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Article ; Online: Corrigendum: Ribosome biogenesis in cancer: new players and therapeutic avenues.

Pelletier, Joffrey / Thomas, George / Volarević, Siniša

2018 Volume 18, Issue 2, Page(s) 134

Abstract: This corrects the article DOI: 10.1038/nrc.2017.104. ...

Abstract	This corrects the article DOI: 10.1038/nrc.2017.104.
Language	English
Publishing date	2018-01-22
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc.2018.3
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Article ; Online: Lysosomal degradation ensures accurate chromosomal segregation to prevent chromosomal instability.

Almacellas, Eugènia / Pelletier, Joffrey / Day, Charles / Ambrosio, Santiago / Tauler, Albert / Mauvezin, Caroline

Autophagy

2020 Volume 17, Issue 3, Page(s) 796–813

Abstract: Lysosomes, as primary degradative organelles, are the endpoint of different converging pathways, including macroautophagy. To date, lysosome degradative function has been mainly studied in interphase cells, while their role during mitosis remains ... ...

Abstract	Lysosomes, as primary degradative organelles, are the endpoint of different converging pathways, including macroautophagy. To date, lysosome degradative function has been mainly studied in interphase cells, while their role during mitosis remains controversial. Mitosis dictates the faithful transmission of genetic material among generations, and perturbations of mitotic division lead to chromosomal instability, a hallmark of cancer. Heretofore, correct mitotic progression relies on the orchestrated degradation of mitotic factors, which was mainly attributed to ubiquitin-triggered proteasome-dependent degradation. Here, we show that mitotic transition also relies on lysosome-dependent degradation, as impairment of lysosomes increases mitotic timing and leads to mitotic errors, thus promoting chromosomal instability. Furthermore, we identified several putative lysosomal targets in mitotic cells. Among them, WAPL, a cohesin regulatory protein, emerged as a novel SQSTM1-interacting protein for targeted lysosomal degradation. Finally, we characterized an atypical nuclear phenotype, the toroidal nucleus, as a novel biomarker for genotoxic screenings. Our results establish lysosome-dependent degradation as an essential event to prevent chromosomal instability.
MeSH term(s)	Animals ; Autophagy/physiology ; Chromosomal Instability/physiology ; Fibroblasts/metabolism ; HeLa Cells ; Humans ; Lysosomes/metabolism ; Mitosis/physiology ; Proteasome Endopeptidase Complex/metabolism ; Transcription Factors/metabolism ; Ubiquitin/metabolism
Chemical Substances	Transcription Factors ; Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1764727
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Article ; Online: Ribosome biogenesis in cancer: new players and therapeutic avenues.

Pelletier, Joffrey / Thomas, George / Volarević, Siniša

Nature reviews. Cancer

2017 Volume 18, Issue 1, Page(s) 51–63

Abstract: The ribosome is a complex molecular machine composed of numerous distinct proteins and nucleic acids and is responsible for protein synthesis in every living cell. Ribosome biogenesis is one of the most multifaceted and energy- demanding processes in ... ...

Abstract	The ribosome is a complex molecular machine composed of numerous distinct proteins and nucleic acids and is responsible for protein synthesis in every living cell. Ribosome biogenesis is one of the most multifaceted and energy- demanding processes in biology, involving a large number of assembly and maturation factors, the functions of which are orchestrated by multiple cellular inputs, including mitogenic signals and nutrient availability. Although causal associations between inherited mutations affecting ribosome biogenesis and elevated cancer risk have been established over the past decade, mechanistic data have emerged suggesting a broader role for dysregulated ribosome biogenesis in the development and progression of most spontaneous cancers. In this Opinion article, we highlight the most recent findings that provide new insights into the molecular basis of ribosome biogenesis in cancer and offer our perspective on how these observations present opportunities for the design of new targeted cancer treatments.
MeSH term(s)	Animals ; Cell Proliferation/physiology ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein Biosynthesis/physiology ; Ribosomal Proteins/metabolism ; Ribosomes/metabolism ; Ribosomes/physiology ; Signal Transduction/physiology
Chemical Substances	Ribosomal Proteins
Language	English
Publishing date	2017-12-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc.2017.104
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Article ; Online: Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.

Almacellas, Eugènia / Pelletier, Joffrey / Manzano, Anna / Gentilella, Antonio / Ambrosio, Santiago / Mauvezin, Caroline / Tauler, Albert

iScience

2019 Volume 20, Page(s) 434–448

Abstract: Cancer cells rely on mTORC1 activity to coordinate mitogenic signaling with nutrients availability for growth. Based on the metabolic function of E2F1, we hypothesize that glucose catabolism driven by E2F1 could participate on mTORC1 activation. Here, we ...

Abstract	Cancer cells rely on mTORC1 activity to coordinate mitogenic signaling with nutrients availability for growth. Based on the metabolic function of E2F1, we hypothesize that glucose catabolism driven by E2F1 could participate on mTORC1 activation. Here, we demonstrate that glucose potentiates E2F1-induced mTORC1 activation by promoting mTORC1 translocation to lysosomes, a process that occurs independently of AMPK activation. We showed that E2F1 regulates glucose metabolism by increasing aerobic glycolysis and identified the PFKFB3 regulatory enzyme as an E2F1-regulated gene important for mTORC1 activation. Furthermore, PFKFB3 and PFK1 were found associated to lysosomes and we demonstrated that modulation of PFKFB3 activity, either by substrate accessibility or expression, regulates the translocation of mTORC1 to lysosomes by direct interaction with Rag B and subsequent mTORC1 activity. Our results support a model whereby a glycolytic metabolon containing phosphofructokinases transiently interacts with the lysosome acting as a sensor platform for glucose catabolism toward mTORC1 activity.
Language	English
Publishing date	2019-10-01
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2019.09.040
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Article ; Online: The 40

Fuentes, Pedro / Pelletier, Joffrey / Martinez-Herráez, Carolina / Diez-Obrero, Virginia / Iannizzotto, Flavia / Rubio, Teresa / Garcia-Cajide, Marta / Menoyo, Sandra / Moreno, Victor / Salazar, Ramón / Tauler, Albert / Gentilella, Antonio

Science advances

2021 Volume 7, Issue 48, Page(s) eabg9275

Abstract: Ribosomes execute the transcriptional program in every cell. Critical to sustain nearly all cellular activities, ribosome biogenesis requires the translation of ~200 factors of which 80 are ribosomal proteins (RPs). As ribosome synthesis depends on RP ... ...

Abstract	Ribosomes execute the transcriptional program in every cell. Critical to sustain nearly all cellular activities, ribosome biogenesis requires the translation of ~200 factors of which 80 are ribosomal proteins (RPs). As ribosome synthesis depends on RP mRNA translation, a priority within the translatome architecture should exist to ensure the preservation of ribosome biogenesis capacity, particularly under adverse growth conditions. Here, we show that under critical metabolic constraints characterized by mTOR inhibition, LARP1 complexed with the 40
Language	English
Publishing date	2021-11-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abg9275
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Article ; Online: Erratum for Brahimi-Horn et al., "Local Mitochondrial-Endolysosomal Microfusion Cleaves the Voltage-Dependent Anion Channel 1 To Promote Survival in Hypoxia".

Brahimi-Horn, M Christiane / Lacas-Gervais, Sandra / Adaixo, Ricardo / Ilc, Karine / Rouleau, Matthieu / Notte, Annick / Dieu, Marc / Michiels, Carine / Voeltzel, Thibault / Maguer-Satta, Véronique / Pelletier, Joffrey / Ilie, Marius / Hofman, Paul / Manoury, Bénédicte / Schmidt, Alexander / Hiller, Sebastian / Pouysségur, Jacques / Mazure, Nathalie M

Molecular and cellular biology

2022 Volume 42, Issue 1, Page(s) e0051521

Language	English
Publishing date	2022-01-20
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00515-21
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Article ; Online: Biochemical titration of glycogen in vitro.

Pelletier, Joffrey / Bellot, Grégory / Pouysségur, Jacques / Mazure, Nathalie M

Journal of visualized experiments : JoVE

2013 , Issue 81, Page(s) e50465

Abstract: Glycogen is the main energetic polymer of glucose in vertebrate animals and plays a crucial role in whole body metabolism as well as in cellular metabolism. Many methods to detect glycogen already exist but only a few are quantitative. We describe here a ...

Abstract	Glycogen is the main energetic polymer of glucose in vertebrate animals and plays a crucial role in whole body metabolism as well as in cellular metabolism. Many methods to detect glycogen already exist but only a few are quantitative. We describe here a method using the Abcam Glycogen assay kit, which is based on specific degradation of glycogen to glucose by glucoamylase. Glucose is then specifically oxidized to a product that reacts with the OxiRed probe to produce fluorescence. Titration is accurate, sensitive and can be achieved on cell extracts or tissue sections. However, in contrast to other techniques, it does not give information about the distribution of glycogen in the cell. As an example of this technique, we describe here the titration of glycogen in two cell lines, Chinese hamster lung fibroblast CCL39 and human colon carcinoma LS174, incubated in normoxia (21% O2) versus hypoxia (1% O2). We hypothesized that hypoxia is a signal that prepares cells to synthesize and store glycogen in order to survive(1).
MeSH term(s)	Animals ; Cell Hypoxia/physiology ; Cell Line ; Cell Line, Tumor ; Colonic Neoplasms/chemistry ; Colonic Neoplasms/metabolism ; Cricetinae ; Cricetulus ; Fibroblasts/chemistry ; Fibroblasts/metabolism ; Fluorescence ; Glucose/analysis ; Glucose/chemistry ; Glucose/metabolism ; Glycogen/analysis ; Glycogen/chemistry ; Glycogen/metabolism ; Humans ; Hydrolysis ; Oxidation-Reduction ; Reagent Kits, Diagnostic ; Titrimetry/methods
Chemical Substances	Reagent Kits, Diagnostic ; Glycogen (9005-79-2) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2013-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/50465
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Article ; Online: Impaired ribosome biogenesis checkpoint activation induces p53-dependent MCL-1 degradation and MYC-driven lymphoma death.

Domostegui, Ana / Peddigari, Suresh / Mercer, Carol A / Iannizzotto, Flavia / Rodriguez, Marta L / Garcia-Cajide, Marta / Amador, Virginia / Diepstraten, Sarah T / Kelly, Gemma L / Salazar, Ramón / Kozma, Sara C / Kusnadi, Eric P / Kang, Jian / Gentilella, Antonio / Pearson, Richard B / Thomas, George / Pelletier, Joffrey

Blood

2021 Volume 137, Issue 24, Page(s) 3351–3364

Abstract: MYC-driven B-cell lymphomas are addicted to increased levels of ribosome biogenesis (RiBi), offering the potential for therapeutic intervention. However, it is unclear whether inhibition of RiBi suppresses lymphomagenesis by decreasing translational ... ...

Abstract	MYC-driven B-cell lymphomas are addicted to increased levels of ribosome biogenesis (RiBi), offering the potential for therapeutic intervention. However, it is unclear whether inhibition of RiBi suppresses lymphomagenesis by decreasing translational capacity and/or by p53 activation mediated by the impaired RiBi checkpoint (IRBC). Here we generated Eμ-Myc lymphoma cells expressing inducible short hairpin RNAs to either ribosomal protein L7a (RPL7a) or RPL11, the latter an essential component of the IRBC. The loss of either protein reduced RiBi, protein synthesis, and cell proliferation to similar extents. However, only RPL7a depletion induced p53-mediated apoptosis through the selective proteasomal degradation of antiapoptotic MCL-1, indicating the critical role of the IRBC in this mechanism. Strikingly, low concentrations of the US Food and Drug Administration-approved anticancer RNA polymerase I inhibitor Actinomycin D (ActD) dramatically prolonged the survival of mice harboring Trp53+/+;Eμ-Myc but not Trp53-/-;Eμ-Myc lymphomas, which provides a rationale for treating MYC-driven B-cell lymphomas with ActD. Importantly, the molecular effects of ActD on Eμ-Myc cells were recapitulated in human B-cell lymphoma cell lines, highlighting the potential for ActD as a therapeutic avenue for p53 wild-type lymphoma.
MeSH term(s)	Animals ; Cell Cycle Checkpoints/drug effects ; Cell Cycle Checkpoints/genetics ; Cell Line, Tumor ; Dactinomycin/pharmacology ; Lymphoma, B-Cell/drug therapy ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/metabolism ; Male ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Proteolysis/drug effects ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Neoplasm/genetics ; RNA, Neoplasm/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Ribosomal Proteins/antagonists & inhibitors ; Ribosomal Proteins/genetics ; Ribosomal Proteins/metabolism ; Ribosomes/genetics ; Ribosomes/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Mcl1 protein, mouse ; Myc protein, mouse ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-myc ; RNA, Neoplasm ; RNA, Small Interfering ; Ribosomal Proteins ; Rpl7a protein, mouse ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Dactinomycin (1CC1JFE158)
Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020007452
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Article ; Online: AMP-activated protein kinase is dispensable for maintaining ATP levels and for survival following inhibition of glycolysis, but promotes tumour engraftment of Ras-transformed fibroblasts.

Pelletier, Joffrey / Roux, Danièle / Viollet, Benoit / Mazure, Nathalie M / Pouysségur, Jacques

Oncotarget

2015 Volume 6, Issue 14, Page(s) 11833–11847

Abstract: Lactic acid generated by highly glycolytic tumours is exported by the MonoCarboxylate Transporters, MCT1 and MCT4, to maintain pHi and energy homeostasis. We report that MCT1 inhibition combined with Mct4 gene disruption severely reduced glycolysis and ... ...

Abstract	Lactic acid generated by highly glycolytic tumours is exported by the MonoCarboxylate Transporters, MCT1 and MCT4, to maintain pHi and energy homeostasis. We report that MCT1 inhibition combined with Mct4 gene disruption severely reduced glycolysis and tumour growth without affecting ATP levels. Because of the key role of the 5'-AMP-activated protein kinase (AMPK) in energy homeostasis, we hypothesized that targeting glycolysis (MCT-blockade) in AMPK-null (Ampk(-/-)) cells should kill tumour cells from 'ATP crisis'. We show that Ampk(-/-)-Ras-transformed mouse embryonic fibroblasts (MEFs) maintained ATP levels and viability when glycolysis was inhibited. In MCT-inhibited MEFs treated with OXPHOS inhibitors the ATP level and viability collapsed in both Ampk(+/+) and Ampk(-/-) cells. We therefore propose that the intracellular acidification resulting from lactic acid sequestration mimicks AMPK by blocking mTORC1, a major component of an ATP consuming pathway, thereby preventing 'ATP crisis'. Finally we showed that genetic disruption of Mct4 and/or Ampk dramatically reduced tumourigenicity in a xenograft mouse model suggesting a crucialrolefor these two actors in establishment of tumours in a nutrient-deprived environment. These findings demonstrated that blockade of lactate transport is an efficient anti-cancer strategy that highlights the potential in targeting Mct4 in a context of impaired AMPK activity.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Line, Tumor ; Cell Transformation, Neoplastic/metabolism ; Fibroblasts/pathology ; Gene Knockout Techniques ; Glycolysis/physiology ; Heterografts ; Humans ; Immunohistochemistry ; Mice ; Mice, Nude ; Monocarboxylic Acid Transporters/metabolism ; Muscle Proteins/metabolism
Chemical Substances	Monocarboxylic Acid Transporters ; Muscle Proteins ; SLC16A4 protein, human ; Adenosine Triphosphate (8L70Q75FXE) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2015-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.3738
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Article: Biochemical titration of glycogen In vitro

Pelletier, Joffrey / Bellot, Grégory / Pouysségur, Jacques / Mazure, Nathalie M

Journal of visualized experiments. 2013 Nov. 24, , no. 81

2013

Abstract	Glycogen is the main energetic polymer of glucose in vertebrate animals and plays a crucial role in whole body metabolism as well as in cellular metabolism. Many methods to detect glycogen already exist but only a few are quantitative. We describe here a method using the Abcam Glycogen assay kit, which is based on specific degradation of glycogen to glucose by glucoamylase. Glucose is then specifically oxidized to a product that reacts with the OxiRed probe to produce fluorescence. Titration is accurate, sensitive and can be achieved on cell extracts or tissue sections. However, in contrast to other techniques, it does not give information about the distribution of glycogen in the cell. As an example of this technique, we describe here the titration of glycogen in two cell lines, Chinese hamster lung fibroblast CCL39 and human colon carcinoma LS174, incubated in normoxia (21% O2) versus hypoxia (1% O2). We hypothesized that hypoxia is a signal that prepares cells to synthesize and store glycogen in order to survive1.
Keywords	Chinese hamsters ; cell lines ; colorectal neoplasms ; fibroblasts ; fluorescence ; glucan 1,4-alpha-glucosidase ; glucose ; glycogen ; humans ; hypoxia ; lungs ; metabolism ; normoxia ; oxygen ; polymers ; titration
Language	English
Dates of publication	2013-1124
Size	p. e50465.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/50465
Database	NAL-Catalogue (AGRICOLA)

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