Relevant bibliographies by topics / EBAG9

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'EBAG9'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "EBAG9"

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Rüder, Constantin, Tatiana Reimer, Ignacio Delgado-Martinez, Ricardo Hermosilla, Arne Engelsberg, Ralf Nehring, Bernd Dörken, and Armin Rehm. "EBAG9 Adds a New Layer of Control on Large Dense-Core Vesicle Exocytosis via Interaction with Snapin." Molecular Biology of the Cell 16, no. 3 (March 2005): 1245–57. http://dx.doi.org/10.1091/mbc.e04-09-0817.

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Regulated exocytosis is subject to several modulatory steps that include phosphorylation events and transient protein–protein interactions. The estrogen receptor-binding fragment-associated gene9 (EBAG9) gene product was recently identified as a modulator of tumor-associated O-linked glycan expression in nonneuronal cells; however, this molecule is expressed physiologically in essentially all mammalian tissues. Particular interest has developed toward this molecule because in some human tumor entities high expression levels correlated with clinical prognosis. To gain insight into the cellular function of EBAG9, we scored for interaction partners by using the yeast two-hybrid system. Here, we demonstrate that EBAG9 interacts with Snapin, which is likely to be a modulator of Synaptotagmin-associated regulated exocytosis. Strengthening of this interaction inhibited regulated secretion of neuropeptide Y from PC12 cells, whereas evoked neurotransmitter release from hippocampal neurons remained unaltered. Mechanistically, EBAG9 decreased phosphorylation of Snapin; subsequently, association of Snapin with synaptosome-associated protein of 25 kDa (SNAP25) and SNAP23 was diminished. We suggest that the occurrence of SNAP23, Snapin, and EBAG9 also in nonneuronal cells might extend the modulatory role of EBAG9 to a broad range of secretory cells. The conjunction between EBAG9 and Snapin adds an additional layer of control on exocytosis processes; in addition, mechanistic evidence is provided that inhibition of phosphorylation has a regulatory function in exocytosis.
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Aoki, T., S. Inoue, H. Imamura, J. Fukushima, S. Takahashi, T. Urano, K. Hasegawa, T. Ogushi, Y. Ouchi, and M. Makuuchi. "EBAG9/RCAS1 expression in hepatocellular carcinoma." European Journal of Cancer 39, no. 11 (July 2003): 1552–61. http://dx.doi.org/10.1016/s0959-8049(03)00362-9.

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Ikeda, Kazuhiro, Masako Sato, Osamu Tsutsumi, Fujiko Tsuchiya, Michiko Tsuneizumi, Mitsuru Emi, Issei Imoto, Johji Inazawa, Masami Muramatsu, and Satoshi Inoue. "Promoter Analysis and Chromosomal Mapping of Human EBAG9 Gene." Biochemical and Biophysical Research Communications 273, no. 2 (July 2000): 654–60. http://dx.doi.org/10.1006/bbrc.2000.2920.

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Takahashi, Satoru, Tomohiko Urano, Fujiko Tsuchiya, Tetsuya Fujimura, Tadaichi Kitamura, Yasuyoshi Ouchi, Masami Muramatsu, and Satoshi Inoue. "EBAG9/RCAS1 expression and its prognostic significance in prostatic cancer." International Journal of Cancer 106, no. 3 (July 1, 2003): 310–15. http://dx.doi.org/10.1002/ijc.11205.

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Ogushi, Tetsuo, Takahashi Satoru, Takumi Takeuchi, Tetsuya Fujimura, Tomohiko Urano, Satoshi Inoue, and Tadaichi Kitamura. "655: EBAG9/RCAS1 Expression Enhances Tumor Growth in Renal Cell Carcinoma." Journal of Urology 173, no. 4S (April 2005): 178–79. http://dx.doi.org/10.1016/s0022-5347(18)34895-x.

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Kumagai, Jinpei, Tomohiko Urano, Tetsuo Ogushi, Satoru Takahashi, Kuniko Horie-Inoue, Tetsuya Fujimura, Kotaro Azuma, et al. "EBAG9 IS A TUMOR-PROMOTING AND PROGNOSTIC FACTOR FOR BLADDER CANCER." Journal of Urology 181, no. 4S (April 2009): 310. http://dx.doi.org/10.1016/s0022-5347(09)60882-x.

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Kumagai, Jinpei, Tomohiko Urano, Tetsuo Ogushi, Satoru Takahashi, Kuniko Horie-Inoue, Tetsuya Fujimura, Kotaro Azuma, et al. "EBAG9 is a tumor-promoting and prognostic factor for bladder cancer." International Journal of Cancer 124, no. 4 (February 15, 2009): 799–805. http://dx.doi.org/10.1002/ijc.23982.

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Aoki, T., S. Inoue, H. Imamura, J. Fukushima, T. Urano, K. Hasegawa, and M. Makuuchi. "EBAG9/RCAS1 expression in hepatocellular carcinoma: Correlation with tumor dedifferentiation and proliferation." Journal of Hepatology 38 (April 2003): 74. http://dx.doi.org/10.1016/s0168-8278(03)80308-2.

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Suzuki, T., S. Inoue, W. Kawabata, J. Akahira, T. Moriya, F. Tsuchiya, S. Ogawa, M. Muramatsu, and H. Sasano. "EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions." British Journal of Cancer 85, no. 11 (November 27, 2001): 1731–37. http://dx.doi.org/10.1054/bjoc.2001.2176.

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Akahira, J.-i., M. Aoki, T. Suzuki, T. Moriya, H. Niikura, K. Ito, S. Inoue, K. Okamura, H. Sasano, and N. Yaegashi. "Expression of EBAG9/RCAS1 is associated with advanced disease in human epithelial ovarian cancer." British Journal of Cancer 90, no. 11 (May 26, 2004): 2197–202. http://dx.doi.org/10.1038/sj.bjc.6601832.

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Dissertations / Theses on the topic "EBAG9"

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Wolf, Jana. "Role of EBAG9 in COPI-dependent glycoprotein maturation and secretion processes in tumor cells." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16227.

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EBAG9 (estrogen receptor-binding fragment-associated gene 9) hat als unabhängiger prognostischer Marker viel Aufmerksamkeit erregt, da in einigen Tumoren hohe Expressionsraten und Tumorentwicklung korrelieren. In diesen Fällen ist eine hohe EBAG9 Expression häufig mit einer schlechten klinischen Prognose verbunden. EBAG9 ist ein ubiquitär exprimiertes Golgi Protein. Aktuelle Daten demonstrieren, dass es in sekretorischen Zellen an der regulierten Exozytose und an der zytotoxischen Funktion von Lymphozyten beteiligt ist. In epithelialen Zellen führt es zur Generierung von Tumor-assoziierten O-Glykanen, welche ein Erkennungsmerkmal vieler Krebsarten sind. In dieser Arbeit wurde der pathogenetische Zusammenhang zwischen EBAG9 Expression und der Veränderung des zellulären Glykoms untersucht. Um einen tieferen Einblick in die zelluläre Funktion von EBAG9 in epithelialen Zellen zu gewinnen, wurden Zellen mit tumorähnlicher EBAG9 Expression verwendet. Innerhalb dieser Arbeit wurde demonstriert, dass EBAG9 mit anterograden COPI Vesikeln assoziiert und zwischen dem ER-Golgi intermediären Kompartiment und cis-Golgi pendelt. EBAG9 verursacht eine Verzögerung des anterograden Transportes vom ER zum Golgi und verändert die Lokalisation von Komponenten der ER Qualitätskontrolle und des Glycosylierungsapparates. Auf der anderen Seite beschleunigt die verminderte Expression von EBAG9 den Proteintransport durch den Golgi und verstärkt die Aktivität von Mannosidase II. Mechanistisch betrachtet verhindert EBAG9 die Rekrutierung von ArfGAP1 an die Membran. Dies beeinträchtigt das Auflösen der COPI Vesikelhülle und somit die Fusion von Vesikeln am cis-Golgi. Damit agiert EBAG9 in epithelialen Zellen als negativer Regulator des COPI-abhängigen ERGolgi Transportes und stellt damit ein neues phatogenetisches Prinzip dar, bei dem die Beeinflussung des intrazellulären Transportes zu der Entstehung von Tumor-assoziierten Glykanen führt.
The estrogen receptor-binding fragment-associated gene 9 (EBAG9) has received increased attention as an independent prognostic marker for disease-specific survival since in some human tumor entities high expression levels correlate with tumor progression and poor clinical prognosis. Interestingly, EBAG9 was identified as an ubiquitously expressed Golgi protein. Recent data demonstrate an involvement in regulated exocytosis in secretory cells and the cytotoxic functions of lymphocytes. However, EBAG9 is expressed in essentially all mammalian tissues, and in epithelial cells it has been identified as a modulator of tumorassociated O-linked glycan expression, a hallmark of many carcinomas. This thesis addresses the pathogenetic link between EBAG9 expression and the alteration of the cellular glycome. To gain further insights into the cellular functions of EBAG9 in epithelial cells, tumor-associated EBAG9 overexpression was mimicked in living cells. It was demonstrated that EBAG9 associates with anterograde COPI-coated carriers and shuttles between the ER-Golgi intermediate compartment and cis-Golgi stacks. EBAG9 overexpression imposes a delay in anterograde ER-to-Golgi transport and mislocalizes components of the ER quality-control and glycosylation machinery. Conversely, EBAG9 downregulation accelerates glycoprotein transport through the Golgi and enhances mannosidase activity. Functionally, EBAG9 impairs ArfGAP1 recruitment to membranes and consequently, interferes with the disassembly of the coat lattice at the cis-Golgi prior to fusion. Thus, EBAG9 acts as a negative regulator of a COPI-dependent ER-to-Golgi transport pathway in epithelial cells and represents a novel pathogenetic principle in which interference with intracellular membrane trafficking results in the emergence of a tumor-associated glycome.
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Rüder, Constantin. "Charakterisierung der physiologischen Funktion des putativ tumorassoziierten Moleküls EBAG9 als Modulator der Exozytosefunktion in vitro und in vivo." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2006/62/index.html.

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Bauer, Christof Peter [Verfasser]. "Einfluss der Deletion von EBAG9 auf die zytotoxische Effektorfunktion von CD8+-T-Lymphozyten im E.G-7 Tumormodell / Christof Peter Bauer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/114842556X/34.

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Ricketts, Jessie. "Reciprocal development in vocabulary and reading skills." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:ef73c787-eba9-4ddf-bc85-1700de9c6d3a.

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Data are presented in seven chapters that address the reciprocal relationship between oral vocabulary and reading development. Chapter 2 explores exception word reading in poor comprehenders longitudinally, finding deficits that are pervasive over a period of two years. The results support the hypothesis that weak oral vocabulary skills are causally related to poor exception word reading in this group. In Chapter 3, orthographic and semantic skills in poor comprehenders are investigated in a word learning paradigm. This chapter provides evidence that poor comprehenders have more difficulty learning and retaining semantic information than orthographic information. A similar paradigm is described in Chapter 4 to investigate predictors of orthographic and semantic learning. In a large group of typically developing readers, this demonstrates that decoding is the strongest predictor of orthographic learning while existing oral vocabulary knowledge is the strongest predictor of semantic learning. In Chapters 5 and 6 orthographic and semantic skills in poor comprehenders and children with dyslexia are compared using standard off-line tasks (Chapter 5) and an online word learning experiment (Chapter 6). These chapters indicate similarities as well as differences in the reading and language profiles of these groups. Chapter 7 adopts a different approach by using a word learning study to investigate the benefit of teaching new oral vocabulary in the presence of orthography.
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Wolf, Jana [Verfasser]. "Role of EBAG9 in COPI-dependent glycoprotein maturation and secretion processes in tumor cells / von Jana Wolf, geb. Göttert." 2010. http://d-nb.info/101060631X/34.

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Rüder, Constantin [Verfasser]. "Charakterisierung der physiologischen Funktion des putativ tumorassoziierten Moleküls EBAG9 als Modulator der Exozytosefunktion in vitro und in vivo / vorgelegt von Constantin Rüder." 2005. http://d-nb.info/979252237/34.

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Book chapters on the topic "EBAG9"

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Aoki, Taku, Hiroshi Imamura, Masatoshi Makuuchi, and Satoshi Inoue. "Immunohistochemical Detection of EBAG9/RCAS1 Expression in Hepatocellular Carcinoma." In Handbook of Immunohistochemistry and in situ Hybridization of Human Carcinomas, Volume 3 - Molecular Genetics, Liver Carcinoma, and Pancreatic Carcinoma, 261–68. Elsevier, 2005. http://dx.doi.org/10.1016/s1874-5784(05)80031-5.

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"eBags." In Internet Retail Operations, 231–44. Taylor & Francis, 2011. http://dx.doi.org/10.1201/9781439800911-19.

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"eBags: Managing Growth." In Internet Retail Operations, 245–58. CRC Press, 2011. http://dx.doi.org/10.1201/b11029-21.

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Conference papers on the topic "EBAG9"

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Laaber, Karin, Taronish D. Dubash, Anna Maria Melzer, Tania Christiansen, Nati Ha, Benedikt Brors, Martin Schneider, Friederike Herbst, Hanno Glimm, and Claudia R. Ball. "Abstract 2852: A gene activatingin vivoscreen identifies EBAG9 as novel metastasis regulator in human colorectal cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2852.

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Shigekawa, T., N. Ijichi, K. Ikeda, T. Miyazaki, K. Horie-Inoue, C. Shimizu, S. Saji, et al. "Abstract P6-04-27: EBAG9 immunoreactivity is a potential prognostic factor for poor outcome of breast cancer patients with adjuvant tamoxifen therapy." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p6-04-27.

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Brodersen, Christina, Bent G. Christensen, Kaj Grønbæk, Christian Dindler, and Balasuthas Sundararajah. "eBag." In the 14th international conference. New York, New York, USA: ACM Press, 2005. http://dx.doi.org/10.1145/1060745.1060791.

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Jeanne, Florian, Yann Soullard, Ali Oker, and Indira Thouvenin. "EBAGG: Error-Based Assistance for Gesture Guidance in Virtual Environments." In 2017 IEEE 17th International Conference on Advanced Learning Technologies (ICALT). IEEE, 2017. http://dx.doi.org/10.1109/icalt.2017.32.

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Hadjitchoneva, Juliana, Claudio Ruff, Marcelo Ruiz, and Alexis Matheu. "The use of artificial intelligence in the online retail sector: the case of the eBag supermarket." In 2021 16th Iberian Conference on Information Systems and Technologies (CISTI). IEEE, 2021. http://dx.doi.org/10.23919/cisti52073.2021.9476484.

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