Search

Your search keyword '"Tasdemir, Ezgi"' showing total 29 results
Start Over Author "Tasdemir, Ezgi"
29 results on '"Tasdemir, Ezgi"'

1. Supplementary Methods and Materials from A Novel Epidermal Growth Factor Receptor Inhibitor Promotes Apoptosis in Non–Small Cell Lung Cancer Cells Resistant to Erlotinib

Author

de La Motte Rouge, Thibault, primary, Galluzzi, Lorenzo, primary, Olaussen, Ken A., primary, Zermati, Yael, primary, Tasdemir, Ezgi, primary, Robert, Thomas, primary, Ripoche, Hugues, primary, Lazar, Vladimir, primary, Dessen, Philippe, primary, Harper, Francis, primary, Pierron, Gerard, primary, Pinna, Guillaume, primary, Araujo, Natalia, primary, Harel-Belan, Annick, primary, Armand, Jean-Pierre, primary, Wong, Tai Wai, primary, Soria, Jean Charles, primary, and Kroemer, Guido, primary

Published
2023
Full Text
View/download PDF

2. Data from A Novel Epidermal Growth Factor Receptor Inhibitor Promotes Apoptosis in Non–Small Cell Lung Cancer Cells Resistant to Erlotinib

Author

de La Motte Rouge, Thibault, primary, Galluzzi, Lorenzo, primary, Olaussen, Ken A., primary, Zermati, Yael, primary, Tasdemir, Ezgi, primary, Robert, Thomas, primary, Ripoche, Hugues, primary, Lazar, Vladimir, primary, Dessen, Philippe, primary, Harper, Francis, primary, Pierron, Gerard, primary, Pinna, Guillaume, primary, Araujo, Natalia, primary, Harel-Belan, Annick, primary, Armand, Jean-Pierre, primary, Wong, Tai Wai, primary, Soria, Jean Charles, primary, and Kroemer, Guido, primary

Published
2023
Full Text
View/download PDF

3. Supplementary Table 1 from A Novel Epidermal Growth Factor Receptor Inhibitor Promotes Apoptosis in Non–Small Cell Lung Cancer Cells Resistant to Erlotinib

Author

de La Motte Rouge, Thibault, primary, Galluzzi, Lorenzo, primary, Olaussen, Ken A., primary, Zermati, Yael, primary, Tasdemir, Ezgi, primary, Robert, Thomas, primary, Ripoche, Hugues, primary, Lazar, Vladimir, primary, Dessen, Philippe, primary, Harper, Francis, primary, Pierron, Gerard, primary, Pinna, Guillaume, primary, Araujo, Natalia, primary, Harel-Belan, Annick, primary, Armand, Jean-Pierre, primary, Wong, Tai Wai, primary, Soria, Jean Charles, primary, and Kroemer, Guido, primary

Published
2023
Full Text
View/download PDF

6. Physical and morphological Properties of Polycarbonate (PC)/Acrylonitrile-Butadiene-Styrene (ABS)/Waste Urea Formaldehyde (WUF) Polymer Blends

Author

TASDEMIR, Ezgi, AKYOL, Nevriye Seyma, YUCE, Sena, and TASDEMIR, Munir

Subjects
Engineering, Mühendislik, Polycarbonate,Acrylonitrile butadiene styrene,Urea formaldehyde,Physical properties,Polymer blends
Abstract

In this study, high density polyethylene matrixcontributes to ground urea formaldehyde powder is handled as 0, 5, 10, 20 and30 wt% ratio will be mixed in the extruder. Mixture obtained from the extruderto be granulated and then the granules will be obtained as appropriate standardtest sample of the injection molding machine. Physical and morphological testswill be applied such as heat deflection temperature, vicat softening point,melt flow index, moisture content, limit oxygen index, war rate and static coefficient offriction. Also, SEMexamination will be conducted to evaluate the microstructure of ureaformaldehyde particles as well as material distribution in theseexperiments.&nbsp

Published
2018

8. Erratum to Morselli E, et al. Cell Cycle 2008; 7:3056–61

Author

Morselli, Eugenia, primary, Tasdemir, Ezgi, additional, Maiuri, Maria Chiara, additional, Galluzzi, Lorenzo, additional, Kepp, Oliver, additional, Criollo, Alfredo, additional, Vicencio, José Miguel, additional, Soussi, Thierry, additional, and Kroemer, Guido, additional

Published
2014
Full Text
View/download PDF

9. IKK connects autophagy to major stress pathways

Author

Criollo, Alfredo, primary, Senovilla, Laura, additional, Authier, Hélène, additional, Maiuri, Maria Chiara, additional, Morselli, Eugenia, additional, Vitale, Ilio, additional, Kepp, Oliver, additional, Tasdemir, Ezgi, additional, Galluzzi, Lorenzo, additional, Shen, Shensi, additional, Tailler, Maximilien, additional, Delahaye, Nicolas, additional, Tesnière, Antoine, additional, De Stefano, Daniela, additional, BenYounès, Amena, additional, Harper, Francis, additional, Pierron, Gérard, additional, Lavandero, Sergio, additional, Zitvogel, Laurence, additional, Israel, Alain, additional, Baud, Véronique, additional, and Kroemer, Guido, additional

Published
2010
Full Text
View/download PDF

10. The IKK complex contributes to the induction of autophagy

Author

Criollo, Alfredo, primary, Senovilla, Laura, additional, Authier, Hélène, additional, Maiuri, Maria Chiara, additional, Morselli, Eugenia, additional, Vitale, Ilio, additional, Kepp, Oliver, additional, Tasdemir, Ezgi, additional, Galluzzi, Lorenzo, additional, Shen, Shensi, additional, Tailler, Maximilien, additional, Delahaye, Nicolas, additional, Tesniere, Antoine, additional, De Stefano, Daniela, additional, Younes, Aména Ben, additional, Harper, Francis, additional, Pierron, Gérard, additional, Lavandero, Sergio, additional, Zitvogel, Laurence, additional, Israel, Alain, additional, Baud, Véronique, additional, and Kroemer, Guido, additional

Published
2009
Full Text
View/download PDF

11. Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors

Author

Ghiringhelli, François, primary, Apetoh, Lionel, additional, Tesniere, Antoine, additional, Aymeric, Laetitia, additional, Ma, Yuting, additional, Ortiz, Carla, additional, Vermaelen, Karim, additional, Panaretakis, Theocharis, additional, Mignot, Grégoire, additional, Ullrich, Evelyn, additional, Perfettini, Jean-Luc, additional, Schlemmer, Frédéric, additional, Tasdemir, Ezgi, additional, Uhl, Martin, additional, Génin, Pierre, additional, Civas, Ahmet, additional, Ryffel, Bernhard, additional, Kanellopoulos, Jean, additional, Tschopp, Jürg, additional, André, Fabrice, additional, Lidereau, Rosette, additional, McLaughlin, Nicole M, additional, Haynes, Nicole M, additional, Smyth, Mark J, additional, Kroemer, Guido, additional, and Zitvogel, Laurence, additional

Published
2009
Full Text
View/download PDF

15. A dual role of p53 in the control of autophagy

Author

Tasdemir, Ezgi, primary, Maiuri, M. Chiara, additional, Morselli, Eugenia, additional, Criollo, Alfredo, additional, D'Amelio, Marcello, additional, Djavaheri-Mergny, Mojgan, additional, Cecconi, Francesco, additional, Tavernarakis, Nektarios, additional, and Kroemer, Guido, additional

Published
2008
Full Text
View/download PDF

16. Regulation of autophagy by cytoplasmic p53

Author

Tasdemir, Ezgi, primary, Maiuri, M. Chiara, additional, Galluzzi, Lorenzo, additional, Vitale, Ilio, additional, Djavaheri-Mergny, Mojgan, additional, D'Amelio, Marcello, additional, Criollo, Alfredo, additional, Morselli, Eugenia, additional, Zhu, Changlian, additional, Harper, Francis, additional, Nannmark, Ulf, additional, Samara, Chrysanthi, additional, Pinton, Paolo, additional, Vicencio, José Miguel, additional, Carnuccio, Rosa, additional, Moll, Ute M., additional, Madeo, Frank, additional, Paterlini-Brechot, Patrizia, additional, Rizzuto, Rosario, additional, Szabadkai, Gyorgy, additional, Pierron, Gérard, additional, Blomgren, Klas, additional, Tavernarakis, Nektarios, additional, Codogno, Patrice, additional, Cecconi, Francesco, additional, and Kroemer, Guido, additional

Published
2008
Full Text
View/download PDF

18. Senescence, Apoptosis or Autophagy?

Author

Vicencio, José Miguel, primary, Galluzzi, Lorenzo, additional, Tajeddine, Nicolas, additional, Ortiz, Carla, additional, Criollo, Alfredo, additional, Tasdemir, Ezgi, additional, Morselli, Eugenia, additional, Ben Younes, Amena, additional, Maiuri, Maria Chiara, additional, Lavandero, Sergio, additional, and Kroemer, Guido, additional

Published
2008
Full Text
View/download PDF

22. A Novel Epidermal Growth Factor Receptor Inhibitor Promotes Apoptosis in Non–Small Cell Lung Cancer Cells Resistant to Erlotinib

Author

de La Motte Rouge, Thibault, primary, Galluzzi, Lorenzo, additional, Olaussen, Ken A., additional, Zermati, Yael, additional, Tasdemir, Ezgi, additional, Robert, Thomas, additional, Ripoche, Hugues, additional, Lazar, Vladimir, additional, Dessen, Philippe, additional, Harper, Francis, additional, Pierron, Gerard, additional, Pinna, Guillaume, additional, Araujo, Natalia, additional, Harel-Belan, Annick, additional, Armand, Jean-Pierre, additional, Wong, Tai Wai, additional, Soria, Jean Charles, additional, and Kroemer, Guido, additional

Published
2007
Full Text
View/download PDF

23. Functional and physical interaction between Bcl-XL and a BH3-like domain in Beclin-1

Author

Maiuri, M Chiara, primary, Le Toumelin, Gaëtane, additional, Criollo, Alfredo, additional, Rain, Jean-Christophe, additional, Gautier, Fabien, additional, Juin, Philippe, additional, Tasdemir, Ezgi, additional, Pierron, Gérard, additional, Troulinaki, Kostoula, additional, Tavernarakis, Nektarios, additional, Hickman, John A, additional, Geneste, Olivier, additional, and Kroemer, Guido, additional

Published
2007
Full Text
View/download PDF

26. The IKK complex contributes to the induction of autophagy.

Author

Criollo, Alfredo, Senovilla, Laura, Authier, Hélène, Maiuri, Maria Chiara, Morselli, Eugenia, Vitale, Ilio, Kepp, Oliver, Tasdemir, Ezgi, Galluzzi, Lorenzo, Shen, Shensi, Tailler, Maximilien, Delahaye, Nicolas, Tesniere, Antoine, De Stefano, Daniela, Younes, Aména Ben, Harper, Francis, Pierron, Gérard, Lavandero, Sergio, Zitvogel, Laurence, and Israel, Alain

Subjects
IMMUNOSUPPRESSIVE agents, TRANSCRIPTION factors, MACROLIDE antibiotics, CELLS, PHARMACOLOGY
Abstract

In response to stress, cells start transcriptional and transcription-independent programs that can lead to adaptation or death. Here, we show that multiple inducers of autophagy, including nutrient depletion, trigger the activation of the IKK (IκB kinase) complex that is best known for its essential role in the activation of the transcription factor NF-κB by stress. Constitutively active IKK subunits stimulated autophagy and transduced multiple signals that operate in starvation-induced autophagy, including the phosphorylation of AMPK and JNK1. Genetic inhibition of the nuclear translocation of NF-κB or ablation of the p65/RelA NF-κB subunit failed to suppress IKK-induced autophagy, indicating that IKK can promote the autophagic pathway in an NF-κB-independent manner. In murine and human cells, knockout and/or knockdown of IKK subunits (but not that of p65) prevented the induction of autophagy in response to multiple stimuli. Moreover, the knockout of IKK-β suppressed the activation of autophagy by food deprivation or rapamycin injections in vivo, in mice. Altogether, these results indicate that IKK has a cardinal role in the stimulation of autophagy by physiological and pharmacological stimuli. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

27. Functional and physical interaction between Bcl-XL and a BH3-like domain in Beclin-1.

Author

Maiuri, M Chiara, Le Toumelin, Gaëtane, Criollo, Alfredo, Rain, Jean-Christophe, Gautier, Fabien, Juin, Philippe, Tasdemir, Ezgi, Pierron, Gérard, Troulinaki, Kostoula, Tavernarakis, Nektarios, Hickman, John A., Geneste, Olivier, and Kroemer, Guido

Subjects
CAENORHABDITIS elegans, AUTOPHAGY, APOPTOSIS, HYDROLASES, CELL death, CELLS, GENETIC mutation
Abstract

The anti-apoptotic proteins Bcl-2 and Bcl-XL bind and inhibit Beclin-1, an essential mediator of autophagy. Here, we demonstrate that this interaction involves a BH3 domain within Beclin-1 (residues 114–123). The physical interaction between Beclin-1 and Bcl-XL is lost when the BH3 domain of Beclin-1 or the BH3 receptor domain of Bcl-XL is mutated. Mutation of the BH3 domain of Beclin-1 or of the BH3 receptor domain of Bcl-XL abolishes the Bcl-XL-mediated inhibition of autophagy triggered by Beclin-1. The pharmacological BH3 mimetic ABT737 competitively inhibits the interaction between Beclin-1 and Bcl-2/Bcl-XL, antagonizes autophagy inhibition by Bcl-2/Bcl-XL and hence stimulates autophagy. Knockout or knockdown of the BH3-only protein Bad reduces starvation-induced autophagy, whereas Bad overexpression induces autophagy in human cells. Gain-of-function mutation of the sole BH3-only protein from Caenorhabditis elegans, EGL-1, induces autophagy, while deletion of EGL-1 compromises starvation-induced autophagy. These results reveal a novel autophagy-stimulatory function of BH3-only proteins beyond their established role as apoptosis inducers. BH3-only proteins and pharmacological BH3 mimetics induce autophagy by competitively disrupting the interaction between Beclin-1 and Bcl-2 or Bcl-XL. [ABSTRACT FROM AUTHOR]

Published
2007
Full Text
View/download PDF

28. To Die or Not to Die: That is the Autophagic Question

Author

Kroemer, Guido, Galluzzi, Lorenzo, Vicencio, Jose, Kepp, Oliver, Tasdemir, Ezgi, and Maiuri, Maria

Abstract

Macroautophagy (commonly referred to as autophagy) is the process by which intact organelles and/or large portions of the cytoplasm are engulfed within double-membraned autophagic vacuoles for degradation. Whereas basal levels of autophagy ensure the physiological turnover of old and damaged organelles, the massive accumulation of autophagic vacuoles may represent either an alternative pathway of cell death or an ultimate attempt for cells to survive by adapting to stress. The activation of the autophagic pathway beyond a certain threshold may promote cell death directly, by causing the collapse of cellular functions as a result of cellular atrophy (autophagic, or type II, cell death). Alternatively, autophagy can lead to the execution of apoptotic (type I) or necrotic (type III) cell death programs, presumably via common regulators such as proteins from the Bcl-2 family. On the other hand, limited self-eating can provide cells with metabolic substrates to meet their energetic demands under stressful conditions, such as nutrient deprivation, or favor the selective elimination of damaged (and potentially dangerous) organelles. In these instances, autophagy operates as a pro-survival mechanism. The coordinate regulation of these opposite effects of autophagy relies upon a complex network of signal transducers, most of which also participate in non-autophagic signaling cascades. Thus, autophagy occupies a crucial position within the cells metabolism, and its modulation may represent an alternative therapeutic strategy in several pathological settings including cancer and neurodegeneration. Here, we present a general outline of autophagy followed by a detailed analysis of organelle-specific autophagic pathways and of their intimate connections with cell death.

Published
2008

29. To die or not to die: that is the autophagic question.

Author

Galluzzi L, Vicencio JM, Kepp O, Tasdemir E, Maiuri MC, and Kroemer G

Subjects
Animals, Humans, Models, Biological, Organelles metabolism, Signal Transduction, Apoptosis physiology, Autophagy physiology
Abstract

Macroautophagy (commonly referred to as autophagy) is the process by which intact organelles and/or large portions of the cytoplasm are engulfed within double-membraned autophagic vacuoles for degradation. Whereas basal levels of autophagy ensure the physiological turnover of old and damaged organelles, the massive accumulation of autophagic vacuoles may represent either an alternative pathway of cell death or an ultimate attempt for cells to survive by adapting to stress. The activation of the autophagic pathway beyond a certain threshold may promote cell death directly, by causing the collapse of cellular functions as a result of cellular atrophy (autophagic, or type II, cell death). Alternatively, autophagy can lead to the execution of apoptotic (type I) or necrotic (type III) cell death programs, presumably via common regulators such as proteins from the Bcl-2 family. On the other hand, limited self-eating can provide cells with metabolic substrates to meet their energetic demands under stressful conditions, such as nutrient deprivation, or favor the selective elimination of damaged (and potentially dangerous) organelles. In these instances, autophagy operates as a pro-survival mechanism. The coordinate regulation of these opposite effects of autophagy relies upon a complex network of signal transducers, most of which also participate in non-autophagic signaling cascades. Thus, autophagy occupies a crucial position within the cell's metabolism, and its modulation may represent an alternative therapeutic strategy in several pathological settings including cancer and neurodegeneration. Here, we present a general outline of autophagy followed by a detailed analysis of organelle-specific autophagic pathways and of their intimate connections with cell death.

Published
2008
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results