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Article ; Online: High Expression of the Lysosomal Protease Cathepsin D Confers Better Prognosis in Neuroblastoma Patients by Contrasting EGF-Induced Neuroblastoma Cell Growth.

Secomandi, Eleonora / Salwa, Amreen / Vidoni, Chiara / Ferraresi, Alessandra / Follo, Carlo / Isidoro, Ciro

International journal of molecular sciences

2022 Volume 23, Issue 9

Abstract: Neuroblastoma is a malignant extracranial solid tumor arising from the sympathoadrenal lineage of the neural crest and is often associated ... ...

Abstract	Neuroblastoma is a malignant extracranial solid tumor arising from the sympathoadrenal lineage of the neural crest and is often associated with
MeSH term(s)	Cathepsin D/genetics ; Cathepsin D/metabolism ; Cell Cycle/genetics ; Child ; Epidermal Growth Factor/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Humans ; Lysosomes/metabolism ; Neuroblastoma/metabolism ; Peptide Hydrolases/metabolism
Chemical Substances	Epidermal Growth Factor (62229-50-9) ; ErbB Receptors (EC 2.7.10.1) ; Peptide Hydrolases (EC 3.4.-) ; CTSD protein, human (EC 3.4.23.5) ; Cathepsin D (EC 3.4.23.5)
Language	English
Publishing date	2022-04-26
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/ijms23094782
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Article ; Online: Isolation, Characterization, and Autophagy Function of BECN1-Splicing Isoforms in Cancer Cells.

Maheshwari, Chinmay / Vidoni, Chiara / Titone, Rossella / Castiglioni, Andrea / Lora, Claudia / Follo, Carlo / Isidoro, Ciro

Biomolecules

2022 Volume 12, Issue 8

Abstract: Alternative splicing allows the synthesis of different protein variants starting from a single gene. Human Beclin 1 ( ...

Abstract	Alternative splicing allows the synthesis of different protein variants starting from a single gene. Human Beclin 1 (
MeSH term(s)	Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy ; Beclin-1/genetics ; Beclin-1/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Neoplasms ; Protein Isoforms/genetics
Chemical Substances	Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Membrane Proteins ; Protein Isoforms
Language	English
Publishing date	2022-08-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12081069
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Article ; Online: Autophagy facilitates the release of immunogenic signals following chemotherapy in 3D models of mesothelioma.

Follo, Carlo / Cheng, Yao / Richards, William G / Bueno, Raphael / Broaddus, V Courtney

Molecular carcinogenesis

2019 Volume 58, Issue 10, Page(s) 1754–1769

Abstract: We have previously shown that nearly half of mesothelioma patients have tumors with low autophagy and that these patients have a significantly worse outcome than those with high autophagy. We hypothesized that autophagy may be beneficial by facilitating ... ...

Abstract	We have previously shown that nearly half of mesothelioma patients have tumors with low autophagy and that these patients have a significantly worse outcome than those with high autophagy. We hypothesized that autophagy may be beneficial by facilitating immunogenic cell death (ICD) of tumor cells following chemotherapy. An important hallmark of ICD is that death of tumor cells is preceded or accompanied by the release of damage-associated molecular pattern molecules (DAMPs), which then can stimulate an antitumor immune response. Therefore, we measured how autophagy affected the release of three major DAMPs: high mobility group box 1 (HMGB1), ATP, and calreticulin following chemotherapy. We found that autophagy in three-dimensional (3D) models with low autophagy at baseline could be upregulated with the cell-permeant Tat-BECN1 peptide and confirmed that autophagy in 3D models with high autophagy at baseline could be inhibited with MRT 68921 or ATG7 RNAi, as we have previously shown. In in vitro 3D spheroids, we found that, when autophagy was high or upregulated, DAMPs were released following chemotherapy; however, when autophagy was low or inhibited, DAMPs release was significantly impaired. Similarly, in ex vivo tumors, when autophagy was high or upregulated, HMGB1 was released following chemotherapy but, when autophagy was low, HMGB1 release was not seen. We conclude that autophagy can be upregulated in at least some tumors with low autophagy and that upregulation of autophagy can restore the release of DAMPs following chemotherapy. Autophagy may be necessary for ICD in this tumor.
MeSH term(s)	Adenosine Triphosphate/genetics ; Alarmins/genetics ; Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy-Related Protein 7/antagonists & inhibitors ; Autophagy-Related Proteins/genetics ; Beclin-1/genetics ; Calreticulin/genetics ; Cell Culture Techniques ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/drug effects ; HMGB1 Protein/genetics ; Humans ; Immunity, Cellular/genetics ; Immunogenic Cell Death/genetics ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma/pathology ; RNA Interference ; Spheroids, Cellular/drug effects ; Spheroids, Cellular/pathology
Chemical Substances	ATG13 protein, human ; Alarmins ; Antineoplastic Agents ; Autophagy-Related Proteins ; BECN1 protein, human ; Beclin-1 ; Calreticulin ; HMGB1 Protein ; HMGB1 protein, human ; Adenosine Triphosphate (8L70Q75FXE) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
Language	English
Publishing date	2019-06-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.23050
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Article ; Online: Autophagy in 3D In Vitro and Ex Vivo Cancer Models.

Follo, Carlo / Barbone, Dario / Richards, William G / Bueno, Raphael / Courtney Broaddus, V

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

2019 Volume 1880, Page(s) 491–510

Abstract: Three-dimensional (3D) models are acquiring importance in cancer research due to their ability to mimic multiple features of the tumor microenvironment more accurately than standard monolayer two-dimensional (2D) cultures. Several groups, including our ... ...

Abstract	Three-dimensional (3D) models are acquiring importance in cancer research due to their ability to mimic multiple features of the tumor microenvironment more accurately than standard monolayer two-dimensional (2D) cultures. Several groups, including our laboratory, are now accumulating evidence that autophagy in solid tumors is also better represented in 3D than in 2D. Here we detail how we generate 3D models, both in vitro multicellular spheroids generated from cell lines and ex vivo tumor fragment spheroids generated from tumor samples, and how autophagy can be measured in 3D cultures.
MeSH term(s)	Adaptor Proteins, Signal Transducing/analysis ; Adaptor Proteins, Signal Transducing/metabolism ; Autophagy/physiology ; Autophagy-Related Proteins/analysis ; Autophagy-Related Proteins/metabolism ; Cell Culture Techniques/instrumentation ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Humans ; Mesothelioma/pathology ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Microtubule-Associated Proteins/analysis ; Microtubule-Associated Proteins/metabolism ; Spheroids, Cellular/pathology ; Tubulin/analysis ; Tubulin/metabolism
Chemical Substances	ATG13 protein, human ; Adaptor Proteins, Signal Transducing ; Autophagy-Related Proteins ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; Tubulin
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8873-0_31
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Article ; Online: Amino acid response by Halofuginone in Cancer cells triggers autophagy through proteasome degradation of mTOR.

Follo, Carlo / Vidoni, Chiara / Morani, Federica / Ferraresi, Alessandra / Seca, Christian / Isidoro, Ciro

Cell communication and signaling : CCS

2019 Volume 17, Issue 1, Page(s) 39

Abstract: Background: In the event of amino acid starvation, the cell activates two main protective pathways: Amino Acid starvation Response (AAR), to inhibit global translation, and autophagy, to recover the essential substrates from degradation of redundant ... ...

Abstract	Background: In the event of amino acid starvation, the cell activates two main protective pathways: Amino Acid starvation Response (AAR), to inhibit global translation, and autophagy, to recover the essential substrates from degradation of redundant self-components. Whether and how AAR and autophagy (ATG) are cross-regulated and at which point the two regulatory pathways intersect remain unknown. Here, we provide experimental evidence that the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) specifically located at the lysosome level links the AAR with the autophagy pathway. Methods: As an inducer of the AAR, we used halofuginone (HF), an alkaloid that binds to the prolyl-tRNA synthetase thus mimicking the unavailability of proline (PRO). Induction of AAR was determined assessing the phosphorylation of the eukaryotic translation initiation factor (eIF) 2α. Autophagy was monitored by assessing the processing and accumulation of microtubule-associated protein 1 light chain 3 isoform B (LC3B) and sequestosome-1 (p62/SQSTM1) levels. The activity of mTORC1 was monitored through assessment of the phosphorylation of mTOR, (rp)S6 and 4E-BP1. Global protein synthesis was determined by puromycin incorporation assay. mTORC1 presence on the membrane of the lysosomes was monitored by cell fractionation and mTOR expression was determined by immunoblotting. Results: In three different types of human cancer cells (thyroid cancer WRO cells, ovarian cancer OAW-42 cells, and breast cancer MCF-7 cells), HF induced both the AAR and the autophagy pathways time-dependently. In WRO cells, which showed the strongest induction of autophagy and of AAR, global protein synthesis was little if any affected. Consistently, 4E-BP1 and (rp)S6 were phosphorylated. Concomitantly, mTOR expression and activation declined along with its detachment from the lysosomes and its degradation by the proteasome, and with the nuclear translocation of transcription factor EB (TFEB), a transcription factor of many ATG genes. The extra supplementation of proline rescued all these effects. Conclusions: We demonstrate that the AAR and autophagy are mechanistically linked at the level of mTORC1, and that the lysosome is the central hub of the cross-talk between these two metabolic stress responses.
MeSH term(s)	Amino Acids/deficiency ; Amino Acids/metabolism ; Autophagy/drug effects ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; MCF-7 Cells ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Microtubule-Associated Proteins/metabolism ; Piperidines/pharmacology ; Proteasome Endopeptidase Complex/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Quinazolinones/pharmacology ; Sequestosome-1 Protein/metabolism
Chemical Substances	Amino Acids ; Eukaryotic Initiation Factor-2 ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; Piperidines ; Protein Synthesis Inhibitors ; Quinazolinones ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; halofuginone (L31MM1385E)
Language	English
Publishing date	2019-05-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1478-811X
ISSN (online)	1478-811X
DOI	10.1186/s12964-019-0354-2
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Article ; Online: Inhibition of autophagy initiation potentiates chemosensitivity in mesothelioma.

Follo, Carlo / Cheng, Yao / Richards, William G / Bueno, Raphael / Broaddus, Virginia Courtney

Molecular carcinogenesis

2017 Volume 57, Issue 3, Page(s) 319–332

Abstract: The benefits of inhibiting autophagy in cancer are still controversial, with differences in outcome based on the type of tumor, the context and the particular stage of inhibition. Here, we investigated the impact of inhibiting autophagy at different ... ...

Abstract	The benefits of inhibiting autophagy in cancer are still controversial, with differences in outcome based on the type of tumor, the context and the particular stage of inhibition. Here, we investigated the impact of inhibiting autophagy at different stages on chemosensitivity using 3-dimensional (3D) models of mesothelioma, including ex vivo human tumor fragment spheroids. As shown by LC3B accumulation, we successfully inhibited autophagy using either an early stage ULK1/2 inhibitor (MRT 68921) or a late stage inhibitor (hydroxychloroquine). We found that inhibition of autophagy at the early stage, but not at late stage, potentiated chemosensitivity. This effect was seen only in those spheroids with high autophagy and active initiation at steady state. Inhibition of autophagy alone, at either early or late stage, did not cause cell death, showing that the inhibitors were non-toxic and that mesothelioma did not depend on autophagy at baseline, at least over 24 h. Using ATG13 puncta analysis, we found that autophagy initiation identified tumors that are more chemosensitive at baseline and after autophagy inhibition. Our results highlight a potential role of autophagy initiation in supporting mesothelioma cells during chemotherapy. Our work also highlights the importance of testing the inhibition of different stages in order to uncover the role of autophagy and the potential of its modulation in the treatment of cancer.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Autophagy-Related Protein-1 Homolog/antagonists & inhibitors ; Autophagy-Related Protein-1 Homolog/metabolism ; Humans ; Hydroxychloroquine/pharmacology ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/metabolism ; Mesothelioma/drug therapy ; Mesothelioma/metabolism ; Mesothelioma/pathology ; Protein Kinase Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Protein-Serine-Threonine Kinases/metabolism ; Spheroids, Cellular ; Tumor Cells, Cultured
Chemical Substances	Antineoplastic Agents ; Intracellular Signaling Peptides and Proteins ; Protein Kinase Inhibitors ; Hydroxychloroquine (4QWG6N8QKH) ; 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) ; Ulk2 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2017-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.22757
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Article ; Online: A fast and simple method for simultaneous mixed site-specific mutagenesis of a wide coding sequence.

Follo, Carlo / Isidoro, Ciro

Biotechnology and applied biochemistry

2008 Volume 49, Issue Pt 2, Page(s) 175–183

Abstract: Background: Site-specific mutagenesis at one or multiple sites has recently become an invaluable strategy in functional proteomic studies and genetic engineering.: Results: We describe a novel PCR-based procedure for site-specific mutagenesis that ... ...

Abstract	Background: Site-specific mutagenesis at one or multiple sites has recently become an invaluable strategy in functional proteomic studies and genetic engineering. Results: We describe a novel PCR-based procedure for site-specific mutagenesis that permits in a single-step all three types of nucleotide sequence mutation (deletion, insertion and substitution).The entire procedure is carried out in one tube and takes about 3 to 4 h. The method utilizes two primers, one of which is phosphorylated at the 5'-terminus, that are designed to directly anneal back-to-back to the target sequence inserted in a plasmid. For deletion type of mutagenesis (of virtually no limits of extent), primers anneal at the ends of the sequence to be deleted. For insertion and substitution types of mutagenesis, the primers bear the mutagenic sequences in a tail. The entire circular plasmid, here tested for a maximum length of 7 kbp, is amplified by inverse PCR. The PCR product incorporates the desired mutagenesis and, after ligation, the plasmid is ready for cloning in bacteria. Conclusion: The method has been proved very efficient to delete up to 279 nucleotides, to introduce simultaneously deletions, insertions and substitutions and to perform the alanine-scanning in a wide coding region. The procedure is suitable for applications in gene engineering and for construction of libraries.
MeSH term(s)	DNA Primers/genetics ; Genetic Engineering/methods ; Mutagenesis, Site-Directed/methods ; Open Reading Frames/genetics ; Polymerase Chain Reaction/methods
Chemical Substances	DNA Primers
Language	English
Publishing date	2008-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	883433-7
ISSN	1470-8744 ; 0885-4513
ISSN (online)	1470-8744
ISSN	0885-4513
DOI	10.1042/BA20070045
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Zs.A 1865: Show issues

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Article ; Online: PTEN dephosphorylates AKT to prevent the expression of GLUT1 on plasmamembrane and to limit glucose consumption in cancer cells.

Phadngam, Suratchanee / Castiglioni, Andrea / Ferraresi, Alessandra / Morani, Federica / Follo, Carlo / Isidoro, Ciro

Oncotarget

2016 Volume 7, Issue 51, Page(s) 84999–85020

Abstract: GLUT1 is the facilitative transporter playing the major role in the internalization of glucose. Basally, GLUT1 resides on vesicles located in a para-golgian area, and is translocated onto the plasmamembrane upon activation of the PI3KC1-AKT pathway. In ... ...

Abstract	GLUT1 is the facilitative transporter playing the major role in the internalization of glucose. Basally, GLUT1 resides on vesicles located in a para-golgian area, and is translocated onto the plasmamembrane upon activation of the PI3KC1-AKT pathway. In proliferating cancer cells, which demand a high quantity of glucose for their metabolism, GLUT1 is permanently expressed on the plasmamembrane. This is associated with the abnormal activation of the PI3KC1-AKT pathway, consequent to the mutational activation of PI3KC1 and/or the loss of PTEN. The latter, in fact, could antagonize the phosphorylation of AKT by limiting the availability of Phosphatidylinositol (3,4,5)-trisphosphate. Here, we asked whether PTEN could control the plasmamembrane expression of GLUT1 also through its protein-phosphatase activity on AKT. Experiments of co-immunoprecipitation and in vitro de-phosphorylation assay with homogenates of cells transgenically expressing the wild type or knocked-down mutants (lipid-phosphatase, protein-phosphatase, or both) isoforms demonstrated that indeed PTEN physically interacts with AKT and drives its dephosphorylation, and so limiting the expression of GLUT1 at the plasmamembrane. We also show that growth factors limit the ability of PTEN to dephosphorylate AKT. Our data emphasize the fact that PTEN acts in two distinct steps of the PI3k/AKT pathway to control the expression of GLUT1 at the plasmamembrane and, further, add AKT to the list of the protein substrates of PTEN.
Language	English
Publishing date	2016-12-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.13113
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Article ; Online: The Role of Cathepsin D in the Pathogenesis of Human Neurodegenerative Disorders.

Vidoni, Chiara / Follo, Carlo / Savino, Miriam / Melone, Mariarosa A B / Isidoro, Ciro

Medicinal research reviews

2016 Volume 36, Issue 5, Page(s) 845–870

Abstract: In familial neurodegenerative disorders, protein aggregates form continuously because of genetic mutations that drive the synthesis of truncated or unfolded proteins. The oxidative stress imposed by neurotransmitters and environmental neurotoxins ... ...

Abstract	In familial neurodegenerative disorders, protein aggregates form continuously because of genetic mutations that drive the synthesis of truncated or unfolded proteins. The oxidative stress imposed by neurotransmitters and environmental neurotoxins constitutes an additional threat to the folding of the proteins and the integrity of organelle membranes in neurons. Failure in degrading such altered materials compromises the function of neurons and eventually leads to neurodegeneration. The lysosomal proteolytic enzyme Cathepsin D is the only aspartic-type protease ubiquitously expressed in all the cells of the human body, and it is expressed at high level in the brain. In general, cathepsin D mediated proteolysis is essential to neuronal cell homeostasis through the degradation of unfolded or oxidized protein aggregates delivered to lysosomes via autophagy or endocytosis. More specifically, many altered neuronal proteins that hallmark neurodegenerative diseases (e.g., the amyloid precursor, α-synuclein, and huntingtin) are physiologic substrates of cathepsin D and would abnormally accumulate if not efficiently degraded by this enzyme. Furthermore, experimental evidence indicates that cathepsin D activity is linked to the metabolism of cholesterol and of glycosaminoglycans, which accounts for its involvement in neuronal plasticity. This review focuses on the unique role of cathepsin D mediated proteolysis in the pathogenesis of human neurodegenerative diseases.
MeSH term(s)	Animals ; Cathepsin D/metabolism ; Humans ; Neurodegenerative Diseases/enzymology ; Neurodegenerative Diseases/etiology
Chemical Substances	CTSD protein, human (EC 3.4.23.5) ; Cathepsin D (EC 3.4.23.5)
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603210-2
ISSN	1098-1128 ; 0198-6325
ISSN (online)	1098-1128
ISSN	0198-6325
DOI	10.1002/med.21394
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Article ; Online: Autophagy initiation correlates with the autophagic flux in 3D models of mesothelioma and with patient outcome.

Follo, Carlo / Barbone, Dario / Richards, William G / Bueno, Raphael / Broaddus, V Courtney

Autophagy

2016 Volume 12, Issue 7, Page(s) 1180–1194

Abstract: Understanding the role of autophagy in cancer has been limited by the inability to measure this dynamic process in formalin-fixed tissue. We considered that 3-dimensional models including ex vivo tumor, such as we have developed for studying mesothelioma, ...

Abstract	Understanding the role of autophagy in cancer has been limited by the inability to measure this dynamic process in formalin-fixed tissue. We considered that 3-dimensional models including ex vivo tumor, such as we have developed for studying mesothelioma, would provide valuable insights. Using these models, in which we could use lysosomal inhibitors to measure the autophagic flux, we sought a marker of autophagy that would be valid in formalin-fixed tumor and be used to assess the role of autophagy in patient outcome. Autophagy was studied in mesothelioma cell lines, as 2-dimensional (2D) monolayers and 3-dimensional (3D) multicellular spheroids (MCS), and in tumor from 25 chemonaive patients, both as ex vivo 3D tumor fragment spheroids (TFS) and as formalin-fixed tissue. Autophagy was evaluated as autophagic flux by detection of the accumulation of LC3 after lysosomal inhibition and as autophagy initiation by detection of ATG13 puncta. We found that autophagic flux in 3D, but not in 2D, correlated with ATG13 positivity. In each TFS, ATG13 positivity was similar to that of the original tumor. When tested in tissue microarrays of 109 chemonaive patients, higher ATG13 positivity correlated with better prognosis and provided information independent of known prognostic factors. Our results show that ATG13 is a static marker of the autophagic flux in 3D models of mesothelioma and may also reflect autophagy levels in formalin-fixed tumor. If confirmed, this marker would represent a novel prognostic factor for mesothelioma, supporting the notion that autophagy plays an important role in this cancer.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autophagy/physiology ; Autophagy-Related Proteins/metabolism ; Cell Culture Techniques ; Cell Line ; Formaldehyde ; Humans ; Mesothelioma/metabolism ; Mesothelioma/therapy ; Treatment Outcome
Chemical Substances	ATG13 protein, human ; Adaptor Proteins, Signal Transducing ; Autophagy-Related Proteins ; Formaldehyde (1HG84L3525)
Language	English
Publishing date	2016-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2016.1173799
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