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Article ; Online: The Role of mTORC1 Pathway and Autophagy in Resistance to Platinum-Based Chemotherapeutics.

Pan, Zhenrui / Zhang, Hanxiao / Dokudovskaya, Svetlana

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Cisplatin ( ...

Abstract	Cisplatin (
MeSH term(s)	Humans ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Platinum/pharmacology ; Mechanistic Target of Rapamycin Complex 1 ; Drug Resistance, Neoplasm ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Neoplasms/drug therapy ; Autophagy
Chemical Substances	Cisplatin (Q20Q21Q62J) ; Platinum (49DFR088MY) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Antineoplastic Agents
Language	English
Publishing date	2023-06-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241310651
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Article ; Online: SEA and GATOR 10 Years Later.

Loissell-Baltazar, Yahir A / Dokudovskaya, Svetlana

Cells

2021 Volume 10, Issue 10

Abstract: The SEA complex was described for the first time in ... ...

Abstract	The SEA complex was described for the first time in yeast
MeSH term(s)	Animals ; Disease ; Humans ; Multiprotein Complexes/chemistry ; Multiprotein Complexes/metabolism ; Nutrients ; Phenotype ; Signal Transduction ; Terminology as Topic
Chemical Substances	Multiprotein Complexes
Language	English
Publishing date	2021-10-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10102689
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Article ; Online: Modulation of mTORC1 Signaling Pathway by HIV-1.

Akbay, Burkitkan / Shmakova, Anna / Vassetzky, Yegor / Dokudovskaya, Svetlana

Cells

2020 Volume 9, Issue 5

Abstract: Mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of cellular proliferation and survival which controls cellular response to different stresses, including viral infection. HIV-1 interferes with the mTORC1 pathway at every stage of ... ...

Abstract	Mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of cellular proliferation and survival which controls cellular response to different stresses, including viral infection. HIV-1 interferes with the mTORC1 pathway at every stage of infection. At the same time, the host cells rely on the mTORC1 pathway and autophagy to fight against virus replication and transmission. In this review, we will provide the most up-to-date picture of the role of the mTORC1 pathway in the HIV-1 life cycle, latency and HIV-related diseases. We will also provide an overview of recent trends in the targeting of the mTORC1 pathway as a promising strategy for HIV-1 eradication.
MeSH term(s)	Autophagy/physiology ; HIV Infections/metabolism ; HIV Infections/virology ; HIV-1/metabolism ; Host-Pathogen Interactions ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Virus Replication/physiology
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2020-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9051090
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Article ; Online: The SEACIT complex is involved in the maintenance of vacuole-mitochondria contact sites and controls mitophagy.

Ma, Yinxing / Moors, Alexis / Camougrand, Nadine / Dokudovskaya, Svetlana

Cellular and molecular life sciences : CMLS

2019 Volume 76, Issue 8, Page(s) 1623–1640

Abstract: The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing ... ...

Abstract	The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing and autophagy. Here, we performed analysis of the expression, interactions and localization of SEA complex proteins under different conditions, varying parameters such as sugar source, nitrogen availability and growth phase. Our results show that the SEA complex promotes mitochondria degradation either by mitophagy or by general autophagy. In addition, the SEACIT subcomplex is involved in the maintenance of the vacuole-mitochondria contact sites. Thus, the SEA complex appears to be an important link between the TORC1 pathway and regulation of mitochondria quality control.
MeSH term(s)	Autophagy/physiology ; Gene Deletion ; Glucose/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondrial Degradation/physiology ; Nitrogen/metabolism ; Oxygen/metabolism ; Reactive Oxygen Species/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/growth & development ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Vacuoles/metabolism
Chemical Substances	Membrane Proteins ; Reactive Oxygen Species ; Saccharomyces cerevisiae Proteins ; TORC1 protein complex, S cerevisiae ; Transcription Factors ; Glucose (IY9XDZ35W2) ; Nitrogen (N762921K75) ; Oxygen (S88TT14065)
Language	English
Publishing date	2019-01-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-019-03015-6
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Article: The SEACIT complex is involved in the maintenance of vacuole–mitochondria contact sites and controls mitophagy

Ma, Yinxing / Moors, Alexis / Camougrand, Nadine / Dokudovskaya, Svetlana

Cellular and molecular life sciences. 2019 Apr., v. 76, no. 8

2019

Abstract	The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing and autophagy. Here, we performed analysis of the expression, interactions and localization of SEA complex proteins under different conditions, varying parameters such as sugar source, nitrogen availability and growth phase. Our results show that the SEA complex promotes mitochondria degradation either by mitophagy or by general autophagy. In addition, the SEACIT subcomplex is involved in the maintenance of the vacuole–mitochondria contact sites. Thus, the SEA complex appears to be an important link between the TORC1 pathway and regulation of mitochondria quality control.
Keywords	Saccharomyces cerevisiae ; amino acids ; cell growth ; developmental stages ; metabolism ; mitochondria ; mitophagy ; nitrogen ; proteins ; rapamycin ; signal transduction ; sugars
Language	English
Dates of publication	2019-04
Size	p. 1623-1640.
Publishing place	Springer International Publishing
Document type	Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-019-03015-6
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Article: mTORC1 pathway in DNA damage response.

Ma, Yinxing / Vassetzky, Yegor / Dokudovskaya, Svetlana

Biochimica et biophysica acta. Molecular cell research

2018 Volume 1865, Issue 9, Page(s) 1293–1311

Abstract: Living organisms have evolved various mechanisms to control their metabolism and response to various stresses, allowing them to survive and grow in different environments. In eukaryotes, the highly conserved mechanistic target of rapamycin (mTOR) ... ...

Abstract	Living organisms have evolved various mechanisms to control their metabolism and response to various stresses, allowing them to survive and grow in different environments. In eukaryotes, the highly conserved mechanistic target of rapamycin (mTOR) signaling pathway integrates both intracellular and extracellular signals and serves as a central regulator of cellular metabolism, proliferation and survival. A growing body of evidence indicates that mTOR signaling is closely related to another cellular protection mechanism, the DNA damage response (DDR). Many factors important for the DDR are also involved in the mTOR pathway. In this review, we discuss how these two pathways communicate to ensure an efficient protection of the cell against metabolic and genotoxic stresses. We also describe how anticancer therapies benefit from simultaneous targeting of the DDR and mTOR pathways.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; DNA Damage/drug effects ; DNA Repair/drug effects ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2018-06-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0167-4889 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2018.06.011
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Article ; Online: SEA you later alli-GATOR--a dynamic regulator of the TORC1 stress response pathway.

Dokudovskaya, Svetlana / Rout, Michael P

Journal of cell science

2015 Volume 128, Issue 12, Page(s) 2219–2228

Abstract: Cells constantly adapt to various environmental changes and stresses. The way in which nutrient and stress levels in a cell feed back to control metabolism and growth are, unsurprisingly, extremely complex, as responding with great sensitivity and speed ... ...

Abstract	Cells constantly adapt to various environmental changes and stresses. The way in which nutrient and stress levels in a cell feed back to control metabolism and growth are, unsurprisingly, extremely complex, as responding with great sensitivity and speed to the 'feast or famine, slack or stress' status of its environment is a central goal for any organism. The highly conserved target of rapamycin complex 1 (TORC1) controls eukaryotic cell growth and response to a variety of signals, including nutrients, hormones and stresses, and plays the key role in the regulation of autophagy. A lot of attention has been paid recently to the factors in this pathway functioning upstream of TORC1. In this Commentary, we focus on a major, newly discovered upstream regulator of TORC1--the multiprotein SEA complex, also known as GATOR. We describe the structural and functional features of the yeast complex and its mammalian homolog, and their involvement in the regulation of the TORC1 pathway and TORC1-independent processes. We will also provide an overview of the consequences of GATOR deregulation in cancer and other diseases.
MeSH term(s)	Gene Expression Regulation, Fungal ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/growth & development ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction ; Stress, Physiological ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Saccharomyces cerevisiae Proteins ; TORC1 protein complex, S cerevisiae ; Transcription Factors
Language	English
Publishing date	2015-06-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.168922
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Article ; Online: HIV-1 Tat Activates Akt/mTORC1 Pathway and AICDA Expression by Downregulating Its Transcriptional Inhibitors in B Cells.

Akbay, Burkitkan / Germini, Diego / Bissenbaev, Amangeldy K / Musinova, Yana R / Sheval, Evgeny V / Vassetzky, Yegor / Dokudovskaya, Svetlana

International journal of molecular sciences

2021 Volume 22, Issue 4

Abstract: HIV-1 infects T cells, but the most frequent AIDS-related lymphomas are of B-cell origin. Molecular mechanisms of HIV-1-induced oncogenic transformation of B cells remain largely unknown. HIV-1 Tat protein may participate in this process by penetrating ... ...

Abstract	HIV-1 infects T cells, but the most frequent AIDS-related lymphomas are of B-cell origin. Molecular mechanisms of HIV-1-induced oncogenic transformation of B cells remain largely unknown. HIV-1 Tat protein may participate in this process by penetrating and regulating gene expression in B cells. Both immune and cancer cells can reprogram communications between extracellular signals and intracellular signaling pathways via the Akt/mTORC1 pathway, which plays a key role in the cellular response to various stimuli including viral infection. Here, we investigated the role of HIV-1 Tat on the modulation of the Akt/mTORC1 pathway in B cells. We found that HIV-1 Tat activated the Akt/mTORC1 signaling pathway; this leads to aberrant activation of activation-induced cytidine deaminase (
MeSH term(s)	B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Cells, Cultured ; Cytidine Deaminase/genetics ; Cytidine Deaminase/metabolism ; DNA Damage ; Gene Expression Regulation ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-myb/genetics ; Proto-Oncogene Proteins c-myb/metabolism ; Reactive Oxygen Species/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcriptional Activation ; tat Gene Products, Human Immunodeficiency Virus/genetics ; tat Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	E2F8 protein, human ; MYB protein, human ; Proto-Oncogene Proteins c-myb ; Reactive Oxygen Species ; Repressor Proteins ; tat Gene Products, Human Immunodeficiency Virus ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; AICDA (activation-induced cytidine deaminase) (EC 3.5.4.-) ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2021-02-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22041588
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Article ; Online: Tumor suppressor NPRL2 induces ROS production and DNA damage response.

Ma, Yinxing / Silveri, Licia / LaCava, John / Dokudovskaya, Svetlana

Scientific reports

2017 Volume 7, Issue 1, Page(s) 15311

Abstract: The SEA/GATOR complex is an essential regulator of the mTORC1 pathway. In mammals the GATOR1 complex is composed of the proteins DEPDC5, NPRL2 and NPRL3. GATOR1 serves as an mTORC1 inhibitor and activates the mTORC1-modulating RagA GTPase. However, ... ...

Abstract	The SEA/GATOR complex is an essential regulator of the mTORC1 pathway. In mammals the GATOR1 complex is composed of the proteins DEPDC5, NPRL2 and NPRL3. GATOR1 serves as an mTORC1 inhibitor and activates the mTORC1-modulating RagA GTPase. However, several GATOR members have mTORC1 independent functions. Here we characterize mammalian cells overexpressing the GATOR1 component NPRL2. We demonstrate that, in the cells with active p53, ectopic expression of NPRL2 induces NOX2-dependent production of reactive oxygen species and DNA damage. Overexpressed NPRL2 accumulates in the nucleus, together with apoptosis-inducing factor (AIF). These events are accompanied by phosphorylation of p53, activation of a DNA-damage response and cell cycle arrest in G1 phase, followed by apoptosis. In the cells negative for active p53, NPRL2 ectopic expression leads to activation of CHK1 or CHK2 kinases and cell cycle arrest in S or G2/M phases. Combined, these results demonstrate a new role for the NPRL2, distinct from its function in mTORC1 regulation.
MeSH term(s)	Cell Cycle Checkpoints ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; DNA Damage ; HEK293 Cells ; Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; NADPH Oxidase 2/genetics ; NADPH Oxidase 2/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	NPRL2 protein, human ; Reactive Oxygen Species ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins ; CYBB protein, human (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2017-11-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-15497-0
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Article ; Online: Identification of Small Molecules Inhibiting Cardiomyocyte Necrosis and Apoptosis by Autophagy Induction and Metabolism Reprogramming.

Liu, Dawei / Peyre, Félix / Loissell-Baltazar, Yahir Alberto / Courilleau, Delphine / Lacas-Gervais, Sandra / Nicolas, Valérie / Jacquet, Eric / Dokudovskaya, Svetlana / Taran, Frédéric / Cintrat, Jean-Christophe / Brenner, Catherine

Cells

2022 Volume 11, Issue 3

Abstract: Improvement of anticancer treatments is associated with increased survival of cancer patients at risk of cardiac disease. Therefore, there is an urgent need for new therapeutic molecules capable of preventing acute and long-term cardiotoxicity. Here, ... ...

Abstract	Improvement of anticancer treatments is associated with increased survival of cancer patients at risk of cardiac disease. Therefore, there is an urgent need for new therapeutic molecules capable of preventing acute and long-term cardiotoxicity. Here, using commercial and home-made chemolibraries, we performed a robust phenotypic high-throughput screening in rat cardiomyoblast cell line H9c2, searching for small molecules capable of inhibiting cell death. A screen of 1600 compounds identified six molecules effective in preventing necrosis and apoptosis induced by H
MeSH term(s)	Animals ; Apoptosis ; Autophagy ; Humans ; Hydrogen Peroxide/pharmacology ; Myocytes, Cardiac/metabolism ; Necrosis/metabolism ; Rats
Chemical Substances	Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2022-01-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11030474
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