Thematische Bibliographien / Tbc1D3

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Auswahl der wissenschaftlichen Literatur zum Thema „Tbc1D3“

Autor: Grafiati

Veröffentlicht am 25. Mai 2024

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Zeitschriftenartikel zum Thema "Tbc1D3"

Frittoli, Emanuela, Andrea Palamidessi, Alessandro Pizzigoni, Letizia Lanzetti, Massimiliano Garrè, Flavia Troglio, Albino Troilo et al. „The Primate-specific Protein TBC1D3 Is Required for Optimal Macropinocytosis in a Novel ARF6-dependent Pathway“. Molecular Biology of the Cell 19, Nr. 4 (April 2008): 1304–16. http://dx.doi.org/10.1091/mbc.e07-06-0594.

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The generation of novel genes and proteins throughout evolution has been proposed to occur as a result of whole genome and gene duplications, exon shuffling, and retrotransposition events. The analysis of such genes might thus shed light into the functional complexity associated with highly evolved species. One such case is represented by TBC1D3, a primate-specific gene, harboring a TBC domain. Because TBC domains encode Rab-specific GAP activities, TBC-containing proteins are predicted to play a major role in endocytosis and intracellular traffic. Here, we show that the TBC1D3 gene originated late in evolution, likely through a duplication of the RNTRE locus, and underwent gene amplification during primate speciation. Despite possessing a TBC domain, TBC1D3 is apparently devoid of Rab-GAP activity. However, TBC1D3 regulates the optimal rate of epidermal growth factor–mediated macropinocytosis by participating in a novel pathway involving ARF6 and RAB5. In addition, TBC1D3 binds and colocalize to GGA3, an ARF6-effector, in an ARF6-dependent manner, and synergize with it in promoting macropinocytosis, suggesting that the two proteins act together in this process. Accordingly, GGA3 siRNA-mediated ablation impaired TBC1D3-induced macropinocytosis. We thus uncover a novel signaling pathway that appeared after primate speciation. Within this pathway, a TBC1D3:GGA3 complex contributes to optimal propagation of signals, ultimately facilitating the macropinocytic process.

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Tobias, Irene S., Kara K. Lazauskas, Jeremy Siu, Pablo B. Costa, Jared W. Coburn und Andrew J. Galpin. „Sex and fiber type independently influence AMPK, TBC1D1, and TBC1D4 at rest and during recovery from high-intensity exercise in humans“. Journal of Applied Physiology 128, Nr. 2 (01.02.2020): 350–61. http://dx.doi.org/10.1152/japplphysiol.00704.2019.

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Women and men present different metabolic responses to exercise, yet whether this phenomenon results from differences in fiber type (FT) composition or other sex-specific factors remains unclear. Therefore, our aim was to examine the effects of sex and FT independently on AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), Tre-2/BUB2/CDC1 domain family (TBC1D)1, and TBC1D4 in response to acute exercise. Segregated pools of myosin heavy chain (MHC) I and MHC IIa fibers were prepared from vastus lateralis biopsies of young trained men and women at rest and during recovery (0 min, 45 min, 90 min, or 180 min) from high-intensity interval exercise (6 × 1.5 min at 95% maximum oxygen uptake). In resting MHC I vs. IIa fibers, AMPKα2, AMPKγ3, and TBC1D1 were higher and TBC1D4 expression was lower in both sexes, along with higher phospho (p)-TBC1D1Ser660 and lower p-TBC1D4Thr642. Women expressed higher ACC than men in MHC IIa fibers and higher AMPKβ1, AMPKβ2, TBC1D1, and TBC1D4 in both FTs. Immediately after exercise, p-AMPKαThr172 increased only in MHC IIa fibers, whereas p-ACCSer221 increased in both FTs, with no change in p-TBC1D1Ser660 or p-TBC1D4Thr642. During recovery, delayed responses were observed for p-AMPKαThr172 in MHC I (45 min), p-TBC1D4Thr642 in both FTs (45 min), and p-TBC1D1Ser660 (180 min). FT-specific phosphorylation responses to exercise were similar between men and women. Data indicate that sex and FT independently influence expression of AMPK and its substrates. Thus failing to account for sex or FT may reduce accuracy and precision of metabolic protein measurements and conceal key findings. NEW & NOTEWORTHY This investigation is the first to compare muscle fiber type (FT)-specific analysis of proteins between the sexes, providing comprehensive data on AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), Tre-2/BUB2/CDC1 domain family (TBC1D)1, and TBC1D4 before and in the hours following high-intensity interval exercise (HIIT). Expression and phosphorylation of specific AMPK isoforms, ACC, TBC1D1, and TBC1D4 were shown to be FT dependent, sex dependent, or both, and TBC1D1 showed an unexpected delay in FT-dependent phosphorylation in the time period following HIIT.

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Penisson, Maxime, Mingyue Jin, Shengming Wang, Shinji Hirotsune, Fiona Francis und Richard Belvindrah. „Lis1 mutation prevents basal radial glia-like cell production in the mouse“. Human Molecular Genetics 31, Nr. 6 (12.10.2021): 942–57. http://dx.doi.org/10.1093/hmg/ddab295.

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Abstract Human cerebral cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Progenitor cells include apical radial glia, intermediate progenitors and basal (or outer) radial glia (bRGs or oRGs). bRGs are few in number in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 (coding for a RAB-GAP protein) at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 expression in wild-type (WT) brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, using the same approach, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Indeed, we observe perturbation of the ventricular zone (VZ) in the mutant. Lis1 depletion altered adhesion proteins and mitotic spindle orientations at the ventricular surface and increased the proportion of abventricular mitoses. Progenitor outcome could not be further altered by TBC1D3. We conclude that disruption of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis.

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Espelage, Lena, Hadi Al-Hasani und Alexandra Chadt. „RabGAPs in skeletal muscle function and exercise“. Journal of Molecular Endocrinology 64, Nr. 1 (Januar 2020): R1—R19. http://dx.doi.org/10.1530/jme-19-0143.

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The two closely related RabGAPs TBC1D1 and TBC1D4 are key signaling factors of skeletal muscle substrate utilization. In mice, deficiency in both RabGAPs leads to reduced skeletal muscle glucose transport in response to insulin and lower GLUT4 abundance. Conversely, Tbc1d1 and Tbc1d4 deficiency results in enhanced lipid use as fuel in skeletal muscle, through yet unknown mechanisms. In humans, variants in TBC1D1 and TBC1D4 are linked to obesity, insulin resistance and type 2 diabetes. While the specific function in metabolism of each of the two RabGAPs remains to be determined, TBC1D1 emerges to be controlling exercise endurance and physical capacity, whereas TBC1D4 may rather be responsible for maintaining muscle insulin sensitivity, muscle contraction, and exercise. There is growing evidence that TBC1D1 also plays an important role in skeletal muscle development, since it has been found to be associated to meat production traits in several livestock species. In addition, TBC1D1 protein abundance in skeletal muscle is regulated by both, insulin receptor and insulin-like growth factor-1 (IGF-1) receptor signaling. This review focuses on the specific roles of the two key signaling factors TBC1D1 and TBC1D4 in skeletal muscle metabolism, development and exercise physiology.

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Mikłosz, Agnieszka, Bartłomiej Łukaszuk, Elżbieta Supruniuk, Kamil Grubczak, Marcin Moniuszko, Barbara Choromańska, Piotr Myśliwiec und Adrian Chabowski. „Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?“ Cells 10, Nr. 6 (16.06.2021): 1515. http://dx.doi.org/10.3390/cells10061515.

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TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of TBC1D4 increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation.

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Zhou, Qiong L., Zhen Y. Jiang, John Holik, Anil Chawla, G. Nana Hagan, John Leszyk und Michael P. Czech. „Akt substrate TBC1D1 regulates GLUT1 expression through the mTOR pathway in 3T3-L1 adipocytes“. Biochemical Journal 411, Nr. 3 (14.04.2008): 647–55. http://dx.doi.org/10.1042/bj20071084.

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Multiple studies have suggested that the protein kinase Akt/PKB (protein kinase B) is required for insulin-stimulated glucose transport in skeletal muscle and adipose cells. In an attempt to understand links between Akt activation and glucose transport regulation, we applied mass spectrometry-based proteomics and bioinformatics approaches to identify potential Akt substrates containing the phospho-Akt substrate motif RXRXXpS/T. The present study describes the identification of the Rab GAP (GTPase-activating protein)-domain containing protein TBC1D1 [TBC (Tre-2/Bub2/Cdc16) domain family, member 1], which is closely related to TBC1D4 [TBC domain family, member 4, also denoted AS160 (Akt substrate of 160 kDa)], as an Akt substrate that is phosphorylated at Thr590. RNAi (RNA interference)-mediated silencing of TBC1D1 elevated basal deoxyglucose uptake by approx. 61% in 3T3-L1 mouse embryo adipocytes, while the suppression of TBC1D4 and RapGAP220 under the same conditions had little effect on basal and insulin-stimulated deoxyglucose uptake. Silencing of TBC1D1 strongly increased expression of the GLUT1 glucose transporter but not GLUT4 in cultured adipocytes, whereas the decrease in TBC1D4 had no effect. Remarkably, loss of TBC1D1 in 3T3-L1 adipocytes activated the mTOR (mammalian target of rapamycin)-p70 S6 protein kinase pathway, and the increase in GLUT1 expression in the cells treated with TBC1D1 siRNA (small interfering RNA) was blocked by the mTOR inhibitor rapamycin. Furthermore, overexpression of the mutant TBC1D1-T590A, lacking the putative Akt/PKB phosphorylation site, inhibited insulin stimulation of p70 S6 kinase phosphorylation at Thr389, a phosphorylation induced by mTOR. Taken together, our data suggest that TBC1D1 may be involved in controlling GLUT1 glucose transporter expression through the mTOR-p70 S6 kinase pathway.

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Mafakheri, Samaneh, Alexandra Chadt und Hadi Al-Hasani. „Regulation of RabGAPs involved in insulin action“. Biochemical Society Transactions 46, Nr. 3 (21.05.2018): 683–90. http://dx.doi.org/10.1042/bst20170479.

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Rab (Ras-related proteins in brain) GTPases are key proteins responsible for a multiplicity of cellular trafficking processes. Belonging to the family of monomeric GTPases, they are regulated by cycling between their active GTP-bound and inactive GDP-bound conformations. Despite possessing a slow intrinsic GTP hydrolysis activity, Rab proteins rely on RabGAPs (Rab GTPase-activating proteins) that catalyze GTP hydrolysis and consequently inactivate the respective Rab GTPases. Two related RabGAPs, TBC1D1 and TBC1D4 (=AS160) have been described to be associated with obesity-related traits and type 2 diabetes in both mice and humans. Inactivating mutations of TBC1D1 and TBC1D4 lead to substantial changes in trafficking and subcellular distribution of the insulin-responsive glucose transporter GLUT4, and to subsequent alterations in energy substrate metabolism. The activity of the RabGAPs is controlled through complex phosphorylation events mediated by protein kinases including AKT and AMPK, and by putative regulatory interaction partners. However, the dynamics and downstream events following phosphorylation are not well understood. This review focuses on the specific role and regulation of TBC1D1 and TBC1D4 in insulin action.

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Qin, Shu, Robert A. Dorschner, Irene Masini, Ophelia Lavoie‐Gagne, Philip D. Stahl, Todd W. Costantini, Andrew Baird und Brian P. Eliceiri. „TBC1D3 regulates the payload and biological activity of extracellular vesicles that mediate tissue repair“. FASEB Journal 33, Nr. 5 (04.02.2019): 6129–39. http://dx.doi.org/10.1096/fj.201802388r.

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Shen, Y., L. Zhang, H. Zhao und C. L. Shen. „TC-1 mediate the TBC1D3 oncogene induced migration of MCF-7 breast cancer cells“. Annals of Oncology 29 (November 2018): ix19. http://dx.doi.org/10.1093/annonc/mdy428.017.

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Kong, Chen, Jeffrey J. Lange, Dmitri Samovski, Xiong Su, Jialiu Liu, Sinju Sundaresan und Philip D. Stahl. „Ubiquitination and degradation of the hominoid-specific oncoprotein TBC1D3 is regulated by protein palmitoylation“. Biochemical and Biophysical Research Communications 434, Nr. 2 (Mai 2013): 388–93. http://dx.doi.org/10.1016/j.bbrc.2013.04.001.

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Dissertationen zum Thema "Tbc1D3"

Penisson, Maxime. „Mécanismes de LIS1 dans les progéniteurs neuraux contribuant aux malformations de développement du cortex“. Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS415.

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Les malformations du développement du cortex sont associées à des troubles de la prolifération des progéniteurs et de la migration neuronale. Les glies radiaires basales (bRGs), un type de progéniteur, sont limités dans les espèces lissencéphaliques mais abondants dans les cerveaux gyrencéphaliques. Le gène LIS1, codant pour un régulateur de la dynéine, est muté dans la lissencéphalie humaine. LIS1 a un rôle dans la division cellulaire et la migration neuronale. Dans cette étude, nous avons généré des cellules bRG-like dans le cerveau embryonnaire murin, pour étudier le rôle de Lis1 dans leur production. Ceci fut réalisé par électroporation in utero du gène hominoïde-spécifique TBC1D3 au jour embryonnaire (E) 14.5. Nous avons confirmé que l’expression de TBC1D3 dans des cerveaux WT induit un grand nombre de cellules bRG-like basales. Puis, nous avons étudié la production des bRGs-like dans des cerveaux murins hétérozygotes pour Lis1. Nos résultats novateurs montrent que la déplétion de Lis1 à partir de E9.5 empêche la production de cellules bRG-like induites par TBC1D3. La déplétion de Lis1 change l’orientation du fuseau mitotique, accroit le nombre de mitoses abventriculaires et altère l’expression de N-Cadhérine. Nous concluons que la perturbation du dosage de Lis1 pourrait perturber le nombre et la position corrects des progéniteurs, contribuant à la pathogenèse de Lis1
Human cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Basal radial glia (bRGs), a type of progenitor cells, are limited in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 overexpression in WT brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Lis1 depletion changed mitotic spindle orientations at the ventricular surface, increased the proportion of abventricular mitoses, and altered N-Cadherin expression, altering TBC1D3 function. We conclude that perturbation of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis

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Benninghoff, Tim [Verfasser], Michael [Gutachter] Feldbrügge und Hadi [Gutachter] Al-Hasani. „Role of the Rab GTPase activating proteins TBC1D1 and TBC1D4 in the regulation of skeletal muscle fatty acid metabolism / Tim Benninghoff ; Gutachter: Michael Feldbrügge, Hadi Al-Hasani“. Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1208505483/34.

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Leicht, Katja. „Positionelle Klonierung von Tbc1d1 als Kandidatengen für Adipositas“. Phd thesis, Universität Potsdam, 2008. http://opus.kobv.de/ubp/volltexte/2009/3461/.

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Nob1 (New Zealand obese 1) bezeichnet einen Adipositas-QTL auf Chr. 5 der Maus (LODBMI >3,3), der in einem Rückkreuzungsexperiment der Mausstämme NZO (adipös) und SJL (schlank) identifiziert wurde. Um Kandidatengene für Adipositas zu finden, wurden mehr als 300 Nob1-Transkripte mit Hilfe von Genexpressionsanalysen auf Unterschiede in stoffwechselrelevanten Geweben zwischen beiden Mausstämmen untersucht. Sieben Gene zeigten eine differentielle Expression: 2310045A20Rik, Tbc1d1, Ppp1cb, Mll5, Insig1, Abhd1 und Alox5ap. Die codierenden Bereiche dieser Gene wurden anschließend auf Sequenzunterschiede zwischen NZO und SJL untersucht. Nur im Gen Tbc1d1, das im Peak-Bereich des Nob1 lokalisiert ist, wurde eine SJL-spezifische Deletion von sieben Basen detektiert, die zu einer Leserasterverschiebung und einem vorzeitigen Abbruch des Proteins in der funktionellen Rab-GAP-Domäne führt (Loss-of-Function-Mutation). Interessanterweise wurde eine Variante von TBC1D1 (R125W) in Kopplungsanalysen mit Adipositas beim Menschen assoziiert (Stone et al., 2006). TBC1D1 zeigt eine hohe Homologie zu TBC1D4 (AS160), das im Insulinsignalweg eine wichtige Rolle spielt. In 17 weiteren Genen im Peak-Bereich des Nob1 wurde keine weitere SJL-spezifischen Mutation detektiert. Bei NZO-Tieren erfolgte die Tbc1d1-mRNA-Expression vorwiegend in glycolytischen Fasern des Skelettmuskels. Zudem wurden zwei gewebsspezifisch exprimierte Tbc1d1-Isoformen identifiziert, die sich durch alternatives Splicen der Exone 12 und 13 unterscheiden. Die im Rahmen dieser Arbeit gefundenen Ergebnisse machen Tbc1d1 zu einem plausiblen Kandidatengen für den Nob1-QTL. Welche Funktion Tbc1d1 im Glucose- und Fettstoffwechsel des Skelettmuskels hat, muss in weiteren Analysen untersucht werden.
Nob1 (New Zealand obese 1) has been identified as an obesity QTL on chromosome 5 (LODBMI >3,3) in a backcross experiment of obese NZO and lean SJL mice. To identify candidate genes for obesity expression profiling experiments with RNA from metabolic tissues were performed with more than 300 Nob1-genes. Seven genes showed differences in mRNA expression levels between both strains: 2310045A20Rik, Tbc1d1, Ppp1cb, Mll5, Insig1, Abhd1, and Alox5ap. Sequencing of the coding regions of these genes revealed a SJL-specific deletion of seven basepairs in the Tbc1d1 gene that is located in the peak region of Nob1. This mutation leads to a frameshift resulting in a truncated protein that lacks the important Rab-GAP-domain (Loss-of-Function-mutation). Interestingly, linkage analysis of the R125W-variant of TBC1D1 has been recently associated with human obesity. TBC1D1 shows high homology to TBC1D4 (AS160) that plays an important role in the insulin signaling pathway. No other SJL-specific mutations were detected in 17 further genes in the Nob1 peak region. In NZO mice Tbc1d1 mRNA is predominantly expressed in glycolytic fibres of skeletal muscle. Two isoformes were identified differing in alternative spliced exons 12 and 13 and showing a tissue specific mRNA expression. The results presented in this work make Tbc1d1 a very feasible candidate gene to be causal for Nob1. The function of Tbc1d1 in the metabolism of carbohydrates and fat has yet to be analyzed.

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Dash, Satya. „Analysis of TBC1D4 genetic variants in patients with severe insulin resistance“. Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609172.

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Câmara, Ana Isabel Rodrigues. „Estudo de padrões de expressão de transcritos alternativos do gene tbccd1 em tecidos humanos e linhas celulares cancerígenas“. Master's thesis, Escola Superior de Saúde Egas Moniz, 2013. http://hdl.handle.net/10400.26/6142.

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Dissertação para obtenção do grau de Mestre em Biologia Molecular em Saúde
O centrossoma é um organito essencial nos eucariotas sendo o principal centro organizador de microtúbulos nas células animais. É composto por um par de centríolos e rodeado por uma matriz pericentriolar. Em células em interfase, os centrossomas estão envolvidos na nucleação/organização dos microtúbulos, no posicionamento dos organitos, e.g. o complexo de Golgi, no estabelecimento da polaridade e ainda na migração e adesão, por sua vez em mitose facilitam a formação dos fusos mitóticos.
Estudos realizados pelo nosso grupo, identificaram uma nova proteína humana, que contem o domínio TBCC (TBCCD1), a qual está relacionada com o cofator C da tubulina, o qual participa na via de folding da tubulina apresentando uma atividade GAP (GTPase activating protein) para a β-tubulina. O TBCCD1 é um componente centrossomal, localizando-se também na zona mediana do fuso, corpo médio e corpos basais/zona de transição de cílios primários e móveis. O silenciamento do TBCCD1 em células RPE-1 provocou um aumento acentuado da distância núcleo-centrossoma, um atraso no ciclo celular, desorganização do complexo de Golgi e baixa eficiência para formar cílios primários. Através de técnicas de análise mutacional identificou-se o domínio mínimo necessário à localização do TBCCD1 no centrossoma, o qual corresponde aos 20 primeiros resíduos de aminoácidos da sua região N-terminal.
O splicing alternativo do pré-mRNA é um passo crítico para a expressão de genes sendo a principal fonte para a diversidade de proteínas nos eucariotas superiores. Atualmente pensa-se que ocorre em mais de 90% dos genes humanos. A proteína TBCCD1 humana é codificada por um gene localizado no cromossoma 3 (3q27.3) e apresenta a sua região codificante interrompida por 7 intrões. O presente estudo permitiu verificar que este gene origina três transcritos diferentes pelo processo de splicing alternativo. Um destes transcritos resulta do facto que existem dois primeiros exões alternativos, que originam duas proteínas putativas diferindo nos primeiros resíduos de aminoácidos da sua N-terminal. Esta sequência de aminoácidos alternativos corresponde no TBCCD1 ao domínio envolvido na sua localização centrossomal. De facto, as duas novas variantes apresentam uma localização citoplasmática não se localizando no centrossoma.

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Longatti, Andrea D. „The RabGAP TBC1D14 regulates autophagosome formation via recycling endosomes and Rab11“. Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/642300/.

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Autophagy is a bulk degradation process characterised by the formation of double membrane vesicles called autophagosomes. Autophagosomes derive from a small precursor structure called phagophore, which is expanded to enclose a portion of cytoplasm or organelle, and finally fuses with the endo-lysosomal system to acquire degradative capacity. Autophagy is often studied as a response to starvation, since the degraded components can be re-used for biosynthetic pathways. However, in multicellular organisms, it has many additional functions in tissue homeostasis, during development, in infection and immunity, and in programmed cell death. Regarding autophagy many questions remain such as the origin of the autophagosomal membrane, the mechanism of phagophore extension and many of the signalling pathways that lead to autophagosome assembly. To better understand the membrane trafficking events involved in autophagosome formation I did an over-expression screen for Rab GTPase activating proteins (RabGAPs) inhibiting this process. RabGAPs act inhibitory on Rab GTPases, which are major regulators of intracellular membrane traffic. I have identified 11 RabGAPs that inhibit autophagosome formation, one of which is TBC1D14, which binds to ULK1, an important kinase for initiation of autophagy. TBC1D14 also binds to Rab11 and tubulates recycling endosomes when over-expressed. I found that both ULK1 and another essential autophagy protein mAtg9 localise to recycling endosomes under normal conditions. I propose that recycling endosomes can signal through both ULK1 and mAtg9 to initiate autophagosome formation upon starvation and may be important in monitory cellular nutrient status, and/or provide membrane to autophagosomes. Investigating the role of ULK1 in vivo, I found that ULK1 knock-out mice are able to undergo basal autophagy as assessed by LC3 lipidation in various tissues. However, ULK1 knock-out mice have less CD4 and CD8-positive mature T cells and their response to TCR stimulation is impaired compared to T cells from wild type animals.

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Negra, Maria Lúcia Mourão Barriga. „" Caracterização da proteína centrossomal TBCCD1 durante o desenvolvimento embrionário do peixe zebra"“. Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2010. http://hdl.handle.net/10216/62269.

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Negra, Maria Lúcia Mourão Barriga. „" Caracterização da proteína centrossomal TBCCD1 durante o desenvolvimento embrionário do peixe zebra"“. Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2010. http://hdl.handle.net/10216/62269.

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Stermann, Torben [Verfasser], Hadi [Akademischer Betreuer] Al-Hasani und Eckhard [Gutachter] Lammert. „The role of TBC1D1 in insulin secretion from mouse pancreatic islets / Torben Stermann ; Gutachter: Eckhard Lammert ; Betreuer: Hadi Al-Hasani“. Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2016. http://d-nb.info/1121745598/34.

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Roy, Michèle. „Étude de l'expression et du rôle de TBC1D25 et de ses isoformes dans les ostéoclastes humains“. Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/10639.

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La maladie de Paget est caractérisée par un remodelage osseux anarchique débutant par une phase de résorption excessive suivie d’une phase de formation désordonnée. Comme les ostéoclastes sont recrutés en plus grand nombre et sont hyperactifs aux sites affectés par la maladie, cette cellule a été incriminée dans ce désordre osseux. Le phénotype de l’ostéoclaste pagétique comporte de plus un défaut du processus autophagique, de même qu'une résistance à l'apoptose, dont les mécanismes restent mal connus. Certains facteurs génétiques et environnementaux contribuent en partie au phénotype, mais d'autres facteurs pourraient y être associés. Des travaux du laboratoire ont mis en évidence six événements de l’épissage alternatif associés à la maladie de Paget. Parmi les gènes identifiés, le gène TBC1D25 et ses deux isoformes connus n’ont jamais été étudiés dans l’ostéoclaste. Le gène TBC1D25 possède un domaine hautement conservé TBC régulant l’activité des petites GTPases Rabs dans le transport vésiculaire et un domaine LIR liant la protéine LC3 durant le processus de l’autophagie. Ces domaines fonctionnels se retrouvent seulement dans l’isoforme long. L’hypothèse de recherche est que l’altération de l’épissage alternatif du gène TBC1D25 dans les ostéoclastes pagétiques explique en partie le phénotype de la cellule. Le changement dans le ratio de l’expression des isoformes affecterait le processus de l’autophagie, en plus d’affecter la principale fonction de l’ostéoclaste, la résorption osseuse. L’objectif principal de l’étude est de caractériser l’expression et la fonction de TBC1D25 dans les ostéoclastes humains. Des ostéoclastes humains différenciés à partir de monocytes fœtaux ont été utilisés pour l’étude de la fonction de TBC1D25 dans l’autophagie, l’apoptose et la résorption osseuse. Les travaux ont permis de localiser les protéines dans l’ostéoclaste dans des conditions maintenant un niveau basal de l’autophagie et dans des conditions induisant l’autophagie. L’interaction entre TBC1D25 et Rab34 a été confirmée pour la première fois dans les ostéoclastes. De plus, une variation de cette interaction a été observée dans les différentes conditions modulant le niveau d’induction de l'autophagie. Les résultats préliminaires montrent une augmentation du ratio LC3II/LC3I lors de la diminution de l’expression de TBC1D25 dans des conditions augmentant l’induction de l'autophagie. Par contre, aucun effet a été observé sur la résorption osseuse ou sur l'apoptose lors de la diminution de l’expression de TBC1D25. En conclusion, les résultats préliminaires montrent que TBC1D25 préviendrait l’augmentation du ratio LC3II/LC3I dans l’ostéoclaste soit en inhibant l’induction de l’autophagie ou en favorisant la dégradation des autophagosomes par l’entremise de son action sur Rab34.
Abstract : Paget’s disease of bone (PDB) is characterized by increases in bone turnover starting with excessive resorption followed by disorganized bone formation. Because the initial phase of PDB involves excessive bone resorption, osteoclasts have been identified as the cells primarily affected in PDB. Pagetic osteoclasts are overactive, resistant to apoptosis and exhibit defects in autophagy, but the mechanisms involved are still unclear. While genetic and environmental factors associated with PDB may partially account for the osteoclast phenotype, other genetic contributors have been identified. Recent work from our laboratory has identified six alternative splicing events associated with PDB. Among those genes, TBC1D25 and its two known isoforms have never been studied in osteoclasts. The two functional domains of TBC1D25 (TBC and LIR) are only present in the long isoform. The highly conserved TBC domain regulates small Rab GTPases in vesicular transport and the LIR domain interacts with LC3 during autophagy. Our research hypothesis is that altered alternative splicing of TBC1D25 in pagetic osteoclasts could contribute to phenotype. Differential isoform expression could affect osteoclast autophagy and bone resorption. The aim of the study is to characterize the expression and function of TBC1D25 proteins in human osteoclasts. Osteoclasts differentiated from cord blood monocytes were used to investigate the function of TBC1D25 in autophagy, apoptosis and bone resorption. First, the localization of the protein has been characterized in conditions maintaining basal autophagy and in rapamycin-induced autophagy. Interactions between TBC1D25 and Rab34 have been observed for the first time in osteoclasts. Moreover, changes in the interaction were observed with autophagy induction. Preliminary results suggest increases in LC3II/LC3I ratio with decreasing TBC1D25 expression when autophagy induction is stimulated. On the other hand, preliminary results showed that decreased expression of TBC1D25 did not affect bone resorption, nor apoptosis. In conclusion, preliminary results show that in osteoclasts, TBC1D25 could prevent the increase of LC3II/LC3I ratio by inhibiting autophagy induction or by promoting the clearance of autophagosomes through its action on Rab34.

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Bücher zum Thema "Tbc1D3"

Davey, K. General Science: Introductory Facts and Concepts, Volume 1 TBCE3-1. 2016.

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Buchteile zum Thema "Tbc1D3"

Suski, W., und T. Palewski. „TbCrS3“. In Pnictides and Chalcogenides II, 1040–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_280.

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Gonçalves, João, und Helena Soares. „TBCCD1“. In Encyclopedia of Signaling Molecules, 5321–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_551.

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Gonçalves, João, und Helena Soares. „TBCCD1“. In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_551-1.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra et al. „TBCCD1“. In Encyclopedia of Signaling Molecules, 1831–36. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_551.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk und R. Zaremba. „TbCl3 ht“. In Structure Types. Part 10: Space Groups (140) I4/mcm – (136) P42/mnm, 797. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19662-1_670.

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Kawazoe, Yoshiyuki, Takeshi Kanomata und Ryunosuke Note. „TbCoO3 (Synthesized Under Pressure)“. In High Pressure Materials Properties: Magnetic Properties of Oxides Under Pressure, 645–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-64593-2_171.

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Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, Arti N. Shah, Bharat K. Kantharia, Ulrich Salzer, Bodo Grimbacher et al. „TBCD“. In Encyclopedia of Molecular Mechanisms of Disease, 2027. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7897.

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Cavalcante, F. H. M., A. W. Carbonari, R. F. L. Malavasi, G. A. Cabrera-Pasca, J. Mestnik-Filho und R. N. Saxena. „Temperature dependence of electric field gradient in TbCoO3“. In HFI/NQI 2007, 253–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-85320-6_38.

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Fontanesi, Luca, und Francesca Bertolini. „The TBC1D1 Gene“. In Vitamins & Hormones, 77–95. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-407766-9.00004-3.

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Aligianis, Irene, und Mark Handley. „RAB3GAP1, RAB3GAP2, RAB18, TBC1D20, and the Warburg Micro and Martsolf Syndromes“. In Epstein's Inborn Errors of Development, 1191–96. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199934522.003.0181.

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Konferenzberichte zum Thema "Tbc1D3"

Stermann, T., D. Grittner, L. Scholten, A. Cramer, A. Chadt, D. Pesta, K. Bódis et al. „Expressionsmuster von TBC1D1- und TBC1D4-Isoformen in primären humanen Skelettmuskelzellen während der Differenzierung“. In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688316.

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Mafakheri, S., R. Flörke, S. Kanngießer, S. Hartwig, L. Espelage, C. De Wendt, T. Schönberger et al. „Regulation of recombinant TBC1D1, the RabGAP involved in GLUT4 translocation“. In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688318.

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Eickelschulte, S., S. Hartwig, B. Leiser, S. Lehr, V. Joschko, A. Chadt und H. Al-Hasani. „Phosphorylation pattern and biological activity of TBC1D4, the RabGAP regulating GLUT4 translocation“. In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727357.

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Peifer-Weiß, Leon, Stefan Lehr, Sonja Hartwig, Michael Turewicz, Ulrike Kettel, Martina Schiller, Hadi Al-Hasani und Alexandra Chadt. „Identification of contraction-specific phosphorylation pattern of TBC1D1 in murine C2C12 myotubes“. In Diabetes. Umwelt. Leben. Perspektiven aus allen Blickwinkeln. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1785378.

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Binsch, C., D. Barbosa, K. Jeruschke, J. Weiß, M. Hubert, G. Hansen, SM Hodge et al. „Absence of TBC1D4/AS160 impairs cardiac substrate metabolism and increases ischemia/reperfusion-induced myocardial damage“. In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688288.

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Binsch, C., D. Barbosa, K. Jeruschke, J. Weiß, M. Hubert, G. Hansen, S. Gorressen et al. „Deletion von TBC1D4/AS160 erhöht den Myokardschaden nach Ischämie/Reperfusion und verschlechtert den kardialen Substratmetabolismus“. In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641777.

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Kim, Beom Kyu, Byung Gi Park, Hwa Jeong Han, Ji Hye Park und Won Ki Kim. „An Effect of Bismuth Ion on the Reduction of Terbium Ion in Molten LiCl-KCl Eutectic Salt“. In 2018 26th International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/icone26-82468.

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A salt waste generated from the pyroprocess contains residual actinides and needs to be purified for recycling of the salt and waste conditioning. A co-reduction process could be considered for removal of residual actinides from the salt waste, which contains lanthanides and residual actinides. In the study, specifically, an effect of Bi(III) ion on the electrochemical reaction of Tb(III) ion was investigated in the molten LiCl-KCl eutectic with BiCl3 and TbCl3 at 773 K using electrochemical techniques of cyclic voltammetry, square wave voltammetry and open circuit chronopotentiometry. Tb(III) has a single redox couple without Bi(III). However, the cyclic voltammograms obtained at tungsten electrode in LiCl-KCl-BiCl3-TbCl3 showed four redox couples. The square wave voltammogram in same condition also showed five reduction peaks. Cyclic voltammogram and square wave voltammogram was resolved to find the accurate peaks for redox reaction. Each peak indicates the formation of Tb-Bi intermetallic compound except Tb(III) reduction peak. From the phase diagram of Tb-Bi, it is inferred that each peak corresponds to TbBi2, TbBi, Tb4Bi3, and Tb5Bi3. The open circuit chronopotentiometry was conducted to estimate Gibbs free energy of formation of Tb-Bi intermetallic compound. The experimental results obtained from three kind of the electrochemical techniques showed that Tb-Bi intermetallic compounds were electrochemically formed under potential of Tb(III) reduction potential by co-reduction of Bi(III) and Tb(III). These results indicate that underpotential deposition by co-reduction could be used for Tb(III) removal from the salt waste with Bi(III).

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Li, Angela S., Jason A. Reuter, Can Cenik und Michael P. Synder. „Abstract 2457: Investigating the functional significance of novel, recurrent noncoding mutations of TBC1D12 in bladder cancer“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2457.

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Machida, Keigo, Hifzur R. Siddique, Mengmei Zheng, Peleg Winer, Dinesh Babu Uthaya Kumar, Ahmed Rokan, Linda Sher et al. „Abstract 1984: Cell fate reprogramming of liver tumor-initiating stem-like cells via phosphorylated NUMB and TBC1D15“. In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1984.

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Elangovan, S. G., F. Fereydouni-Forouzandeh und O. Ait-Mohamed. „Performance analysis of TBCD protocol over Wireless Body channel“. In 2012 IEEE 55th International Midwest Symposium on Circuits and Systems (MWSCAS). IEEE, 2012. http://dx.doi.org/10.1109/mwscas.2012.6292203.

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