor Stage Efficiency and Rotor Stiffness Augmentation via Artificial Neural Networks." In ASME Turbo Expo 2021: Turbomachinery Technical Conference and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/gt2021-59998.

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Abstract Centrifugal compressor stages with high rotor stiffness (i.e. impeller hub-to-outer-diameter ratio) may represent a crucial element to cope with tight rotordynamic requirements and constraints that are needed for certain applications. On the other hand, high-stiffness has a detrimental effect on the aerodynamic performance. Thus, an accurate design and optimization are required to minimize the performance gap with respect to low-stiffness stages. This paper shows a redesign and optimization procedure of a centrifugal compressor stage aimed at increasing the impeller stiffness while keeping high aerodynamic performance. Two different optimization steps are employed to consider a wide design space while keeping the computational cost as low as possible. At first the attention is focused on the impeller only, then the diffuser and the return channel are taken into account. The multi-objective and multi-operating point optimization makes use of artificial neural networks (ANNs) as a surrogate model to obtain the response surfaces. RANS calculations are carried out using the TRAF code and are employed to create the training dataset. Once the ANN has been trained, an optimization strategy is used to find the constrained optimum geometries for the impeller and the static components. The optimized high-stiffness stage is finally compared to the low-stiffness one to assess its applicability.
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Reports on the topic "TRAF"

1

Fujiwara, Ippei, Tomoyuki Nakajima, Nao Sudo, and Yuki Teranishi. Global Liquidity Trap. Cambridge, MA: National Bureau of Economic Research, March 2011. http://dx.doi.org/10.3386/w16867.

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Caballero, Ricardo, and Emmanuel Farhi. The Safety Trap. Cambridge, MA: National Bureau of Economic Research, February 2014. http://dx.doi.org/10.3386/w19927.

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Boissay, Frédéric, and Russell Cooper. The Collateral Trap. Cambridge, MA: National Bureau of Economic Research, November 2014. http://dx.doi.org/10.3386/w20703.

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Kıbrıs, Arzu. The polarization trap. Sabancı University, September 2012. http://dx.doi.org/10.5900/su_fass_wp.2012.19320.

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Badel, Alejandro. An American Inequality Trap. Federal Reserve Bank of St. Louis, 2010. http://dx.doi.org/10.20955/wp.2010.047.

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Burger, Leland L., and Randall D. Scheele. HWVP Iodine Trap Evaluation. Office of Scientific and Technical Information (OSTI), September 2004. http://dx.doi.org/10.2172/15009659.

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Hamlet, Benjamin Roger. Ion trap simulation tools. Office of Scientific and Technical Information (OSTI), February 2009. http://dx.doi.org/10.2172/983695.

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Lagos-Kutz, Doris, and David Voegtlin. Midwest Suction Trap Network. Ames: Iowa State University, Digital Repository, 2015. http://dx.doi.org/10.31274/farmprogressreports-180814-1811.

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Lagos-Kutz, Doris, and David Voegtlin. Midwest Suction Trap Network. Ames: Iowa State University, Digital Repository, 2015. http://dx.doi.org/10.31274/farmprogressreports-180814-2711.

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Lagos-Kutz, Doris, and David Voegtlin. Midwest Suction Trap Network. Ames: Iowa State University, Digital Repository, 2015. http://dx.doi.org/10.31274/farmprogressreports-180814-437.

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Journal articles Dissertations / Theses Books
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