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Article ; Online: Computational prediction and experimental validation of

Demeter, Amanda / Jacomin, Anne-Claire / Gul, Lejla / Lister, Ashleigh / Lipscombe, James / Invernizzi, Rachele / Branchu, Priscilla / Macaulay, Iain / Nezis, Ioannis P / Kingsley, Robert A / Korcsmaros, Tamas / Hautefort, Isabelle

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 834895

Abstract: Macroautophagy is a ubiquitous homeostasis and health-promoting recycling process of eukaryotic cells, targeting misfolded proteins, damaged organelles and intracellular infectious agents. Some intracellular pathogens such ... ...

Abstract	Macroautophagy is a ubiquitous homeostasis and health-promoting recycling process of eukaryotic cells, targeting misfolded proteins, damaged organelles and intracellular infectious agents. Some intracellular pathogens such as
MeSH term(s)	Autophagy/physiology ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Epithelial Cells/metabolism ; Humans ; Salmonella Infections ; Salmonella typhimurium/genetics
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2022-08-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.834895
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Article ; Online: ULK1 and ULK2 are less redundant than previously thought: computational analysis uncovers distinct regulation and functions of these autophagy induction proteins.

Demeter, Amanda / Romero-Mulero, Mari Carmen / Csabai, Luca / Ölbei, Márton / Sudhakar, Padhmanand / Haerty, Wilfried / Korcsmáros, Tamás

Scientific reports

2020 Volume 10, Issue 1, Page(s) 10940

Abstract: Macroautophagy, the degradation of cytoplasmic content by lysosomal fusion, is an evolutionary conserved process promoting homeostasis and intracellular defence. Macroautophagy is initiated primarily by a complex containing ULK1 or ULK2 (two paralogs of ... ...

Abstract	Macroautophagy, the degradation of cytoplasmic content by lysosomal fusion, is an evolutionary conserved process promoting homeostasis and intracellular defence. Macroautophagy is initiated primarily by a complex containing ULK1 or ULK2 (two paralogs of the yeast Atg1 protein). To understand the differences between ULK1 and ULK2, we compared the human ULK1 and ULK2 proteins and their regulation. Despite the similarity in their enzymatic domain, we found that ULK1 and ULK2 have major differences in their autophagy-related interactors and their post-translational and transcriptional regulators. We identified 18 ULK1-specific and 7 ULK2-specific protein motifs serving as different interaction interfaces. We found that interactors of ULK1 and ULK2 all have different tissue-specific expressions partially contributing to diverse and ULK-specific interaction networks in various tissues. We identified three ULK1-specific and one ULK2-specific transcription factor binding sites, and eight sites shared by the regulatory region of both genes. Importantly, we found that both their post-translational and transcriptional regulators are involved in distinct biological processes-suggesting separate functions for ULK1 and ULK2. Unravelling differences between ULK1 and ULK2 could lead to a better understanding of how ULK-type specific dysregulation affects autophagy and other cellular processes that have been implicated in diseases such as inflammatory bowel disease and cancer.
MeSH term(s)	Autophagy ; Autophagy-Related Protein-1 Homolog/chemistry ; Autophagy-Related Protein-1 Homolog/metabolism ; Autophagy-Related Proteins/chemistry ; Autophagy-Related Proteins/metabolism ; Computational Biology/methods ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/metabolism ; Lysosomes ; Protein Binding ; Protein Conformation ; Protein Interaction Mapping ; Protein Serine-Threonine Kinases/chemistry ; Protein Serine-Threonine Kinases/metabolism
Chemical Substances	Autophagy-Related Proteins ; Intracellular Signaling Peptides and Proteins ; 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	2020-07-02
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/s41598-020-67780-2
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Article ; Online: AutophagyNet: high-resolution data source for the analysis of autophagy and its regulation.

Autophagy

2023 Volume 20, Issue 1, Page(s) 188–201

Abstract: Macroautophagy/autophagy is a highly-conserved catabolic procss eliminating dysfunctional cellular components and invading pathogens. Autophagy malfunction contributes to disorders such as cancer, neurodegenerative and inflammatory diseases. ... ...

Abstract	Macroautophagy/autophagy is a highly-conserved catabolic procss eliminating dysfunctional cellular components and invading pathogens. Autophagy malfunction contributes to disorders such as cancer, neurodegenerative and inflammatory diseases. Understanding autophagy regulation in health and disease has been the focus of the last decades. We previously provided an integrated database for autophagy research, the Autophagy Regulatory Network (ARN). For the last eight years, this resource has been used by thousands of users. Here, we present a new and upgraded resource, AutophagyNet. It builds on the previous database but contains major improvements to address user feedback and novel needs due to the advancement in omics data availability. AutophagyNet contains updated interaction curation and integration of over 280,000 experimentally verified interactions between core autophagy proteins and their protein, transcriptional and post-transcriptional regulators as well as their potential upstream pathway connections. AutophagyNet provides annotations for each core protein about their role: 1) in different types of autophagy (mitophagy, xenophagy, etc.); 2) in distinct stages of autophagy (initiation, expansion, termination, etc.); 3) with subcellular and tissue-specific localization. These annotations can be used to filter the dataset, providing customizable download options tailored to the user's needs. The resource is available in various file formats (e.g. CSV, BioPAX and PSI-MI), and data can be analyzed and visualized directly in Cytoscape. The multi-layered regulation of autophagy can be analyzed by combining AutophagyNet with tissue- or cell type-specific (multi-)omics datasets (e.g. transcriptomic or proteomic data). The resource is publicly accessible at http://autophagynet.org.
MeSH term(s)	Autophagy/physiology ; Proteomics ; Beclin-1 ; Mitophagy ; Signal Transduction/genetics ; MicroRNAs
Chemical Substances	Beclin-1 ; MicroRNAs
Language	English
Publishing date	2023-08-17
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	10.1080/15548627.2023.2247737
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Article: Epigenetic Dysregulation of Trophoblastic Gene Expression in Gestational Trophoblastic Disease.

Szabolcsi, Zoltan / Demeter, Amanda / Kiraly, Peter / Balogh, Andrea / Wilson, Melissa L / King, Jennifer R / Hetey, Szabolcs / Gelencser, Zsolt / Matsuo, Koji / Hargitai, Beata / Mhawech-Fauceglia, Paulette / Hupuczi, Petronella / Szilagyi, Andras / Papp, Zoltan / Roman, Lynda D / Cortessis, Victoria K / Than, Nandor Gabor

Biomedicines

2021 Volume 9, Issue 12

Abstract: Gestational trophoblastic diseases (GTDs) have not been investigated for their epigenetic marks and consequent transcriptomic changes. Here, we analyzed genome-wide DNA methylation and transcriptome data to reveal the epigenetic basis of disease pathways ...

Abstract	Gestational trophoblastic diseases (GTDs) have not been investigated for their epigenetic marks and consequent transcriptomic changes. Here, we analyzed genome-wide DNA methylation and transcriptome data to reveal the epigenetic basis of disease pathways that may lead to benign or malignant GTDs. RNA-Seq, mRNA microarray, and Human Methylation 450 BeadChip data from complete moles and choriocarcinoma cells were bioinformatically analyzed. Paraffin-embedded tissues from complete moles and control placentas were used for tissue microarray construction, DNMT3B immunostaining and immunoscoring. We found that DNA methylation increases with disease severity in GTDs. Differentially expressed genes are mainly upregulated in moles while predominantly downregulated in choriocarcinoma. DNA methylation principally influences the gene expression of villous trophoblast differentiation-related or predominantly placenta-expressed genes in moles and choriocarcinoma cells. Affected genes in these subsets shared focal adhesion and actin cytoskeleton pathways in moles and choriocarcinoma. In moles, cell cycle and differentiation regulatory pathways, essential for trophoblast/placental development, were enriched. In choriocarcinoma cells, hormone biosynthetic, extracellular matrix-related, hypoxic gene regulatory, and differentiation-related signaling pathways were enriched. In moles, we found slight upregulation of DNMT3B protein, a developmentally important de novo DNA methylase, which is strongly overexpressed in choriocarcinoma cells that may partly be responsible for the large DNA methylation differences. Our findings provide new insights into the shared and disparate molecular pathways of disease in GTDs and may help in designing new diagnostic and therapeutic tools.
Language	English
Publishing date	2021-12-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines9121935
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Article ; Online: Targeted interplay between bacterial pathogens and host autophagy.

Sudhakar, Padhmanand / Jacomin, Anne-Claire / Hautefort, Isabelle / Samavedam, Siva / Fatemian, Koorosh / Ari, Eszter / Gul, Leila / Demeter, Amanda / Jones, Emily / Korcsmaros, Tamas / Nezis, Ioannis P

Autophagy

2019 Volume 15, Issue 9, Page(s) 1620–1633

Abstract: Due to the critical role played by autophagy in pathogen clearance, pathogens have developed diverse strategies to subvert it. Despite previous key findings of bacteria-autophagy interplay, asystems-level insight into selective targeting by the host and ... ...

Abstract	Due to the critical role played by autophagy in pathogen clearance, pathogens have developed diverse strategies to subvert it. Despite previous key findings of bacteria-autophagy interplay, asystems-level insight into selective targeting by the host and autophagy modulation by the pathogens is lacking. We predicted potential interactions between human autophagy proteins and effector proteins from 56 pathogenic bacterial species by identifying bacterial proteins predicted to have recognition motifs for selective autophagy receptors SQSTM1/p62, CALCOCO2/NDP52 and MAP1LC3/LC3. Using structure-based interaction prediction, we identified bacterial proteins capable to modify core autophagy components. Our analysis revealed that autophagy receptors in general potentially target mostly genus-specific proteins, and not those present in multiple genera. The complementarity between the predicted SQSTM1/p62 and CALCOCO2/NDP52 targets, which has been shown for
MeSH term(s)	Amino Acid Motifs ; Autophagy/genetics ; Bacillus/metabolism ; Bacillus/pathogenicity ; Bacterial Proteins/metabolism ; Cluster Analysis ; Computational Biology ; Evolution, Molecular ; Host-Pathogen Interactions/genetics ; Humans ; Listeria/metabolism ; Listeria/pathogenicity ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Protein Binding/genetics ; Protein Interaction Maps ; Salmonella/metabolism ; Salmonella/pathogenicity ; Sequestosome-1 Protein/genetics ; Sequestosome-1 Protein/metabolism ; Shigella/metabolism ; Shigella/pathogenicity ; Virulence Factors/metabolism
Chemical Substances	Bacterial Proteins ; CALCOCO2 protein, human ; MAP1LC3A protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Nuclear Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Virulence Factors
Language	English
Publishing date	2019-03-25
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2019.1590519
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Article ; Online: Placenta-Specific Genes, Their Regulation During Villous Trophoblast Differentiation and Dysregulation in Preterm Preeclampsia.

Szilagyi, Andras / Gelencser, Zsolt / Romero, Roberto / Xu, Yi / Kiraly, Peter / Demeter, Amanda / Palhalmi, Janos / Gyorffy, Balazs A / Juhasz, Kata / Hupuczi, Petronella / Kekesi, Katalin Adrienna / Meinhardt, Gudrun / Papp, Zoltan / Draghici, Sorin / Erez, Offer / Tarca, Adi Laurentiu / Knöfler, Martin / Than, Nandor Gabor

International journal of molecular sciences

2020 Volume 21, Issue 2

Abstract: The human placenta maintains pregnancy and supports the developing fetus by providing nutrition, gas-waste exchange, hormonal regulation, and an immunological barrier from the maternal immune system. The villous syncytiotrophoblast carries most of these ... ...

Abstract	The human placenta maintains pregnancy and supports the developing fetus by providing nutrition, gas-waste exchange, hormonal regulation, and an immunological barrier from the maternal immune system. The villous syncytiotrophoblast carries most of these functions and provides the interface between the maternal and fetal circulatory systems. The syncytiotrophoblast is generated by the biochemical and morphological differentiation of underlying cytotrophoblast progenitor cells. The dysfunction of the villous trophoblast development is implicated in placenta-mediated pregnancy complications. Herein, we describe gene modules and clusters involved in the dynamic differentiation of villous cytotrophoblasts into the syncytiotrophoblast. During this process, the immune defense functions are first established, followed by structural and metabolic changes, and then by peptide hormone synthesis. We describe key transcription regulatory molecules that regulate gene modules involved in placental functions. Based on transcriptomic evidence, we infer how villous trophoblast differentiation and functions are dysregulated in preterm preeclampsia, a life-threatening placenta-mediated obstetrical syndrome for the mother and fetus. In the conclusion, we uncover the blueprint for villous trophoblast development and its impairment in preterm preeclampsia, which may aid in the future development of non-invasive biomarkers for placental functions and early identification of women at risk for preterm preeclampsia as well as other placenta-mediated pregnancy complications.
MeSH term(s)	Cell Differentiation ; Female ; Gene Expression Regulation ; Genetic Markers ; Humans ; Placenta/metabolism ; Placenta/pathology ; Pre-Eclampsia/genetics ; Pre-Eclampsia/pathology ; Pregnancy ; Transcriptome ; Trophoblasts/metabolism ; Trophoblasts/pathology
Chemical Substances	Genetic Markers
Language	English
Publishing date	2020-01-17
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/ijms21020628
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Article: SalmoNet, an integrated network of ten

Métris, Aline / Sudhakar, Padhmanand / Fazekas, David / Demeter, Amanda / Ari, Eszter / Olbei, Marton / Branchu, Priscilla / Kingsley, Rob A / Baranyi, Jozsef / Korcsmáros, Tamas

NPJ systems biology and applications

2017 Volume 3, Page(s) 31

Abstract: Salmonella ... ...

Abstract	Salmonella enterica
Language	English
Publishing date	2017
Publishing country	England
Document type	Journal Article
ISSN	2056-7189
ISSN	2056-7189
DOI	10.1038/s41540-017-0034-z
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Article ; Online: SignaLink3: a multi-layered resource to uncover tissue-specific signaling networks.

Csabai, Luca / Fazekas, Dávid / Kadlecsik, Tamás / Szalay-Bekő, Máté / Bohár, Balázs / Madgwick, Matthew / Módos, Dezső / Ölbei, Márton / Gul, Lejla / Sudhakar, Padhmanand / Kubisch, János / Oyeyemi, Oyebode James / Liska, Orsolya / Ari, Eszter / Hotzi, Bernadette / Billes, Viktor A / Molnár, Eszter / Földvári-Nagy, László / Csályi, Kitti /

Demeter, Amanda / Pápai, Nóra / Koltai, Mihály / Varga, Máté / Lenti, Katalin / Farkas, Illés J / Türei, Dénes / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás

Nucleic acids research

2021 Volume 50, Issue D1, Page(s) D701–D709

Abstract: Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key ...

Abstract	Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key interactions or processes. Hence, we have developed SignaLink3 (http://signalink.org/), a value-added knowledge-base that provides manually curated data on signaling pathways and integrated data from several types of databases (interaction, regulation, localisation, disease, etc.) for humans, and three major animal model organisms. SignaLink3 contains over 400 000 newly added human protein-protein interactions resulting in a total of 700 000 interactions for Homo sapiens, making it one of the largest integrated signaling network resources. Next to H. sapiens, SignaLink3 is the only current signaling network resource to provide regulatory information for the model species Caenorhabditis elegans and Danio rerio, and the largest resource for Drosophila melanogaster. Compared to previous versions, we have integrated gene expression data as well as subcellular localization of the interactors, therefore uniquely allowing tissue-, or compartment-specific pathway interaction analysis to create more accurate models. Data is freely available for download in widely used formats, including CSV, PSI-MI TAB or SQL.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Databases, Genetic ; Drosophila melanogaster/genetics ; Gene Regulatory Networks/genetics ; Humans ; Protein Interaction Maps/genetics ; Signal Transduction/genetics ; Zebrafish/genetics
Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkab909
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Article ; Online: SignaFish: A Zebrafish-Specific Signaling Pathway Resource.

Csályi, Kitti / Fazekas, Dávid / Kadlecsik, Tamás / Türei, Dénes / Gul, Leila / Horváth, Balázs / Módos, Dezső / Demeter, Amanda / Pápai, Nóra / Lenti, Katalin / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás / Varga, Máté

Zebrafish

2016 Volume 13, Issue 6, Page(s) 541–544

Abstract: Understanding living systems requires an in-depth knowledge of the signaling networks that drive cellular homeostasis, regulate intercellular communication, and contribute to cell fates during development. Several resources exist to provide high- ... ...

Abstract	Understanding living systems requires an in-depth knowledge of the signaling networks that drive cellular homeostasis, regulate intercellular communication, and contribute to cell fates during development. Several resources exist to provide high-throughput data sets or manually curated interaction information from human or invertebrate model organisms. We previously developed SignaLink, a uniformly curated, multi-layered signaling resource containing information for human and for the model organisms nematode Caenorhabditis elegans and fruit fly Drosophila melanogaster. Until now, the use of the SignaLink database for zebrafish pathway analysis was limited. To overcome this limitation, we created SignaFish ( http://signafish.org ), a fish-specific signaling resource, built using the concept of SignaLink. SignaFish contains more than 200 curation-based signaling interactions, 132 further interactions listed in other resources, and it also lists potential miRNA-based regulatory connections for seven major signaling pathways. From the SignaFish website, users can reach other web resources, such as ZFIN. SignaFish provides signaling or signaling-related interactions that can be examined for each gene or downloaded for each signaling pathway. We believe that the SignaFish resource will serve as a novel navigating point for experimental design and evaluation for the zebrafish community and for researchers focusing on nonmodel fish species, such as cyclids.
MeSH term(s)	Animals ; Databases, Genetic ; Gene Regulatory Networks ; Internet ; Signal Transduction ; Zebrafish/genetics
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2156020-1
ISSN	1557-8542 ; 1545-8547
ISSN (online)	1557-8542
ISSN	1545-8547
DOI	10.1089/zeb.2016.1277
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Article ; Online: Autophagy Regulatory Network - a systems-level bioinformatics resource for studying the mechanism and regulation of autophagy.

Türei, Dénes / Földvári-Nagy, László / Fazekas, Dávid / Módos, Dezső / Kubisch, János / Kadlecsik, Tamás / Demeter, Amanda / Lenti, Katalin / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás

Autophagy

2015 Volume 11, Issue 1, Page(s) 155–165

Abstract: Autophagy is a complex cellular process having multiple roles, depending on tissue, physiological, or pathological conditions. Major post-translational regulators of autophagy are well known, however, they have not yet been collected comprehensively. The ...

Abstract	Autophagy is a complex cellular process having multiple roles, depending on tissue, physiological, or pathological conditions. Major post-translational regulators of autophagy are well known, however, they have not yet been collected comprehensively. The precise and context-dependent regulation of autophagy necessitates additional regulators, including transcriptional and post-transcriptional components that are listed in various datasets. Prompted by the lack of systems-level autophagy-related information, we manually collected the literature and integrated external resources to gain a high coverage autophagy database. We developed an online resource, Autophagy Regulatory Network (ARN; http://autophagy-regulation.org), to provide an integrated and systems-level database for autophagy research. ARN contains manually curated, imported, and predicted interactions of autophagy components (1,485 proteins with 4,013 interactions) in humans. We listed 413 transcription factors and 386 miRNAs that could regulate autophagy components or their protein regulators. We also connected the above-mentioned autophagy components and regulators with signaling pathways from the SignaLink 2 resource. The user-friendly website of ARN allows researchers without computational background to search, browse, and download the database. The database can be downloaded in SQL, CSV, BioPAX, SBML, PSI-MI, and in a Cytoscape CYS file formats. ARN has the potential to facilitate the experimental validation of novel autophagy components and regulators. In addition, ARN helps the investigation of transcription factors, miRNAs and signaling pathways implicated in the control of the autophagic pathway. The list of such known and predicted regulators could be important in pharmacological attempts against cancer and neurodegenerative diseases.
MeSH term(s)	Apoptosis Regulatory Proteins/metabolism ; Autophagy/genetics ; Beclin-1 ; Computational Biology/methods ; Databases, Genetic ; Gene Regulatory Networks ; Humans ; Internet ; Membrane Proteins/metabolism ; Protein Binding ; Signal Transduction/genetics ; Statistics as Topic
Chemical Substances	Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Membrane Proteins
Language	English
Publishing date	2015-01-30
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	10.4161/15548627.2014.994346
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