Academic literature on the topic 'Tbc1D3'
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Journal articles on the topic "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, no. 4 (April 2008): 1304–16. http://dx.doi.org/10.1091/mbc.e07-06-0594.
Full textTobias, Irene S., Kara K. Lazauskas, Jeremy Siu, Pablo B. Costa, Jared W. Coburn, and 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, no. 2 (February 1, 2020): 350–61. http://dx.doi.org/10.1152/japplphysiol.00704.2019.
Full textPenisson, Maxime, Mingyue Jin, Shengming Wang, Shinji Hirotsune, Fiona Francis, and Richard Belvindrah. "Lis1 mutation prevents basal radial glia-like cell production in the mouse." Human Molecular Genetics 31, no. 6 (October 12, 2021): 942–57. http://dx.doi.org/10.1093/hmg/ddab295.
Full textEspelage, Lena, Hadi Al-Hasani, and Alexandra Chadt. "RabGAPs in skeletal muscle function and exercise." Journal of Molecular Endocrinology 64, no. 1 (January 2020): R1—R19. http://dx.doi.org/10.1530/jme-19-0143.
Full textMikłosz, Agnieszka, Bartłomiej Łukaszuk, Elżbieta Supruniuk, Kamil Grubczak, Marcin Moniuszko, Barbara Choromańska, Piotr Myśliwiec, and 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, no. 6 (June 16, 2021): 1515. http://dx.doi.org/10.3390/cells10061515.
Full textZhou, Qiong L., Zhen Y. Jiang, John Holik, Anil Chawla, G. Nana Hagan, John Leszyk, and Michael P. Czech. "Akt substrate TBC1D1 regulates GLUT1 expression through the mTOR pathway in 3T3-L1 adipocytes." Biochemical Journal 411, no. 3 (April 14, 2008): 647–55. http://dx.doi.org/10.1042/bj20071084.
Full textMafakheri, Samaneh, Alexandra Chadt, and Hadi Al-Hasani. "Regulation of RabGAPs involved in insulin action." Biochemical Society Transactions 46, no. 3 (May 21, 2018): 683–90. http://dx.doi.org/10.1042/bst20170479.
Full textQin, Shu, Robert A. Dorschner, Irene Masini, Ophelia Lavoie‐Gagne, Philip D. Stahl, Todd W. Costantini, Andrew Baird, and Brian P. Eliceiri. "TBC1D3 regulates the payload and biological activity of extracellular vesicles that mediate tissue repair." FASEB Journal 33, no. 5 (February 4, 2019): 6129–39. http://dx.doi.org/10.1096/fj.201802388r.
Full textShen, Y., L. Zhang, H. Zhao, and 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.
Full textKong, Chen, Jeffrey J. Lange, Dmitri Samovski, Xiong Su, Jialiu Liu, Sinju Sundaresan, and Philip D. Stahl. "Ubiquitination and degradation of the hominoid-specific oncoprotein TBC1D3 is regulated by protein palmitoylation." Biochemical and Biophysical Research Communications 434, no. 2 (May 2013): 388–93. http://dx.doi.org/10.1016/j.bbrc.2013.04.001.
Full textDissertations / Theses on the topic "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.
Full textHuman 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
Benninghoff, Tim [Verfasser], Michael [Gutachter] Feldbrügge, and 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.
Full textLeicht, Katja. "Positionelle Klonierung von Tbc1d1 als Kandidatengen für Adipositas." Phd thesis, Universität Potsdam, 2008. http://opus.kobv.de/ubp/volltexte/2009/3461/.
Full textNob1 (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.
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.
Full textCâmara, 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.
Full textO 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.
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/.
Full textNegra, 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.
Full textNegra, 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.
Full textStermann, Torben [Verfasser], Hadi [Akademischer Betreuer] Al-Hasani, and 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.
Full textRoy, 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.
Full textAbstract : 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.
Books on the topic "Tbc1D3"
Davey, K. General Science: Introductory Facts and Concepts, Volume 1 TBCE3-1. 2016.
Find full textBook chapters on the topic "Tbc1D3"
Suski, W., and T. Palewski. "TbCrS3." In Pnictides and Chalcogenides II, 1040–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_280.
Full textGonçalves, João, and 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.
Full textGonçalves, João, and 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.
Full textGonçalves, 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.
Full textVillars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk, I. Savysyuk, and 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.
Full textKawazoe, Yoshiyuki, Takeshi Kanomata, and 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.
Full textRaj, 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.
Full textCavalcante, F. H. M., A. W. Carbonari, R. F. L. Malavasi, G. A. Cabrera-Pasca, J. Mestnik-Filho, and 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.
Full textFontanesi, Luca, and 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.
Full textAligianis, Irene, and 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.
Full textConference papers on the topic "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.
Full textMafakheri, 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.
Full textEickelschulte, S., S. Hartwig, B. Leiser, S. Lehr, V. Joschko, A. Chadt, and 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.
Full textPeifer-Weiß, Leon, Stefan Lehr, Sonja Hartwig, Michael Turewicz, Ulrike Kettel, Martina Schiller, Hadi Al-Hasani, and 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.
Full textBinsch, 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.
Full textBinsch, 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.
Full textKim, Beom Kyu, Byung Gi Park, Hwa Jeong Han, Ji Hye Park, and 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.
Full textLi, Angela S., Jason A. Reuter, Can Cenik, and 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.
Full textMachida, 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.
Full textElangovan, S. G., F. Fereydouni-Forouzandeh, and 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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