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Academic literature on the topic 'MTOB'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "MTOB"

1

ROCH, Anne-Marie, Gerard QUASH, Yvonne MICHAL, Jacqueline CHANTEPIE, Bernard CHANTEGREL, Christian DESHAYES, Alain DOUTHEAU, and Jacqueline MARVEL. "Altered methional homoeostasis is associated with decreased apoptosis in BAF3 bcl2 murine lymphoid cells." Biochemical Journal 313, no. 3 (February 1, 1996): 973–81. http://dx.doi.org/10.1042/bj3130973.

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Methional is a potent inducer of apoptosis in an interleukin 3-dependent murine lymphoid cell line BAF3 b0 when it is added to the culture medium. In these cells transfected with the bcl2 gene, BAF3 bcl2, the apoptotic-inducing activity of methional is dramatically reduced. The addition of disulfiram (an inhibitor of aldehyde dehydrogenase) in order to reduce methional oxidation brought about an increase in apoptosis in BAF3 b0 but not in BAF3 bcl2 cells. In contrast, the addition of quercetin (an inhibitor of aldehyde reductase) in an attempt to diminish methional reduction increased apoptosis in both BAF3 b0 and BAF3 bcl2 cells. The extent of DNA fragmentation in BAF3 bcl2 cells approached that in BAF3 b0 cells in the presence of quercetin and exogenous methional, suggesting a defect in methional biosynthesis in BAF3 bcl2 cells. Direct evidence for this was obtained by measuring labelled methional in cells incubated with the sodium salt of [U-14C]4-methylthio-2-oxobutanoic acid (MTOB), the precursor of methional. The 80% decrease in labelled methional in BAF3 bcl2 compared with BAF3 b0 cells was accompanied by a concomitant rise in the transamination of [14C]MTOB to [14C]methionine in BAF3 bcl2 cells. Inhibition of the transaminase, however, by a synthetic transition-state-type compound, pyridoxal-L-methionine ethyl ester, induced apoptosis in BAF3 b0 but not in BAF3 bcl2 cells, confirming that the defect in BAF3 bcl2 cells was not in the transaminase itself but rather in the oxidative decarboxylation step MTOB →methional. In addition, no evidence was obtained for the synthesis of [14C]malondialdehyde from [14C]methional in BAF3 bcl2 cells. As these cells show no deficiency in their content of reactive oxygen species compared with that of BAF3 b0 cells, they may possess some other defect in the β-hydroxylase enzyme system itself.

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Zhu, Lin, Jing Wu, and Hong Liu. "Downregulation of HERC5 E3 ligase attenuates the ubiquitination of CtBP1 to inhibit apoptosis in colorectal cancer cells." Carcinogenesis 42, no. 8 (June 19, 2021): 1119–30. http://dx.doi.org/10.1093/carcin/bgab053.

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Abstract The homologous to E6AP C-terminus (HECT) domain and RCC1-like domain-containing (HERC) proteins can function as tumour suppressors and as oncogenes, depending on the cancer type. However, the expression patterns of HERCs in colorectal cancer (CRC) cells are unclear. Here, we show that only HERC1 and HERC5 are downregulated in CRC tumours, and we focus our study on revealing HERC5-mediating signalling because the change in downregulation is much more obvious for HERC5 than for HERC1. We demonstrate that HERC5 recruits an adaptor protein, CREB-binding protein, to ubiquitinate C-terminal binding protein 1 (CtBP1) in non-cancerous colon cells. The downregulation of HERC5 in CRC cells attenuates the ubiquitination of CtBP1, which then accumulates and assembles into a transcriptional complex with histone deacetylase 1 and a transcription factor c-MYC. This transcriptional complex binds to the promoters of three proapoptotic genes, Bcl2 associated X (BAX), Bcl2 interacting killer (BIK) and p53upregulated modulator of apoptosis (PUMA), and inhibits their expression, thereby suppressing apoptotic signalling and promoting tumourigenesis. Overexpression of HERC5, downregulation of CtBP1 or blocking of the CtBP1 function with its inhibitors (NSC95397 and 4-methylthio-2-oxobutyric acid [MTOB]) significantly prevents CRC cell proliferation in vitro and tumour growth in vivo. Combining NSC95397 (or MTOB) with chemotherapeutic drugs (oxaliplatin or capecitabine) gives a much stronger inhibition of cell proliferation and tumour growth compared with their single treatments. Collectively, our results reveal that downregulation of HERC5 E3 ligase attenuates the ubiquitination of CtBP1 to inhibit apoptosis. Therefore, CtBP1 may be a promising target in CRC chemotherapy.

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Hilbert, Brendan J., Steven R. Grossman, Celia A. Schiffer, and William E. Royer. "Crystal structures of human CtBP in complex with substrate MTOB reveal active site features useful for inhibitor design." FEBS Letters 588, no. 9 (March 19, 2014): 1743–48. http://dx.doi.org/10.1016/j.febslet.2014.03.026.

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Reyes-Hernández, Blanca Jazmín, Svetlana Shishkova, Rachel Amir, Aranza Xhaly Quintana-Armas, Selene Napsucialy-Mendivil, Rocio Guadalupe Cervantes-Gamez, Héctor Hugo Torres-Martínez, Jesús Montiel, Christopher D. Wood, and Joseph G. Dubrovsky. "Root stem cell niche maintenance and apical meristem activity critically depend on THREONINE SYNTHASE1." Journal of Experimental Botany 70, no. 15 (April 11, 2019): 3835–49. http://dx.doi.org/10.1093/jxb/erz165.

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AbstractIndeterminate root growth depends on the stem cell niche (SCN) and root apical meristem (RAM) maintenance whose regulation permits plasticity in root system formation. Using a forward genetics approach, we isolated the moots koom1 (‘short root’ in Mayan) mutant that shows complete primary RAM exhaustion and abolished SCN activity. We identified that this phenotype is caused by a point mutation in the METHIONINE OVERACCUMULATOR2 (MTO2) gene that encodes THREONINE SYNTHASE1 and renamed the mutant as mto2-2. The amino acid profile showed drastic changes, most notorious of which was accumulation of methionine. In non-allelic mto1-1 (Arabidopsis thaliana cystathionine gamma-synthetase1) and mto3-1 (S-adenosylmethionine synthetase) mutants, both with an increased methionine level, the RAM size was similar to that of the wild type, suggesting that methionine overaccumulation itself did not cause RAM exhaustion in mto2 mutants. When mto2-2 RAM is not yet completely exhausted, exogenous threonine induced de novo SCN establishment and root growth recovery. The threonine-dependent RAM re-establishment in mto2-2 suggests that threonine is a limiting factor for RAM maintenance. In the root, MTO2 was predominantly expressed in the RAM. The essential role of threonine in mouse embryonic stem cells and in RAM maintenance suggests that common regulatory mechanisms may operate in plant and animal SCN maintenance.

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Cerni, Stephen, Dylan Shafer, Kimberly To, and Vishwanath Venketaraman. "Investigating the Role of Everolimus in mTOR Inhibition and Autophagy Promotion as a Potential Host-Directed Therapeutic Target in Mycobacterium tuberculosis Infection." Journal of Clinical Medicine 8, no. 2 (February 11, 2019): 232. http://dx.doi.org/10.3390/jcm8020232.

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Tuberculosis (TB) is a serious infectious disease caused by the pathogen Mycobacterium tuberculosis (Mtb). The current therapy consists of a combination of antibiotics over the course of four months. Current treatment protocols run into problems due to the growing antibiotic resistance of Mtb and poor compliance to the multi-drug-resistant TB treatment protocol. New treatments are being investigated that target host intracellular processes that could be effective in fighting Mtb infections. Autophagy is an intracellular process that is involved in eliminating cellular debris, as well as intracellular pathogens. Mammalian target of rapamycin (mTOR) is an enzyme involved in inhibiting this pathway. Modulation of mTOR and the autophagy cellular machinery are being investigated as potential therapeutic targets for novel Mtb treatments. In this review, we discuss the background of Mtb pathogenesis, including its interaction with the innate and adaptive immune systems, the mTOR and autophagy pathways, the interaction of Mtb with these pathways, and finally, the drug everolimus, which targets these pathways and is a potential novel therapy for TB treatment.

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Yang, Yi, Yingfei Sun, Jinrui Xu, Kangda Bao, Meihui Luo, Xiaoming Liu, and Yujiong Wang. "Epithelial Cells Attenuate Toll-Like Receptor-Mediated Inflammatory Responses in Monocyte-Derived Macrophage-Like Cells to Mycobacterium tuberculosis by Modulating the PI3K/Akt/mTOR Signaling Pathway." Mediators of Inflammation 2018 (September 26, 2018): 1–19. http://dx.doi.org/10.1155/2018/3685948.

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Both alveolar macrophages (AMs) and alveolar epithelial cells (AECs) are main targets of Mycobacterium tuberculosis (M. tuberculosis (Mtb)). Intercellular communications between mucosal AECs and AMs have important implications in cellular responses to exogenous insults. However, molecular mechanisms underpinning interactions responding to Mtb remain largely unknown. In this study, impacts of AECs on Toll-like receptor- (TLR-) mediated inflammatory responses of AMs to Mtb virulent strain H37Rv were interrogated using an air-liquid interface (ALI) coculture model of epithelial A549 cells and U937 monocyte-derived macrophage-like cells. Results showed that Mtb-activated TLR-mediated inflammatory responses in U937 cells were significantly alleviated when A549 cells were coinfected with H37Rv, in comparison with the infection of U937 cells alone. Mechanistically, PI3K/Akt/mTOR signaling was involved in the epithelial cell-modulated Mtb-activated TLR signaling. The epithelial cell-attenuated TLR signaling in U937s could be reversed by PI3K inhibitor LY294002 and mTOR inhibitor rapamycin, but not glycogen synthase kinase 3β inhibitor LiCl, suggesting that the epithelially modulated-TLR signaling in macrophages was in part caused by inhibiting the TLR-triggered PI3K/Akt/mTOR signaling pathway. Together, this study demonstrates that mucosal AEC-derived signals play an important role in modulating inflammatory responses of AMs to Mtb, which thus also offers an insight into cellular communications between AECs and AMs to Mtb infections.

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Kountz, Duncan J., Edward J. Behrman, Liwen Zhang, and Joseph A. Krzycki. "MtcB, a member of the MttB superfamily from the human gut acetogen Eubacterium limosum, is a cobalamin-dependent carnitine demethylase." Journal of Biological Chemistry 295, no. 34 (June 22, 2020): 11971–81. http://dx.doi.org/10.1074/jbc.ra120.012934.

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The trimethylamine methyltransferase MttB is the first described member of a superfamily comprising thousands of microbial proteins. Most members of the MttB superfamily are encoded by genes that lack the codon for pyrrolysine characteristic of trimethylamine methyltransferases, raising questions about the activities of these proteins. The superfamily member MtcB is found in the human intestinal isolate Eubacterium limosum ATCC 8486, an acetogen that can grow by demethylation of l-carnitine. Here, we demonstrate that MtcB catalyzes l-carnitine demethylation. When growing on l-carnitine, E. limosum excreted the unusual biological product norcarnitine as well as acetate, butyrate, and caproate. Cellular extracts of E. limosum grown on l-carnitine, but not lactate, methylated cob-(I)alamin or tetrahydrofolate using l-carnitine as methyl donor. MtcB, along with the corrinoid protein MtqC and the methylcorrinoid:tetrahydrofolate methyltransferase MtqA, were much more abundant in E. limosum cells grown on l-carnitine than on lactate. Recombinant MtcB methylates either cob(I)alamin or Co(I)-MtqC in the presence of l-carnitine and, to a much lesser extent, γ-butyrobetaine. Other quaternary amines were not substrates. Recombinant MtcB, MtqC, and MtqA methylated tetrahydrofolate via l-carnitine, forming a key intermediate in the acetogenic Wood–Ljungdahl pathway. To our knowledge, MtcB methylation of cobalamin or Co(I)-MtqC represents the first described mechanism of biological l-carnitine demethylation. The conversion of l-carnitine and its derivative γ-butyrobetaine to trimethylamine by the gut microbiome has been linked to cardiovascular disease. The activities of MtcB and related proteins in E. limosum might demethylate proatherogenic quaternary amines and contribute to the perceived health benefits of this human gut symbiont.

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Dundon, Samantha E. R., and Thomas D. Pollard. "Microtubule nucleation promoters Mto1 and Mto2 regulate cytokinesis in fission yeast." Molecular Biology of the Cell 31, no. 17 (August 1, 2020): 1846–56. http://dx.doi.org/10.1091/mbc.e19-12-0686.

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Dundon and Pollard show that compromising the Mto1 or Mto2 regulators of the fission yeast γ-tubulin complex reduces or eliminates astral microtubules, exaggerates the effects of a D277N substitution in β-glucan synthase 1 (Cps1/Bgs1) on the rate of cytokinetic furrow formation, and increases Rho1-GTP at the cleavage site.

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Cronin, David. "Are Member States’ Budgetary Policies Adhering to the EU Fiscal Rules?" Applied Economics Quarterly: Volume 66, Issue 1 66, no. 1 (January 1, 2020): 47–64. http://dx.doi.org/10.3790/aeq.66.1.47.

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Harmonised data from the 2013 to 2018 Stability and Convergence Programmes (SCPs) are used to assess whether member states are acting to meet EU fiscal requirements and, in particular, their medium-term objectives (MTOs). EU AMECO data are employed to check whether planned fiscal policy, set out in the SCPs, materialises ex-post. The main finding is that planned changes in the fiscal stance aim towards meeting the MTO when that target has not yet been attained but less effort occurs in practice. Member states who have already met their MTO loosen their fiscal stance. The policy message is that, in general, the enhanced, post-crisis EU fiscal framework is delivering budgetary policy that contributes to avoiding excessive deficit and debt positions. The fiscal consolidation actually undertaken, however, is less than planned and the upside of the economic cycle does not see greater effort towards meeting MTOs. Moreover, those member states with prior excessive deficits do not make, nor plan, any additional fiscal effort over other member states also striving to meet their MTO. The policy reaction to the economic cycle is pro-cyclical in nature.

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LIN, XUE, MENGMENG WEI, FUYANG SONG, DI XUE, and YUJIONG WANG. "N-acetylcysteine (NAC) Attenuating Apoptosis and Autophagy in RAW264.7 Cells in Response to Incubation with Mycolic Acid from Bovine Mycobacterium tuberculosis Complex." Polish Journal of Microbiology 69, no. 2 (June 2020): 223–29. http://dx.doi.org/10.33073/pjm-2020-026.

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Bovine tuberculosis is an airborne infectious disease caused by organisms of the Mycobacterium tuberculosis (MTB) complex. Mycolic acid (MA) is the main lipid component of the cell membrane of MTB. It is non-enzymatically reduced by NAD(P)H and further produces reactive oxygen species (ROS), which can cause oxidative stress in human cells. N-acetylcysteine (NAC) is a synthetic precursor of glutathione (GSH) and exhibits anti-ROS activity. However, the underlying mechanisms of its protective properties remain uncertain. Herein, after pre-incubation of RAW264.7 cells with NAC, the factors associated with apoptosis and autophagy were measured. Mechanistically, NAC could reduce MA-induced expression of pro-apoptotic and pro-autophagy proteins. At the mRNA level, NAC can inhibit AMPK and activate mTOR expression. The results indicate that NAC might regulate autophagy in RAW264.7 cells through the AMPK/mTOR pathway. To further prove the effect of NAC on MA, ICR mice were used to evaluate the lung injury. Hematoxylin-eosin (HE) staining was performed on the lung. The results show that NAC could reduce cell injury induced by MA. In conclusion, our research showed that NAC attenuates apoptosis and autophagy in response to incubation with mycolic acid.

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Dissertations / Theses on the topic "MTOB"

1

Picking, Jonathan William. "Glycine Betaine and Proline Betaine Specific Methyltransferases of the MttB Superfamily." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563468258124346.

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Morris, Benjamin L. "Understanding and targeting the C-terminal Binding Protein (CtBP) substrate-binding domain for cancer therapeutic development." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4434.

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Cancer involves the dysregulated proliferation and growth of cells throughout the body. C-terminal binding proteins (CtBP) 1 and 2 are transcriptional co-regulators upregulated in several cancers, including breast, colorectal, and ovarian tumors. CtBPs drive oncogenic properties, including migration, invasion, proliferation, and survival, in part through repression of tumor suppressor genes. CtBPs encode an intrinsic dehydrogenase activity, utilizing intracellular NADH concentrations and the substrate 4-methylthio-2-oxobutyric acid (MTOB), to regulate the recruitment of transcriptional regulatory complexes. High levels of MTOB inhibit CtBP dehydrogenase function and induce cytotoxicity among cancer cells in a CtBP-dependent manner. While encouraging, a good therapeutic would utilize >100-fold lower concentrations. Therefore, we endeavored to design better CtBP-specific therapeutics. The best of these drugs, 3-Cl and 4-Cl HIPP, exhibit nanomolar enzymatic inhibition and micromolar cytotoxicity and showed that CtBP enzymatic function is subject to allosteric interactions. Additionally, the function of the substrate-binding domain has yet to be examined in context of CtBP’s oncogenic activity. To this end, we created several point mutations in the CtBP substrate-binding pocket and determined key residues for CtBP’s enzymatic activity. We found that a conserved tryptophan in the catalytic domain is imperative for function and unique to CtBPs among dehydrogenases. Knowledge of this and other residues allows the directed synthesis of drugs with increased potency and higher CtBP specificity. Early work interrogated the importance of these residues in cell migration. Taken together, this work addresses the utility of the CtBP substrate-binding domain as a target for cancer therapeutics.

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Borek, Weronika Ewa. "Cell cycle regulation of microtubule nucleation in fission yeast Schizosaccharomyces pombe." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/16873.

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In fission yeast, microtubule (MT) nucleation is regulated in space and time. In interphase, MTs are nucleated in the cytoplasm to regulate cell polarity, whereas in mitosis, nucleation takes place inside the nucleus to form a mitotic spindle. We hypothesize that several non-exclusive mechanisms may be responsible for this differential regulation of MT nucleation. Two fission yeast proteins, Mto1 and Pcp1, are involved in MT nucleation in interphase and mitosis, respectively. These proteins share a sequence motif, called CM1 that is responsible for interaction with the γ-tubulin complex (γ-TuC). In the first part of my project, I tested whether sequence differences between Mto1 and Pcp1 CM1 regions contribute to the differential regulation of MT nucleation in interphase vs. mitosis. I showed that the two CM1 regions are interchangeable and play no role in differential regulation of Mto1 and Pcp1. By generating Pcp1-9A1 mutant, where conserved residues within the Pcp1 CM1 region was replaced with alanines, I showed that Pcp1 CM1 region is required for its function. Moreover, using CM1 regions from two human proteins that are implicated in schizophrenia and microcephaly development, MMGL and CDK5RAP2, I showed that human CM1 domains could rescue yeast protein function, demonstrating that the CM1 region is conserved across evolution. In the second part of my project, I focused on regulation of cytoplasmic MT nucleation. In fission yeast, cytoplasmic MT nucleation occurs from several distinct sites in the cell and is promoted by the Mto1/2 complex. The Mto1/2 complex is composed of multiple copies of Mto1 and Mto2 and interacts with the γ-TuC. Disruption of the interaction of Mto1/2 with the γ-TuC, or of the Mto1-Mto2 interaction, results in a complete loss of interphase cytoplasmic nucleation. As cells enter mitosis, Mto2 is hyperphosphorylated, and the Mto1-Mto2 interaction is disrupted, leading to abolishment of cytoplasmic nucleation. This led to a hypothesis that Mto2 phosphorylation regulated the Mto1/2 complex mitotic disassembly. I showed that Mto2 phosphorylation is used to control levels of cytoplasmic nucleation in both interphase and mitosis. During interphase, I found that Mto2 is phosphorylated in order to reduce levels of MT nucleation. When Mto2 phosphorylation is prevented by mutation of phosphorylatable residues to alanines, Mto1/2 mutant complexes show a more robust interaction with the γ-TuC, and more MTs are nucleated in the cytoplasm. During mitosis, hyperphosphorylation of Mto2 plays a role in the disassembly of Mto1/2 complexes. In particular, while the interaction of wild-type Mto2 with Mto1 is disrupted during mitosis, Mto2-alanine mutants, in which phosphorylation was nearly abolished, are still able to interact with Mto1 in mitosis. Interestingly, Mto1/2 complexes containing Mto2-alanine mutants are still disassembled in mitosis by disruption of Mto2 self-interaction. I used SILAC phosphoproteomics to show that Mto2-alanine is still phosphorylated in mitosis, suggesting the Mto2 self-interaction might also be controlled by phosphorylation. While doing so, I developed a novel SILAC quantification method that is particularly useful for quantification of multiply phosphorylated proteins and peptides. Using data obtained by SILAC, I generated additional Mto2 alanine mutants with more phosphorylation sites mutated. Preliminary analysis showed that these mutants are similar to the alanine mutants analysed previously; however, more analysis is required to generate more definitive conclusions. In summary, in this study I have uncovered the functional conservation of the CM1 region from yeast to human. I also showed that Mto2 phosphorylation regulates cytoplasmic MT nucleation in both interphase and mitosis, by regulating the Mto2-Mto1 interaction and the Mto2-Mto2 self-interaction and therefore remodelling the Mto1/2 complex.

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Olsen, Jessica M. "β-Adrenergic Signalling Through mTOR." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-142169.

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Adrenergic signalling is part of the sympathetic nervous system and is activated upon stimulation by the catecholamines epinephrine and norepinephrine. This regulates heart rate, energy mobilization, digestion and helps to divert blood flow to important organs. Insulin is released to regulate metabolism of carbohydrates, fats and proteins, mainly by taking up glucose from the blood. The insulin and the catecholamine hormone systems are normally working as opposing metabolic regulators and are therefore thought to antagonize each other. One of the major regulators involved in insulin signalling is the mechanistic target of rapamycin (mTOR). There are two different complexes of mTOR; mTORC1 and mTORC2, and they are essential in the control of cell growth, metabolism and energy homeostasis. Since mTOR is one of the major signalling nodes for anabolic actions of insulin it was thought that catecholamines might oppose this action by inhibiting the complexes. However, lately there are studies demonstrating that this may not be the case. mTOR is for instance part of the adrenergic signalling pathway resulting in hypertrophy of cardiac and skeletal muscle cells and inhibition of smooth muscle relaxation and helps to regulate browning in white adipose tissue and thermogenesis in brown adipose tissue (BAT). In this thesis I show that β-adrenergic signalling leading to glucose uptake occurs independently of insulin in skeletal muscle and BAT, and does not activate either Akt or mTORC1, but that the master regulator of this pathway is mTORC2. Further, my co-workers and I demonstrates that β-adrenergic stimulation in skeletal muscle and BAT utilizes different glucose transporters. In skeletal muscle, GLUT4 is translocated to the plasma membrane upon stimulation. However, in BAT, β-adrenergic stimulation results in glucose uptake through translocation of GLUT1. Importantly, in both skeletal muscle and BAT, the role of mTORC2 in β-adrenergic stimulated glucose uptake is to regulate GLUT-translocation.

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.

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Schalm, Stefanie. "Molecular mechanism of mTOR downstream signaling." [S.l. : s.n.], 2003. http://www.diss.fu-berlin.de/2003/249/index.html.

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Joyce, Claire Lois. "Tumour cell responses to mTOR inhibition." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610245.

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März, Andreas. "A new player in mTOR regulation." Diss., Ludwig-Maximilians-Universität München, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-139523.

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Lee, John Hung. "Altered mTOR signaling in Huntington's Disease." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5547.

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Huntington's Disease (HD) is caused by a polyglutamine tract expansion in huntingtin (HTT). Despite HTTs ubiquitous expression, there is selective vulnerability in a specific brain region known as the striatum, the cause of which is poorly understood. Here, we provide evidence that impaired striatal mTORC1 activity underlies varied metabolic and degenerative phenotypes in striatal tissues from HD mouse models and patients, and show that further mTORC1 impairment in mouse models, achieved through the knockdown of Rhes, a striatum-enriched mTORC1 activator, exacerbates disease phenotypes. In contrast, exogenous addition of Rhes or the constitutively active form of the mTORC1 regulator, Rheb, into HD mouse brain, alleviates mitochondrial dysfunction, aberrant cholesterol homeostasis, striatal atrophy, and elicits increased autophagy, and reverses impaired dopamine signaling. Furthermore, while HD has been considered primarily a neurological disease, organs with high metabolic demand, such as heart, are also severely affected. The mechanism by which mHTT disrupts cardiac function remains unknown. I provide evidence that mTORC1 is impaired in HD mouse model hearts, causing hyperactive FoxO1 signaling which may render HD hearts vulnerable to stress induced cardiomyopathy. In sum, my combined work indicates impaired mTORC1 signaling as a primary mechanism underlying the neurodegenerative and heart-related disease phenotypes in HD, and thus presents a rational therapeutic target.

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Marin, Lucas [Verfasser], and J. [Akademischer Betreuer] Gescher. "Charakterisierung des β‑Fass-Proteins MtrB = Characterization of the β‑barrel protein MtrB / Lucas Marin ; Betreuer: J. Gescher." Karlsruhe : KIT-Bibliothek, 2020. http://d-nb.info/122302783X/34.

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Ramsbottom, Ben Alan. "Regulation of pol III transcription by mTOR." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438962.

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Books on the topic "MTOB"

1

Weichhart, Thomas, ed. mTOR. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-430-8.

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Houghton, Peter J., and V. A. Polunovskiĭ. mTOR pathway and mTOR inhibitors in cancer therapy. New York: Humana Press, 2010.

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3

Polunovsky, Vitaly A., and Peter J. Houghton, eds. mTOR Pathway and mTOR Inhibitors in Cancer Therapy. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-271-1.

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4

mTor: Methods and protocols. New York: Humana Press, 2012.

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Transportation, Ontario Ministry of. MTO drainage management manual. [Toronto]: Ministry of Transportation, 1995.

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6

MTTB ve MTTB'liler: Kimler geldi, kimler geçti? Güngören, İstanbul: Hemenora, 2010.

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7

Dey, Nandini, Pradip De, and Brian Leyland-Jones, eds. PI3K-mTOR in Cancer and Cancer Therapy. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34211-5.

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Ontario. Ministry of Transportation. Road User Safety Division. The official MTO motorcycle handbook. [Downsview, Ont.]: Road User Safety Division, Ministry of Transportation of Ontario, 2012.

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Dickens, Peter. Night action: MTB flotilla at war. Barnsley: Seaforth, 2008.

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Bozkurt'tan Kur'an'a Millî Türk Talebe Birliği (MTTB),1916-1980. İstanbul: İstanbul Bilgi Üniversitesi, 2004.

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Book chapters on the topic "MTOB"

1

Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda, et al. "mTOR." In Encyclopedia of Signaling Molecules, 1129–36. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_331.

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Robitaille, Aaron M. "mTOR." In Encyclopedia of Signaling Molecules, 3239–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_331.

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Patel, Nisha R., Michael L. Wong, Anthony E. Dragun, Stephan Mose, Bernadine R. Donahue, Jay S. Cooper, Filip T. Troicki, et al. "mTOR Inhibitors." In Encyclopedia of Radiation Oncology, 516–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_751.

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Kubica, Neil, and John Blenis. "mTORC1: A Signaling Integration Node Involved in Cell Growth." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 1–36. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_1.

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Dowling, Ryan J. O., and Nahum Sonenberg. "Downstream of mTOR: Translational Control of Cancer." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 201–16. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_10.

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Larsson, Ola, and Peter B. Bitterman. "Genome-Wide Analysis of Translational Control." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 217–36. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_11.

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Bitterman, Peter B., and Vitaly A. Polunovsky. "Translational Control of Cancer: Implications for Targeted Therapy." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 237–55. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_12.

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Pelletier, Jerry, and Jeremy R. Graff. "Downstream from mTOR: Therapeutic Approaches to Targeting the eIF4F Translation Initiation Complex." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 257–85. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_13.

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Feng, Zhaohui, and Arnold J. Levine. "The Regulation of the IGF-1/mTOR Pathway by the p53 Tumor Suppressor Gene Functions." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 37–48. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_2.

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Mead, Henry, Mirjana Zeremski, and Markus Guba. "mTOR Signaling in Angiogenesis." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 49–74. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_3.

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Conference papers on the topic "MTOB"

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Zhou, Yuqing, Tsuyoshi Nomura, and Kazuhiro Saitou. "Multi-Component Topology Optimization for Powder Bed Additive Manufacturing (MTO-A)." In ASME 2018 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/detc2018-86284.

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This paper presents a gradient-based multi-component topology optimization (MTO) method for structures assembled from components made by powder bed additive manufacturing. It is built upon our previous work on the continuously-relaxed MTO framework utilizing the concept of fractional component membership. The previous attempt on the integration of the relaxed MTO framework with additive manufacturing constraints, however, suffered from numerical instability for larger size problems, limiting its application to 2D low-resolution examples. To overcome this difficulty, this paper proposes an improved MTO formulation based on a design field regularization and a nonlinear projection of component membership variables, with a focus on powder bed additive manufacturing. For each component, constraints on the maximum allowable build volume (i.e., length, width, and height), the elimination of enclosed voids, and the minimum printable feature size are imposed during the simultaneous optimization of the overall base topology and component partitioning. The scalability of the new MTO formulation is demonstrated by a few 2D examples with much higher resolution than previously reported, and the first reported 3D example of MTO.

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Yeo, Woon-Hong, Fong-Li Chou, Dayong Gao, Amy Q. Shen, Jae-Hyun Chung, and Kyong-Hoon Lee. "Size Specific Immunofluorescence of Mycobacterium Tuberculosis Cells by Using a Microtip-Sensor." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-37719.

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The size-specific capturing mechanism for Mycobacterium tuberculosis (MTB) cells is presented using a microtip-sensor. When a microtip is withdrawn from a solution drop, enriched cells by an alternating current (AC) electric field are selectively captured onto the tip due to capillary- and viscous forces. The size-specificity on the 50 μm-diameter tip is studied by using polystyrene microspheres. The size-specific capturing mechanism is applied to capture MTB cells from a sample mixture containing MTB and Drosophila S2 cells. Under the competition between capillary- and viscous forces, MTB cells are captured onto the microtip by the viscous force, while Drosophila S2 cells are removed from the tip by the capillary force. The microtip-sensor yields the detection limit of 800 cells/mL for MTB cells, which is one of the highest-sensitivity immunosensors.

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Kim, Jong-Hoon, Woon-Hong Yeo, Zhiquan Shu, Shinnosuke Inoue, Kieseok Oh, Dayong Gao, Jae-Hyun Chung, and Kyong-Hoon Lee. "Tip Enrichment System for Rapid Screening of Mycobacterium Tuberculosis." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38403.

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Rapid detection of tuberculosis (TB) has been critically demanded over the last century. To detect TB, numerous methods screening Mycobacterium tuberculosis (MTB) have been developed. However, the methods still have challenges of rapid and specific enrichment of MTB. In this study, we present a novel specific enrichment method of MTB using a microfabricated tip. Through our simulation study, a wavy-shaped microtip is designed to enhance capturing efficiency of bacteria. Using an optimized tip, bacteria are attracted by dielectrophoresis and captured by affinity binding and capillary action. In experiment, a surrogate marker of MTB, Bacilli Calmette-Guerin (BCG), is enriched with the micromachined tip. When a microtip decorated with capturing antibodies is used, BCG cells spiked in saliva are detected at the concentration of 5×105 CFU/mL within 20 minutes. The tip enrichment system demonstrates the potential for rapid, culture-free detection of MTB in a raw sample.

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van der Zijden, Wim, Djoerd Hiemstra, and Maurice van Keulen. "MTCB." In the 9th International Conference. New York, New York, USA: ACM Press, 2017. http://dx.doi.org/10.1145/3149572.3149585.

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Blanco, Elvin, Takafumi Sangai, Funda Meric-Bernstam, and Mauro Ferrari. "Chemotherapeutic Synergy Enhancement Through Micellar Nanotherapeutics." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13263.

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Current chemotherapeutic regimens involve the administration of a combination of agents with hopes of gaining synergistic cell-killing effects observed in vitro. However, drug synergy is rarely realized clinically given the different pharmacokinetic profiles of the drugs. Recent findings show that a combination of rapamycin and paclitaxel proves highly effective at hindering growth of tumors wherein the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. Our objective was to fabricate a micellar nanotherapeutic platform capable of delivering a multitude of agents shown to synergistically affect a specific pathway (PI3K/Akt/mTOR) in breast cancer. We hypothesized that this concomitant delivery strategy will result in increased antitumor efficacy, given the site-specific and controlled delivery of the two agents. Herein, we demonstrate the successful fabrication of a nanotherepeutic strategy for the treatment of breast tumors with aberrant PI3K/Akt/mTOR pathways. Resulting polymer micelles were small in size (∼30 nm) and showed high levels of drug incorporation efficiency of both rapamycin and paclitaxel. Current studies involve the examination of release kinetics and antitumor efficacy in in vitro and in vivo models.

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Kim, Jong-Hoon, Morgan Hiraiwa, Dayong Gao, Kyong-Hoon Lee, and Jae-Hyun Chung. "Dendritic Nanotip for Low-Cost Detection of Mycobacterium Tuberculosis." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-87871.

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Rapid diagnosis of tuberculosis, one of the most widely spread diseases on the globe today, has been critically demanded for over a century. One of the major challenges for screening Mycobacterium tuberculosis (MTB) is in low-cost detection of MTB. In this study, we present an electrical detection method of MTB cells using a dendritic nanotip composed of single-walled carbon nanotubes (SWCNTs) and Si micro- and nanowires. The novelty is in the direct measurement of electric current with a minimal capacitance effect on dendritic nanotip surface. Upon binding of target cells, a gating effect on the nanotip surface decreases the electric current, which is measured directly by a dendritic nanotip. The measurement resolution is aided by reduced interference of an electrical double layer effect, due to the dendritic nanostructure. Using the nanotip, BCG cells could be electrically detected within 15 minutes, which is validated by fluorescence detection. The sensitivity is 1000 cfu/ml for both methods. The presented tip sensor demonstrated the potential for rapid and low-cost detection of MTB.

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Yeo, Woon-Hong, Jae-Hyun Chung, and Kyong-Hoon Lee. "Tuberculosis Diagnostics Using a Nanotip Sensor." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13065.

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Tuberculosis (TB) is one of the most widely spread diseases. In 2006, 9.2 million new TB cases were reported with 1.7 million victims [1]. To diagnose TB, Mycobacterium tuberculosis (MTB) is identified in clinical samples. The challenge of TB diagnostics is high-performance screening conducted by nontrained personnel. Currently, nucleic acid testing with target-amplification strategy such as polymerase chain reaction (PCR) is available for detection of TB. However, this entails cumbersome procedures run by skilled operators with expensive instrumentation and reagents. To overcome these challenges, this paper presents a nanotip sensor to diagnose TB rapidly without target-amplification. The proposed methodology uses a nanostructured tip as a biosensor to detect target analytes. The novelty of this approach is in the superior concentration and detection mechanisms of nucleic acids on the terminal end of a nanotip using an alternating current (AC) electric field, specific chemical binding, and capillary action. Confirmatory identification of MTB is achieved by detecting MTB strains on a nanostructured tip through DNA hybridization. In this paper, the working principle is presented with the demonstration of amplification-free detection of MTB genomic DNA using the nanotip sensor. The performance of the tip sensor is characterized.

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Atkins, N. R. "Investigation of a Radial-Inflow Bleed as a Potential for Compressor Clearance Control." In ASME Turbo Expo 2013: Turbine Technical Conference and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/gt2013-95768.

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The mismatch in thermal response between a High Pressure Compressor (HPC) drum and casing is a limiting factor in the reduction of compressor clearance. An experimental test rig has been used to demonstrate the concept of radial inflow to reduce the thermal time constant of HPC discs. The testing uses a simulated idle - Maximum Take Off (MTO) - idle transient in order to measure the thermal response directly. The testing is fully scaled in the dimensionless sense to engine conditions. A simple closure model based on lumped capacitance is used to illustrate the scope of potential benefits. The proof-of-concept testing shows that HPC disc time constant reductions of the order 2 are feasible with a radial-inflow bleed of only 4% of bore flow at scaled MTO conditions. Using the experimental results, the simple closure modelling suggests that for a stage with a significant mismatch in thermal response, reductions in 2D axis-symmetric clearance of as much as 50% at MTO conditions may be possible along with significant scope for improvements at cruise conditions.

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Martel, Sylvain, and Mahmood Mohammadi. "Towards Mass-Scale Micro-Assembly Systems Using Magnetotactic Bacteria." In ASME 2011 International Manufacturing Science and Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/msec2011-50171.

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Magnetotactic bacteria (MTB) can be used in a coordinated fashion to assemble micro-objects in an orderly manner. To perform micro-assembly tasks, magnetotaxis-based control is used where a directional magnetic field is generated to induce a torque on an embedded chain of membrane-based magnetic nanoparticles (MNP) named magnetosomes. Such chain acts like a nano-compass or a nano-steering system embedded in each bacterium. Such magnetotaxis-based control is then used to orient the MTB in such a way that the laminar flow created by their flagella bundles provides a displacement force on the micro-objects being assembled. Since the force is generated by the bacteria, relatively large micro-objects can be moved with no requirement for electrical energy except for a relatively small value required for inducing a directional torque on the chain of magnetosomes in the cells. Because the energy required to generate the directional torque is independent on the population of MTB being involved but the displacement force can be scaled up with the use of a larger swarm while the total workspace would typically be at microscale dimensions, the energy required for the coils configuration around such workspace and responsible for generating the directional torque can be reduced further to a very low level and hence, makes the implementation of mass-scale bacterial micro-assembly systems, a viable approach. Based on these findings, we propose a corresponding mass-scale system based on many workspaces, each relying on a swarm of MTB to perform micro-assembly tasks in parallel.

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"Proceedings of the National Forum: Military Telemedicine On-Line Today Research, Practice, and Opportunities." In Proceedings of the National Forum: Military Telemedicine On-Line Today Research, Practice, and Opportunities. IEEE, 1995. http://dx.doi.org/10.1109/mtol.1995.504519.

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Reports on the topic "MTOB"

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Guan, Kun-Liang. Regulation of mTOR by Nutrients. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada569533.

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Guan, Kun-Liang. Regulation of mTOR by Nutrients. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada602038.

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Ramesh, Vijaya, and Anat Stemmer-Rachamimov. Role of Merlin/NF2 in mTOR Signaling and Meningioma Growth. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada566365.

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Roberge, Michel. Study of mTOR Signaling Inhibitors as Potential Treatment for TSC. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada601809.

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Costa-Mattioli, Mauro. The Role of the New mTOR Complex, MTORC2, in Autism Spectrum Disorders. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613836.

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Jacob, Josemon. Atom transfer and rearrangement reactions catalyzed by methyltrioxorhenium, MTO. Office of Scientific and Technical Information (OSTI), May 1999. http://dx.doi.org/10.2172/354892.

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Yu, Kyung, Latha Narayanan, John Schlager, Jeffery Gearhart, and Peter Robinson. Kinetic Behavior of Leucine and Other Amino Acids Modulating Cognitive Performance via mTOR Pathway. Fort Belvoir, VA: Defense Technical Information Center, December 2011. http://dx.doi.org/10.21236/ada560396.

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Ellis, Leigh. Inhibition of Histone Deacetylases (HDACs) and mTOR Signaling: Novel Strategies Towards the Treatment of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada562460.

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Jongens, Thomas A. Examination of the mGluR-mTOR Pathway for the Identification of Potential Therapeutic Targets to Treat Fragile X. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612771.

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Tan, Haisong. Kinetics and mechanism of the oxidation of alkenes and silanes by hydrogen peroxide catalyzed by methylrhenium trioxide (MTO) and a novel application of electrospray mass spectrometry to study the hydrolysis of MTO. Office of Scientific and Technical Information (OSTI), November 1999. http://dx.doi.org/10.2172/754781.

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