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Article ; Online: The ATG8 Family Proteins GABARAP and GABARAPL1 Target Antigen to Dendritic Cells to Prime CD4

Fonderflick, Leïla / Baudu, Timothée / Adotévi, Olivier / Guittaut, Michaël / Adami, Pascale / Delage-Mourroux, Régis

2022 Volume 11, Issue 18

Abstract: Vaccine therapy is a promising method of research to promote T cell immune response and to develop novel antitumor immunotherapy protocols. Accumulating evidence has shown that autophagy is involved in antigen processing and presentation to T cells. In ... ...

Abstract	Vaccine therapy is a promising method of research to promote T cell immune response and to develop novel antitumor immunotherapy protocols. Accumulating evidence has shown that autophagy is involved in antigen processing and presentation to T cells. In this work, we investigated the potential role of GABARAP and GABARAPL1, two members of the autophagic ATG8 family proteins, as surrogate tumor antigen delivery vectors to prime antitumor T cells. We showed that bone marrow-derived dendritic cells, expressing the antigen OVALBUMIN (OVA) fused with GABARAP or GABARAPL1, were able to prime OVA-specific CD4
MeSH term(s)	Antigens, Neoplasm/metabolism ; Autophagy-Related Protein 8 Family/metabolism ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; Dendritic Cells ; Ovalbumin ; Peptides/metabolism ; Proteasome Endopeptidase Complex/metabolism
Chemical Substances	Antigens, Neoplasm ; Autophagy-Related Protein 8 Family ; Peptides ; Ovalbumin (9006-59-1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2022-09-06
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/cells11182782
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Article ; Online: Specific or not specific recruitment of DNMTs for DNA methylation, an epigenetic dilemma.

Hervouet, Eric / Peixoto, Paul / Delage-Mourroux, Régis / Boyer-Guittaut, Michaël / Cartron, Pierre-François

Clinical epigenetics

2018 Volume 10, Page(s) 17

Abstract: Our current view of DNA methylation processes is strongly moving: First, even if it was generally admitted that DNMT3A and DNMT3B are associated with de novo methylation and DNMT1 is associated with inheritance DNA methylation, these distinctions are now ...

Abstract	Our current view of DNA methylation processes is strongly moving: First, even if it was generally admitted that DNMT3A and DNMT3B are associated with de novo methylation and DNMT1 is associated with inheritance DNA methylation, these distinctions are now not so clear. Secondly, since one decade, many partners of DNMTs have been involved in both the regulation of DNA methylation activity and DNMT recruitment on DNA. The high diversity of interactions and the combination of these interactions let us to subclass the different DNMT-including complexes. For example, the DNMT3L/DNMT3A complex is mainly related to de novo DNA methylation in embryonic states, whereas the DNMT1/PCNA/UHRF1 complex is required for maintaining global DNA methylation following DNA replication. On the opposite to these unspecific DNA methylation machineries (no preferential DNA sequence), some recently identified DNMT-including complexes are recruited on specific DNA sequences. The coexistence of both types of DNA methylation (un/specific) suggests a close cooperation and an orchestration between these systems to maintain genome and epigenome integrities. Deregulation of these systems can lead to pathologic disorders.
MeSH term(s)	Animals ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Methylation ; DNA Replication ; Embryonic Development ; Epigenesis, Genetic ; Humans
Chemical Substances	DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2018-02-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1868-7083
ISSN (online)	1868-7083
DOI	10.1186/s13148-018-0450-y
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Article: EZH2 and KDM6B Expressions Are Associated with Specific Epigenetic Signatures during EMT in Non Small Cell Lung Carcinomas.

Lachat, Camille / Bruyère, Diane / Etcheverry, Amandine / Aubry, Marc / Mosser, Jean / Warda, Walid / Herfs, Michaël / Hendrick, Elodie / Ferrand, Christophe / Borg, Christophe / Delage-Mourroux, Régis / Feugeas, Jean-Paul / Guittaut, Michaël / Hervouet, Eric / Peixoto, Paul

Cancers

2020 Volume 12, Issue 12

Abstract: The role of Epigenetics in Epithelial Mesenchymal Transition (EMT) has recently emerged. Two epigenetic enzymes with paradoxical roles have previously been associated to EMT, EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 (PRC2) Subunit), a ... ...

Abstract	The role of Epigenetics in Epithelial Mesenchymal Transition (EMT) has recently emerged. Two epigenetic enzymes with paradoxical roles have previously been associated to EMT, EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 (PRC2) Subunit), a lysine methyltranserase able to add the H3K27me3 mark, and the histone demethylase KDM6B (Lysine Demethylase 6B), which can remove the H3K27me3 mark. Nevertheless, it still remains unclear how these enzymes, with apparent opposite activities, could both promote EMT. In this study, we evaluated the function of these two enzymes using an EMT-inducible model, the lung cancer A549 cell line. ChIP-seq coupled with transcriptomic analysis showed that EZH2 and KDM6B were able to target and modulate the expression of different genes during EMT. Based on this analysis, we described INHBB, WTN5B, and ADAMTS6 as new EMT markers regulated by epigenetic modifications and directly implicated in EMT induction.
Language	English
Publishing date	2020-12-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12123649
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Article ; Online: Epigenetic regulation of estrogen signaling in breast cancer.

Hervouet, Eric / Cartron, Pierre-François / Jouvenot, Michèle / Delage-Mourroux, Régis

Epigenetics

2013 Volume 8, Issue 3, Page(s) 237–245

Abstract: Estrogen signaling is mediated by ERα and ERβ in hormone dependent, breast cancer (BC). Over the last decade the implication of epigenetic pathways in BC tumorigenesis has emerged: cancer-related epigenetic modifications are implicated in both gene ... ...

Abstract	Estrogen signaling is mediated by ERα and ERβ in hormone dependent, breast cancer (BC). Over the last decade the implication of epigenetic pathways in BC tumorigenesis has emerged: cancer-related epigenetic modifications are implicated in both gene expression regulation, and chromosomal instability. In this review, the epigenetic-mediated estrogen signaling, controlling both ER level and ER-targeted gene expression in BC, are discussed: (1) ER silencing is frequently observed in BC and is often associated with epigenetic regulations while chemical epigenetic modulators restore ER expression and increase response to treatment;(2) ER-targeted gene expression is tightly regulated by co-recruitment of ER and both coactivators/corepressors including HATs, HDACs, HMTs, Dnmts and Polycomb proteins.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Epigenesis, Genetic ; Estrogens/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Estrogens ; Receptors, Estrogen ; Transcription Factors
Language	English
Publishing date	2013-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.4161/epi.23790
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Article ; Online: Interplay between ROS and autophagy in cancer cells, from tumor initiation to cancer therapy.

Poillet-Perez, Laura / Despouy, Gilles / Delage-Mourroux, Régis / Boyer-Guittaut, Michaël

Redox biology

2015 Volume 4, Page(s) 184–192

Abstract: Cancer formation is a complex and highly regulated multi-step process which is highly dependent of its environment, from the tissue to the patient. This complexity implies the development of specific treatments adapted to each type of tumor. The initial ... ...

Abstract	Cancer formation is a complex and highly regulated multi-step process which is highly dependent of its environment, from the tissue to the patient. This complexity implies the development of specific treatments adapted to each type of tumor. The initial step of cancer formation requires the transformation of a healthy cell to a cancer cell, a process regulated by multiple intracellular and extracellular stimuli. The further steps, from the anarchic proliferation of cancer cells to form a primary tumor to the migration of cancer cells to distant organs to form metastasis, are also highly dependent of the tumor environment but of intracellular molecules and pathways as well. In this review, we will focus on the regulatory role of reactive oxygen species (ROS) and autophagy levels during the course of cancer development, from cellular transformation to the formation of metastasis. These data will allow us to discuss the potential of this molecule or pathway as putative future therapeutic targets.
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Antineoplastic Agents/therapeutic use ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy/genetics ; Autophagy-Related Protein-1 Homolog ; Autophagy-Related Proteins ; Beclin-1 ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cysteine Endopeptidases/genetics ; Cysteine Endopeptidases/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Kelch-Like ECH-Associated Protein 1 ; Lymphatic Metastasis ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Degradation/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents ; Apoptosis Regulatory Proteins ; Autophagy-Related Proteins ; BECN1 protein, human ; Beclin-1 ; Intracellular Signaling Peptides and Proteins ; KEAP1 protein, human ; Kelch-Like ECH-Associated Protein 1 ; Membrane Proteins ; Reactive Oxygen Species ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; ULK1 protein, human (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; ATG4A protein, human (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
Language	English
Publishing date	2015
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2213-2317
ISSN (online)	2213-2317
DOI	10.1016/j.redox.2014.12.003
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Article ; Online: Use of epigenetic modulators as a powerful adjuvant for breast cancer therapies.

Claude-Taupin, Aurore / Boyer-Guittaut, Michael / Delage-Mourroux, Régis / Hervouet, Eric

Methods in molecular biology (Clifton, N.J.)

2015 Volume 1238, Page(s) 487–509

Abstract: Breast cancer (BC) is one of the five most frequent cancers in the world. Despite earlier diagnosis and development of specific treatments, mortality has only declined of about 30 % during the past two decades. Two of the main reasons are the emergence ... ...

Abstract	Breast cancer (BC) is one of the five most frequent cancers in the world. Despite earlier diagnosis and development of specific treatments, mortality has only declined of about 30 % during the past two decades. Two of the main reasons are the emergence of drug resistance and the absence of specific therapy for triple negative breast cancers (TNBC), which are characterized by a poor prognosis due to high proliferation rate. Therefore, the future goal of the fight against BC will be to find new therapeutic approaches to overcome drug resistances and cure TNBC. Recent research on gene expression profiles linked to the different types of BC cells have led to consider the use of epigenetic modulators to modulate the expression of genes deregulated in cancer. The preliminary encouraging results have demonstrated a positive effect of DNA Methyl Transferase (DNMT) and Histone DeAcetylase (HDAC) inhibitors on different types of BC, as well as drug-resistant cells, with low side effects. In this review, we will describe the different epigenetic modulators currently used or investigated in BC therapy research in vitro as well as preclinical and clinical trials, and promising compounds, which might be used in future BC therapies.
MeSH term(s)	Adjuvants, Pharmaceutic/pharmacology ; Adjuvants, Pharmaceutic/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; DNA (Cytosine-5-)-Methyltransferases/antagonists & inhibitors ; Drug Discovery ; Epigenesis, Genetic/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Humans
Chemical Substances	Adjuvants, Pharmaceutic ; Histone Deacetylase Inhibitors ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-1804-1_25
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Article ; Online: Proximity Ligation In situ Assay is a Powerful Tool to Monitor Specific ATG Protein Interactions following Autophagy Induction.

Gauthier, Thierry / Claude-Taupin, Aurore / Delage-Mourroux, Régis / Boyer-Guittaut, Michaël / Hervouet, Eric

PloS one

2015 Volume 10, Issue 6, Page(s) e0128701

Abstract: Macroautophagy is a highly regulated intracellular degradation process which has been extensively studied over the last decade. This pathway has been initially described as a non selective process inducing the degradation of parts of the cytoplasm as ... ...

Abstract	Macroautophagy is a highly regulated intracellular degradation process which has been extensively studied over the last decade. This pathway has been initially described as a non selective process inducing the degradation of parts of the cytoplasm as well as organelles at random. Nevertheless, over the last few years, new research highlighted the existence of a more selective autophagy pathway specifically recruiting some organelles or aggregates to the autophagosomes in order to induce their degradation. These selective autophagy pathways such as aggrephagy, mitophagy, pexophagy or xenophagy, involve the intervention of a cargo, the material to be degraded, cargo adapters, the molecules allowing the recruitment of the cargo to the autophagosome, and the proteins of the ATG8 family which link the cargo adapters to the autophagosome. One of the main questions which now remain is to develop new techniques and protocols able to discriminate between these different types of induced autophagy. In our work, we studied the possibility to use the P-LISA technique, which has been recently developed to study endogenous in vivo protein interactions, as a new technique to characterize the ATG proteins specifically involved in bulk or selective autophagy. In this manuscript, we indeed demonstrate that this technique allows the study of endogenous ATG protein interactions in cells following autophagy induction, but more interestingly that this technique might be used to characterize the ATG proteins involved in selective autophagy.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/physiology ; Autophagy/physiology ; Autophagy-Related Protein 8 Family ; Fluorescent Antibody Technique ; Humans ; MCF-7 Cells ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Membrane Proteins/physiology ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Microfilament Proteins/physiology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Microtubule-Associated Proteins/physiology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins/physiology ; Sequestosome-1 Protein ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/physiology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Autophagy-Related Protein 8 Family ; BNIP3L protein, human ; GABARAP protein, human ; GABARAPL2 protein, human ; MAP1LC3B protein, human ; Membrane Proteins ; Microfilament Proteins ; Microtubule-Associated Proteins ; Proto-Oncogene Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Tumor Suppressor Proteins
Language	English
Publishing date	2015-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0128701
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Article ; Online: Carbon nanotubes as gene carriers: Focus on internalization pathways related to functionalization and properties.

Caoduro, Cécile / Hervouet, Eric / Girard-Thernier, Corine / Gharbi, Tijani / Boulahdour, Hatem / Delage-Mourroux, Régis / Pudlo, Marc

Acta biomaterialia

2017 Volume 49, Page(s) 36–44

Abstract: Carbon nanotubes represent promising transporters for delivery of DNA and other biomolecules into living cells. Various methods of CNTs surface functionalization have been developed. These are essential to improve CNTs dispersibility and permit their ... ...

Abstract	Carbon nanotubes represent promising transporters for delivery of DNA and other biomolecules into living cells. Various methods of CNTs surface functionalization have been developed. These are essential to improve CNTs dispersibility and permit their interactions with biological structures that broaden their use in advanced biomedical applications. The present review discusses the different single walled carbon nanotubes and multiwalled carbon nanotubes functionalization methods, leading to the formation of optimized and functionalized-CNT complexes with DNA. F-CNTs are recognized as efficient and promising gene carriers. Emphasis is then placed on the processes used by f-CNTs/DNA complexes to cross cell membranes. Energy independent pathways and uptake mechanisms dependent on energy, such as endocytosis or phagocytosis, are reported by many studies, and if these mechanisms seem contradictory at first sight, a detailed review of the literature illustrates that they are rather complementary. Preferential use of one or the other depends on the DNA and CNTs chemical nature and physical parameters, experimental procedures and cell types. Statement of significance: Efficient non-viral gene delivery is desirable, yet challenging. CNTs appear as a promising solution to penetrate into cells and successfully deliver DNA. Moreover, the field of use of CNTs as gene carrier is large and is currently growing. This critical review summarizes the development and evaluation of CNTs as intracellular gene delivery system and provides an overview of functionalized CNTs/DNA cellular uptake mechanisms, depending on several parameters of CNTs/DNA complexes.
MeSH term(s)	Animals ; DNA/metabolism ; Endocytosis ; Gene Transfer Techniques ; Humans ; Nanotubes, Carbon/chemistry ; Phagocytosis ; Signal Transduction
Chemical Substances	Nanotubes, Carbon ; DNA (9007-49-2)
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2173841-5
ISSN	1878-7568 ; 1742-7061
ISSN (online)	1878-7568
ISSN	1742-7061
DOI	10.1016/j.actbio.2016.11.013
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Article ; Online: EMT is associated with an epigenetic signature of ECM remodeling genes.

Peixoto, Paul / Etcheverry, Amandine / Aubry, Marc / Missey, Anaïs / Lachat, Camille / Perrard, Jérôme / Hendrick, Elodie / Delage-Mourroux, Régis / Mosser, Jean / Borg, Christophe / Feugeas, Jean-Paul / Herfs, Michaël / Boyer-Guittaut, Michaël / Hervouet, Eric

Cell death & disease

2019 Volume 10, Issue 3, Page(s) 205

Abstract: Type III epithelial-mesenchymal transition (EMT) has been previously associated with increased cell migration, invasion, metastasis, and therefore cancer aggressiveness. This reversible process is associated with an important gene expression ... ...

Abstract	Type III epithelial-mesenchymal transition (EMT) has been previously associated with increased cell migration, invasion, metastasis, and therefore cancer aggressiveness. This reversible process is associated with an important gene expression reprogramming mainly due to epigenetic plasticity. Nevertheless, most of the studies describing the central role of epigenetic modifications during EMT were performed in a single-cell model and using only one mode of EMT induction. In our study, we studied the overall modulations of gene expression and epigenetic modifications in four different EMT-induced cell models issued from different tissues and using different inducers of EMT. Pangenomic analysis (transcriptome and ChIP-sequencing) validated our hypothesis that gene expression reprogramming during EMT is largely regulated by epigenetic modifications of a wide range of genes. Indeed, our results confirmed that each EMT model is unique and can be associated with a specific transcriptome profile and epigenetic program. However, we could select some genes or pathways that are similarly regulated in the different models and that could therefore be used as a common signature of all EMT models and become new biomarkers of the EMT phenotype. As an example, we can cite the regulation of gene-coding proteins involved in the degradation of the extracellular matrix (ECM), which are highly induced in all EMT models. Based on our investigations and results, we identified ADAM19 as a new biomarker of in vitro and in vivo EMT and we validated this biological new marker in a cohort of non-small lung carcinomas.
MeSH term(s)	A549 Cells ; Epidermal Growth Factor/pharmacology ; Epigenesis, Genetic ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Retrospective Studies ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Tumor Necrosis Factor-alpha ; Epidermal Growth Factor (62229-50-9)
Language	English
Publishing date	2019-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-1397-4
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Article: Induction of oxiapoptophagy, a mixed mode of cell death associated with oxidative stress, apoptosis and autophagy, on 7-ketocholesterol-treated 158N murine oligodendrocytes: Impairment by α-tocopherol

Nury, Thomas / Zarrouk, Amira / Vejux, Anne / Doria, Margaux / Riedinger, Jean Marc / Delage-Mourroux, Régis / Lizard, Gérard

Biochemical and biophysical research communications. 2014 Apr. 11, v. 446

2014

Abstract: 7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, ...

Abstract	7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, was to bring new evidence on this mixed form of cell death. On 158N cells, 7KC induces an overproduction of reactive oxygen species (ROS) revealed by dihydroethidium staining, a loss of transmembrane mitochondrial potential measured with DiOC6(3), caspase-3 activation, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC enhances cytoplamic membrane permeability to propidium iodide, and induces acidic vesicular organelle formation evaluated with acridine orange. In addition, 7KC promotes conversion of microtubule-associated protein light chain 3 (LC3-I) to LC3-II which is characteristic of autophagy. These different side effects were impaired by α-tocopherol. Altogether, our data demonstrate that oxiapoptophagy including ROS overproduction, apoptosis and autophagy could be a particular type of cell death activated by 7KC which can be inhibited by α-tocopherol.
Keywords	acridine orange ; adverse effects ; alpha-tocopherol ; apoptosis ; autophagy ; caspase-3 ; membrane permeability ; mice ; mitochondria ; oligodendroglia ; oxidation ; oxidative stress ; propidium ; reactive oxygen species ; staining
Language	English
Dates of publication	2014-0411
Size	p. 714-719.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.11.081
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