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Article ; Online: A gene toolbox for monitoring autophagy transcription.

Bordi, Matteo / De Cegli, Rossella / Testa, Beatrice / Nixon, Ralph A / Ballabio, Andrea / Cecconi, Francesco

2021 Volume 12, Issue 11, Page(s) 1044

Abstract: Autophagy is a highly dynamic and multi-step process, regulated by many functional protein units. Here, we have built up a comprehensive and up-to-date annotated gene list for the autophagy pathway, by combining previously published gene lists and the ... ...

Abstract	Autophagy is a highly dynamic and multi-step process, regulated by many functional protein units. Here, we have built up a comprehensive and up-to-date annotated gene list for the autophagy pathway, by combining previously published gene lists and the most recent publications in the field. We identified 604 genes and created main categories: MTOR and upstream pathways, autophagy core, autophagy transcription factors, mitophagy, docking and fusion, lysosome and lysosome-related genes. We then classified such genes in sub-groups, based on their functions or on their sub-cellular localization. Moreover, we have curated two shorter sub-lists to predict the extent of autophagy activation and/or lysosomal biogenesis; we next validated the "induction list" by Real-time PCR in cell lines during fasting or MTOR inhibition, identifying ATG14, ATG7, NBR1, ULK1, ULK2, and WDR45, as minimal transcriptional targets. We also demonstrated that our list of autophagy genes can be particularly useful during an effective RNA-sequencing analysis. Thus, we propose our lists as a useful toolbox for performing an informative and functionally-prognostic gene scan of autophagy steps.
MeSH term(s)	Autophagy/genetics ; Cell Line, Tumor ; Genetic Techniques ; HEK293 Cells ; Humans ; Lysosomes/metabolism ; Reproducibility of Results ; TOR Serine-Threonine Kinases/metabolism ; Transcription, Genetic
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-11-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41419-021-04121-9
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Article ; Online: Autophagy and cancer stem cells: molecular mechanisms and therapeutic applications.

Nazio, Francesca / Bordi, Matteo / Cianfanelli, Valentina / Locatelli, Franco / Cecconi, Francesco

Cell death and differentiation

2019 Volume 26, Issue 4, Page(s) 690–702

Abstract: Autophagy and mitophagy act in cancer as bimodal processes, whose differential functions strictly depend on cancer ontogenesis, progression, and type. For instance, they can act to promote cancer progression by helping cancer cells survive stress or, ... ...

Abstract	Autophagy and mitophagy act in cancer as bimodal processes, whose differential functions strictly depend on cancer ontogenesis, progression, and type. For instance, they can act to promote cancer progression by helping cancer cells survive stress or, instead, when mutated or abnormal, to induce carcinogenesis by influencing cell signaling or promoting intracellular toxicity. For this reason, the study of autophagy in cancer is the main focus of many researchers and several clinical trials are already ongoing to manipulate autophagy and by this way determine the outcome of disease therapy. Since the establishment of the cancer stem cell (CSC) theory and the discovery of CSCs in individual cancer types, autophagy and mitophagy have been proposed as key mechanisms in their homeostasis, dismissal or spread, even though we still miss a comprehensive view of how and by which regulatory molecules these two processes drive cell fate. In this review, we will dive into the deep water of autophagy, mitophagy, and CSCs and offer novel viewpoints on possible therapeutic strategies, based on the modulation of these degradative systems.
MeSH term(s)	Animals ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy/immunology ; Humans ; Mitophagy/drug effects ; Mitophagy/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/immunology ; Neoplastic Stem Cells/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/immunology ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
Language	English
Publishing date	2019-02-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-019-0292-y
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Article: The Close Interconnection between Mitochondrial Dynamics and Mitophagy in Cancer.

Bordi, Matteo / Nazio, Francesca / Campello, Silvia

Frontiers in oncology

2017 Volume 7, Page(s) 81

Abstract: Recent decades have revealed the shape changes of mitochondria and their regulators to be main players in a plethora of physiological cell processes. Mitochondria are extremely dynamic organelles whose highly controlled morphological changes respond to ... ...

Abstract	Recent decades have revealed the shape changes of mitochondria and their regulators to be main players in a plethora of physiological cell processes. Mitochondria are extremely dynamic organelles whose highly controlled morphological changes respond to specific and diverse pathophysiological needs. Thus, their qualitative control is crucial for the determination of cell function and fate. Moreover, ever-new metabolic changes, mainly attributable to mitochondrial (dys)functions, are strongly connected to cancer and its microenvironment. For this reason, the aspects controlling mitochondria activity and status are in the oncological spotlight. In this review, we elucidate the most intriguing discoveries related to two apparently independent but strictly interconnected processes crucial for the organelle functionality and fate, mitochondrial dynamics, and mitophagy. We will mostly focus on their metabolic interconnections and regulations that can causally foster a tumoral context.
Language	English
Publishing date	2017-05-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2017.00081
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Book ; Online ; Thesis: Investigating the RNA-binding activity of the Drosophila melanogaster germline inducer Oskar

Bordi, Matteo [Verfasser] / Stoecklin, Georg [Akademischer Betreuer]

2018

Author's details	Matteo Bordi ; Betreuer: Georg Stoecklin
Keywords	Naturwissenschaften ; Science
Subject code	sg500
Language	English
Publisher	Universitätsbibliothek Heidelberg
Publishing place	Heidelberg
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Real-world outcomes of Italian patients with advanced non-squamous lung cancer treated with first-line pembrolizumab plus platinum-pemetrexed.

Leonetti, Alessandro / Perrone, Fabiana / Puntoni, Matteo / Maglietta, Giuseppe / Bordi, Paola / Bria, Emilio / Vita, Emanuele / Gelsomino, Francesco / De Giglio, Andrea / Gelibter, Alain / Siringo, Marco / Mazzoni, Francesca / Caliman, Enrico / Genova, Carlo / Bertolini, Federica / Guaitoli, Giorgia / Passiglia, Francesco / Delcuratolo, Marco Donatello / Montrone, Michele /

Cerea, Giulio / Pasello, Giulia / Roca, Elisa / Belluomini, Lorenzo / Cecere, Fabiana Letizia / Guida, Annalisa / Manzo, Anna / Adamo, Vincenzo / Rastelli, Francesca / Bulotta, Alessandra / Citarella, Fabrizio / Toschi, Luca / Zoratto, Federica / Cortinovis, Diego Luigi / Berardi, Rossana / Follador, Alessandro / Carta, Annamaria / Camerini, Andrea / Salerno, Flavio / Silva, Rosa Rita / Baldini, Editta / Cortellini, Alessio / Brighenti, Matteo / Santoni, Matteo / Malorgio, Francesco / Caminiti, Caterina / Tiseo, Marcello

European journal of cancer (Oxford, England : 1990)

2024 Volume 202, Page(s) 114006

Abstract: Purpose: The aim of this multi-center, retrospective/prospective cohort observational study was to evaluate outcomes in routine clinical practice of first-line chemo-immunotherapy with cis/carboplatin, pemetrexed and pembrolizumab in patients with ... ...

Abstract	Purpose: The aim of this multi-center, retrospective/prospective cohort observational study was to evaluate outcomes in routine clinical practice of first-line chemo-immunotherapy with cis/carboplatin, pemetrexed and pembrolizumab in patients with advanced non-squamous non-small cell lung cancer (NSCLC) in 33 Italian centers. Methods: The outcome measure was to evaluate overall survival (OS) in a real-world patient population. Secondary endpoints were: progression-free survival (PFS), objective response rate (ORR), duration of response (DoR) and incidence of treatment-related adverse events (AEs). Results: 1068 patients were enrolled at the time of data cut-off (January 31st, 2023), and 812 (76.0%) belonged to the retrospective cohort. Median age was 66 years (27-85), ECOG PS was ≥ 2 in 91 (8.6%) patients; 254 (23.8%) patients had brain metastases at baseline; 38 (3.6%) patients had tumor with PD-L1 expression ≥ 50%. After a median follow-up of 17.0 months (95% CI, 16.1-17.9), median OS was 16.1 months (95% CI, 14.4-18.8) and PFS was 9.9 months (95% CI, 8.8-11.2). Median DoR (n = 493) was 14.7 months (95% CI, 13.6-17.1). ORR was 43.4% (95% CI, 40.4-46.4). Any-grade AEs occurred in 636 (59.6%) patients and grade ≥ 3 in 253 (23.7%) patients. Most common grade ≥ 3 AEs were neutropenia (6.3%) and anemia (6.3%). Conclusions: First-line chemo-immunotherapy was effective and tolerable in this large, real-world Italian study of patients with advanced non-squamous NSCLC. Our results were in line with the KEYNOTE-189 registration study, also considering the low number of PD-L1 ≥ 50% patients included in our study.
MeSH term(s)	Humans ; Aged ; Lung Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/pathology ; Pemetrexed ; Platinum/therapeutic use ; B7-H1 Antigen ; Prospective Studies ; Retrospective Studies ; Italy ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antibodies, Monoclonal, Humanized
Chemical Substances	Pemetrexed (04Q9AIZ7NO) ; pembrolizumab (DPT0O3T46P) ; Platinum (49DFR088MY) ; B7-H1 Antigen ; Antibodies, Monoclonal, Humanized
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Observational Study ; Multicenter Study ; Journal Article
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2024.114006
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Zs.A 456: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 583: Show issues

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Article ; Online: The long non-coding RNA

Porcù, Elena / Benetton, Maddalena / Bisio, Valeria / Da Ros, Ambra / Tregnago, Claudia / Borella, Giulia / Zanon, Carlo / Bordi, Matteo / Germano, Giuseppe / Manni, Sabrina / Campello, Silvia / Rao, Dinesh S / Locatelli, Franco / Pigazzi, Martina

iScience

2021 Volume 24, Issue 11, Page(s) 103350

Abstract: Patients with acute myeloid leukemia (AML) carrying high-risk genetic lesions or high residual disease levels after therapy are particularly exposed to the risk of relapse. Here, we identified the long non-coding ... ...

Abstract	Patients with acute myeloid leukemia (AML) carrying high-risk genetic lesions or high residual disease levels after therapy are particularly exposed to the risk of relapse. Here, we identified the long non-coding RNA
Language	English
Publishing date	2021-10-26
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103350
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Article ; Online: Effects of ST1936, a selective serotonin-6 agonist, on electrical activity of putative mesencephalic dopaminergic neurons in the rat brain.

Borsini, Franco / Bordi, Fabio / Poggi, Andreina / Di Matteo, Vincenzo

Journal of psychopharmacology (Oxford, England)

2015 Volume 29, Issue 7, Page(s) 802–811

Abstract: The serotonin-6 (5-HT6) receptor is the most recently discovered serotonin receptor, and it represents an increasingly promising target for improving cognition in both normal and disease states. Recently, a new selective 5-HT6 receptor agonist, 2-(5 ... ...

Abstract	The serotonin-6 (5-HT6) receptor is the most recently discovered serotonin receptor, and it represents an increasingly promising target for improving cognition in both normal and disease states. Recently, a new selective 5-HT6 receptor agonist, 2-(5 chloro-2-methyl-1H-indol-3-yl)-N,N-dimethylethanamine (ST1936), with nanomolar affinity for 5-HT6 receptors was described. We performed in-vivo electrophysiological studies to investigate the physiological role of 5-HT6 receptors in the control of the function of the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA). Extracellular single-unit recordings were performed from putative dopamine-containing neurons in the SNc and VTA of anesthetised rats. In the SNc, acute systemic administration of ST1936 had no effects on basal firing activity of these dopamine neurons; however, in the VTA, ST1936 induced either dose-related increases (45% of cells) or decreases in basal activity of these dopaminergic neurons. Local application of ST1936 into the VTA caused excitation in all of the dopamine neurons, but had no effects on non-dopamine VTA neurons. Both effects of systemic and microiontophoretic ST1936 were completely reversed by the potent and selective 5-HT6 receptor antagonist 5-chloro-N-(4-methoxy-3-piperazin-1-ylphenyl)-3-methyl-2- benzothiophene-sulfonamide (SB271046). Systemic application of another 5-HT6 agonist, 2-(1-{6-chloroimidazo[2,1-b] [1,3]thiazole-5-sulfonyl}-1H-indol-3-yl)ethan-1-amine (WAY-181187), induced dose-dependent inhibition of these VTA dopaminergic neurons. ST1936 and WAY-181187 appear to have different effects on these VTA dopaminergic neurons, potentially due to different mechanisms of action or to the complexity of 5-HT6 receptor functions. Our data demonstrate the need for further investigations into the use of 5-HT6 receptor agonists to control cognitive disfunction, such as in schizophrenia and depression.
MeSH term(s)	Animals ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/metabolism ; Dose-Response Relationship, Drug ; Electrophysiological Phenomena/drug effects ; Ethylamines/administration & dosage ; Ethylamines/pharmacology ; Indoles/administration & dosage ; Indoles/pharmacology ; Male ; Pars Compacta/drug effects ; Pars Compacta/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Serotonin/drug effects ; Receptors, Serotonin/metabolism ; Serotonin Receptor Agonists/administration & dosage ; Serotonin Receptor Agonists/pharmacology ; Thiazoles/administration & dosage ; Thiazoles/pharmacology ; Tryptamines/administration & dosage ; Tryptamines/pharmacology ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/metabolism
Chemical Substances	2-(5-chloro-2-methyl-1H-indol-3-yl)-N,N-dimethylethanamine ; Ethylamines ; Indoles ; N(1)-(6-chloroimidazo(2,1-b)(1,3)thiazole-5-sulfonyl)tryptamine ; Receptors, Serotonin ; Serotonin Receptor Agonists ; Thiazoles ; Tryptamines ; serotonin 6 receptor
Language	English
Publishing date	2015-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639313-5
ISSN	1461-7285 ; 0269-8811
ISSN (online)	1461-7285
ISSN	0269-8811
DOI	10.1177/0269881115573804
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Article ; Online: Clinical and molecular characterization of patients with adenylosuccinate lyase deficiency.

Mastrogiorgio, Gerarda / Macchiaiolo, Marina / Buonuomo, Paola Sabrina / Bellacchio, Emanuele / Bordi, Matteo / Vecchio, Davide / Brown, Kari Payne / Watson, Natalie Karen / Contardi, Benedetta / Cecconi, Francesco / Tartaglia, Marco / Bartuli, Andrea

Orphanet journal of rare diseases

2021 Volume 16, Issue 1, Page(s) 112

Abstract: Background: Adenylosuccinate lyase deficiency (ADSLD) is an ultrarare neurometabolic recessive disorder caused by loss-of-function mutations in the ADSL gene. The disease is characterized by wide clinical variability. Here we provide an updated clinical ...

Abstract	Background: Adenylosuccinate lyase deficiency (ADSLD) is an ultrarare neurometabolic recessive disorder caused by loss-of-function mutations in the ADSL gene. The disease is characterized by wide clinical variability. Here we provide an updated clinical profiling of the disorder and discuss genotype-phenotype correlations. Results: Data were collected through "Our Journey with ADSL deficiency Association" by using a dedicated web survey filled-in by parents. Clinical and molecular data were collected from 18 patients (12 males, median age 10.9 years ± 7.3), from 13 unrelated families. The age at onset ranged from birth to the first three years (median age 0.63 years ± 0.84 SD), and age at diagnosis varied from 2 months to 17 years, (median age 6.4 years ± 6.1 SD). The first sign was a psychomotor delay in 8/18 patients, epilepsy in 3/18, psychomotor delay and epilepsy in 3/18, and apneas, hypotonia, nystagmus in single cases. One patient (sibling of a previously diagnosed child) had a presymptomatic diagnosis. The diagnosis was made by exome sequencing in 7/18 patients. All patients were definitively diagnosed with ADSL deficiency based on pathogenic variants and/or biochemical assessment. One patient had a fatal neonatal form of ADSL deficiency, seven showed features fitting type I, and nine were characterized by a milder condition (type II), with two showing a very mild phenotype. Eighteen different variants were distributed along the entire ADSL coding sequence and were predicted to have a variable structural impact by impairing proper homotetramerization or catalytic activity of the enzyme. Six variants had not previously been reported. All but two variants were missense. Conclusions: The study adds more details on the spectrum of ADSLD patients' phenotypes and molecular data.
MeSH term(s)	Adenylosuccinate Lyase/deficiency ; Adenylosuccinate Lyase/genetics ; Adolescent ; Autistic Disorder ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Infant, Newborn ; Male ; Phenotype ; Purine-Pyrimidine Metabolism, Inborn Errors/diagnosis ; Purine-Pyrimidine Metabolism, Inborn Errors/genetics
Chemical Substances	Adenylosuccinate Lyase (EC 4.3.2.2)
Language	English
Publishing date	2021-03-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-021-01731-6
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Article ; Online: Transglutaminase Type 2 regulates the Wnt/β-catenin pathway in vertebrates.

Rossin, Federica / Costa, Roberto / Bordi, Matteo / D'Eletto, Manuela / Occhigrossi, Luca / Farrace, Maria Grazia / Barlev, Nickolai / Ciccosanti, Fabiola / Muccioli, Silvia / Chieregato, Leonardo / Szabo, Ildiko / Fimia, Gian Maria / Piacentini, Mauro / Leanza, Luigi

Cell death & disease

2021 Volume 12, Issue 3, Page(s) 249

Abstract: TG2 is a multifunctional enzyme involved in several cellular processes and has emerging as a potential regulator of gene expression. In this regard, we have recently shown that TG2 is able to activate HSF1, the master transcriptional regulator of the ... ...

Abstract	TG2 is a multifunctional enzyme involved in several cellular processes and has emerging as a potential regulator of gene expression. In this regard, we have recently shown that TG2 is able to activate HSF1, the master transcriptional regulator of the stress-responsive genes; however, its effect on the overall gene expression remains unclear. To address this point, we analyzed, by RNA-seq, the effect of TG2 on the overall transcriptome as well as we characterized the TG2 interactome in the nucleus. The data obtained from these omics approaches reveal that TG2 markedly influences the overall cellular transcriptome profile and specifically the Wnt and HSF1 pathways. In particular, its ablation leads to a drastic downregulation of many key members of these pathways. Interestingly, we found that key components of the Wnt/β-catenin pathway are also downregulated in cells lacking HSF1, thus confirming that TG2 regulates the HSF1 and this axis controls the Wnt signaling. Mechanistic studies revealed that TG2 can regulate the Wnt pathway by physically interacts with β-catenin and its nuclear interactome includes several proteins known to be involved in the regulation of the Wnt signaling. In order to verify whether this effect is playing a role in vivo, we ablated TG2 in Danio rerio. Our data show that the zebrafish lacking TG2 cannot complete the development and their death is associated with an evident downregulation of the Wnt pathway and a defective heat-shock response. Our findings show for the first time that TG2 is essential for the correct embryonal development of lower vertebrates, and its action is mediated by the Wnt/HSF1 axis.
MeSH term(s)	Animals ; Cells, Cultured ; Fibroblasts/enzymology ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Gene Expression Regulation, Developmental ; Heat Shock Transcription Factors/genetics ; Heat Shock Transcription Factors/metabolism ; Heat-Shock Response ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Glutamine gamma Glutamyltransferase 2 ; Transcription, Genetic ; Transcriptome ; Transglutaminases/genetics ; Transglutaminases/metabolism ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; Zebrafish/embryology ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism ; Mice
Chemical Substances	CTNNB1 protein, mouse ; Heat Shock Transcription Factors ; Hsf1 protein, mouse ; Wnt Proteins ; Zebrafish Proteins ; beta Catenin ; Protein Glutamine gamma Glutamyltransferase 2 (EC 2.3.2.13) ; Transglutaminases (EC 2.3.2.13) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2021-03-05
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/s41419-021-03485-2
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Article ; Online: Modulation of autophagy by RTN-1C: role in autophagosome biogenesis.

D' Eletto, Manuela / Risuglia, Anna / Oliverio, Serafina / Mehdawy, Bisan / Nardacci, Roberta / Bordi, Matteo / Di Sano, Federica

Cell death & disease

2019 Volume 10, Issue 12, Page(s) 868

Abstract: The endoplasmic reticulum (ER) is a key organelle fundamental for the maintenance of cellular homeostasis and to determine the cell's fate under stress conditions. Among the known proteins that regulate ER structure and function there is Reticulon-1C ( ... ...

Abstract	The endoplasmic reticulum (ER) is a key organelle fundamental for the maintenance of cellular homeostasis and to determine the cell's fate under stress conditions. Among the known proteins that regulate ER structure and function there is Reticulon-1C (RTN-1C), a member of the reticulon family localized primarily on the ER membrane. We previously demonstrated that RTN-1C expression affects ER function and stress condition. ER is an essential site for the regulation of apoptotic pathways and it has also been recently recognized as an important component of autophagic signaling. Based on these evidences, we have investigated the impact of RTN-1C modulation on autophagy induction. Interestingly we found that reticulon overexpression is able to activate autophagic machinery and its silencing results in a significative inhibition of both basal and induced autophagic response. Using different experimental approaches we demonstrated that RTN-1C colocalizes with ATG16L and LC3II on the autophagosomes. Considering the key role of reticulon proteins in the control of ER membrane shaping and homeostasis, our data suggest the participation of RTN-1C in the autophagic vesicle biogenesis at the level of the ER compartment. Our data indicate a new mechanism by which this structural ER protein modulates cellular stress, that is at the basis of different autophagy-related pathologies.
MeSH term(s)	Autophagosomes/metabolism ; Autophagy/physiology ; Endoplasmic Reticulum/metabolism ; Humans ; Nerve Tissue Proteins/genetics ; Organelle Biogenesis
Chemical Substances	Nerve Tissue Proteins ; RTN1 protein, human
Language	English
Publishing date	2019-11-18
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/s41419-019-2099-7
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