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Article ; Online: The stiff RhoAd from mevalonate to mutant p53.

Sorrentino, Giovanni / Mantovani, Fiamma / Del Sal, Giannino

2018 Volume 25, Issue 4, Page(s) 645–647

MeSH term(s)	Animals ; Humans ; Mevalonic Acid/metabolism ; Mutation ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; rhoA GTP-Binding Protein/genetics ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53 ; RHOA protein, human (124671-05-2) ; rhoA GTP-Binding Protein (EC 3.6.5.2) ; Mevalonic Acid (S5UOB36OCZ)
Language	English
Publishing date	2018-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-018-0091-x
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Hepatic lipid overload triggers biliary epithelial cell activation via E2Fs.

Yildiz, Ece / El Alam, Gaby / Perino, Alessia / Jalil, Antoine / Denechaud, Pierre-Damien / Huber, Katharina / Fajas, Lluis / Auwerx, Johan / Sorrentino, Giovanni / Schoonjans, Kristina

eLife

2023 Volume 12

Abstract: During severe or chronic hepatic injury, biliary epithelial cells (BECs) undergo rapid activation into proliferating progenitors, a crucial step required to establish a regenerative process known as ductular reaction (DR). While DR is a hallmark of ... ...

Abstract	During severe or chronic hepatic injury, biliary epithelial cells (BECs) undergo rapid activation into proliferating progenitors, a crucial step required to establish a regenerative process known as ductular reaction (DR). While DR is a hallmark of chronic liver diseases, including advanced stages of non-alcoholic fatty liver disease (NAFLD), the early events underlying BEC activation are largely unknown. Here, we demonstrate that BECs readily accumulate lipids during high-fat diet feeding in mice and upon fatty acid treatment in BEC-derived organoids. Lipid overload induces metabolic rewiring to support the conversion of adult cholangiocytes into reactive BECs. Mechanistically, we found that lipid overload activates the E2F transcription factors in BECs, which drive cell cycle progression while promoting glycolytic metabolism. These findings demonstrate that fat overload is sufficient to reprogram BECs into progenitor cells in the early stages of NAFLD and provide new insights into the mechanistic basis of this process, revealing unexpected connections between lipid metabolism, stemness, and regeneration.
MeSH term(s)	Animals ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism ; Liver/metabolism ; Epithelial Cells/metabolism ; Cell Division ; Lipids
Chemical Substances	Lipids
Language	English
Publishing date	2023-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.81926
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Article ; Online: p53 orchestrates calcium signaling in vivo.

Sorrentino, Giovanni / Comel, Anna / Del Sal, Giannino

Cell cycle (Georgetown, Tex.)

2015 Volume 14, Issue 9, Page(s) 1343–1344

MeSH term(s)	Animals ; Apoptosis ; Calcium/metabolism ; Calcium Signaling/drug effects ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/metabolism ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Swelling ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Photochemotherapy/methods ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Inositol 1,4,5-Trisphosphate Receptors ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015-04-16
Publishing country	United States
Document type	Editorial
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2015.1024583
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Article ; Online: Mechano-modulatory synthetic niches for liver organoid derivation.

Sorrentino, Giovanni / Rezakhani, Saba / Yildiz, Ece / Nuciforo, Sandro / Heim, Markus H / Lutolf, Matthias P / Schoonjans, Kristina

Nature communications

2020 Volume 11, Issue 1, Page(s) 3416

Abstract: The recent demonstration that primary cells from the liver can be expanded in vitro as organoids holds enormous promise for regenerative medicine and disease modelling. The use of three-dimensional (3D) cultures based on ill-defined and potentially ... ...

Abstract	The recent demonstration that primary cells from the liver can be expanded in vitro as organoids holds enormous promise for regenerative medicine and disease modelling. The use of three-dimensional (3D) cultures based on ill-defined and potentially immunogenic matrices, however, hampers the translation of liver organoid technology into real-life applications. We here use chemically defined hydrogels for the efficient derivation of both mouse and human hepatic organoids. Organoid growth is found to be highly stiffness-sensitive, a mechanism independent of acto-myosin contractility and requiring instead activation of the Src family of kinases (SFKs) and yes-associated protein 1 (YAP). Aberrant matrix stiffness, on the other hand, results in compromised proliferative capacity. Finally, we demonstrate the establishment of biopsy-derived human liver organoids without the use of animal components at any step of the process. Our approach thus opens up exciting perspectives for the establishment of protocols for liver organoid-based regenerative medicine.
MeSH term(s)	Humans ; Hydrogels ; Liver/cytology ; Liver/metabolism ; Organoids/cytology ; Organoids/metabolism ; Tissue Engineering/methods ; Transcription Factors/metabolism ; src-Family Kinases/metabolism
Chemical Substances	Hydrogels ; Transcription Factors ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2020-07-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-17161-0
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Article ; Online: Bile Acids Signal via TGR5 to Activate Intestinal Stem Cells and Epithelial Regeneration.

Sorrentino, Giovanni / Perino, Alessia / Yildiz, Ece / El Alam, Gaby / Bou Sleiman, Maroun / Gioiello, Antimo / Pellicciari, Roberto / Schoonjans, Kristina

Gastroenterology

2020 Volume 159, Issue 3, Page(s) 956–968.e8

Abstract: Background & aims: Renewal and patterning of the intestinal epithelium is coordinated by intestinal stem cells (ISCs); dietary and metabolic factors provide signals to the niche that control ISC activity. Bile acids (BAs), metabolites in the gut, signal ...

Abstract	Background & aims: Renewal and patterning of the intestinal epithelium is coordinated by intestinal stem cells (ISCs); dietary and metabolic factors provide signals to the niche that control ISC activity. Bile acids (BAs), metabolites in the gut, signal nutrient availability by activating the G protein-coupled bile acid receptor 1 (GPBAR1, also called TGR5). TGR5 is expressed in the intestinal epithelium, but it is not clear how its activation affects ISCs and regeneration of the intestinal epithelium. We studied the role of BAs and TGR5 in intestinal renewal, and regulation of ISC function in mice and intestinal organoids. Methods: We derived intestinal organoids from wild-type mice and Tgr5 Results: BAs and TGR5 agonists promoted growth of intestinal organoids. Administration of cholecystokinin to mice resulted in acute release of BAs into the intestinal lumen and increased proliferation of the intestinal epithelium. BAs and Tgr5 expression in ISCs were required for homeostatic intestinal epithelial renewal and fate specification, and for regeneration after colitis induction. Tgr5 Conclusions: BAs promote regeneration of the intestinal epithelium via activation of TGR5 in ISCs, resulting in activation of SRC and YAP and activation of their target genes. Release of endogenous BAs in the intestinal lumen is sufficient to promote ISC renewal and drives regeneration in response to injury.
MeSH term(s)	Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/metabolism ; Adult Stem Cells/physiology ; Animals ; Bile Acids and Salts/metabolism ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Cycle Proteins/metabolism ; Cell Self Renewal/drug effects ; Cell Self Renewal/physiology ; Cells, Cultured ; Cholic Acids/pharmacology ; Colitis/chemically induced ; Colitis/pathology ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Epithelial Cells ; Humans ; Intestinal Mucosa/cytology ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/pathology ; Male ; Mice ; Mice, Knockout ; Organoids ; Primary Cell Culture ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Regeneration/drug effects ; Regeneration/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/metabolism
Chemical Substances	6alpha-ethyl-23(S)-methylcholic acid ; Adaptor Proteins, Signal Transducing ; Bile Acids and Salts ; Cell Cycle Proteins ; Cholic Acids ; Gpbar1 protein, mouse ; Receptors, G-Protein-Coupled ; Yap1 protein, mouse ; Dextran Sulfate (9042-14-2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2020-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2020.05.067
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Zs.MO 572: Show issues

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Article ; Online: GDA, a web-based tool for Genomics and Drugs integrated analysis.

Caroli, Jimmy / Sorrentino, Giovanni / Forcato, Mattia / Del Sal, Giannino / Bicciato, Silvio

Nucleic acids research

2018 Volume 46, Issue W1, Page(s) W148–W156

Abstract: Several major screenings of genetic profiling and drug testing in cancer cell lines proved that the integration of genomic portraits and compound activities is effective in discovering new genetic markers of drug sensitivity and clinically relevant ... ...

Abstract	Several major screenings of genetic profiling and drug testing in cancer cell lines proved that the integration of genomic portraits and compound activities is effective in discovering new genetic markers of drug sensitivity and clinically relevant anticancer compounds. Despite most genetic and drug response data are publicly available, the availability of user-friendly tools for their integrative analysis remains limited, thus hampering an effective exploitation of this information. Here, we present GDA, a web-based tool for Genomics and Drugs integrated Analysis that combines drug response data for >50 800 compounds with mutations and gene expression profiles across 73 cancer cell lines. Genomic and pharmacological data are integrated through a modular architecture that allows users to identify compounds active towards cancer cell lines bearing a specific genomic background and, conversely, the mutational or transcriptional status of cells responding or not-responding to a specific compound. Results are presented through intuitive graphical representations and supplemented with information obtained from public repositories. As both personalized targeted therapies and drug-repurposing are gaining increasing attention, GDA represents a resource to formulate hypotheses on the interplay between genomic traits and drug response in cancer. GDA is freely available at http://gda.unimore.it/.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Genomics/methods ; Humans ; Internet ; Mutation ; Neoplasms/genetics ; Neoplasms/metabolism ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Signal Transduction ; Software ; Transcriptional Activation ; Transcriptome/drug effects
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2018-05-25
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/gky434
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Article ; Online: Sterol regulatory element binding protein 1 couples mechanical cues and lipid metabolism.

Bertolio, Rebecca / Napoletano, Francesco / Mano, Miguel / Maurer-Stroh, Sebastian / Fantuz, Marco / Zannini, Alessandro / Bicciato, Silvio / Sorrentino, Giovanni / Del Sal, Giannino

Nature communications

2019 Volume 10, Issue 1, Page(s) 1326

Abstract: Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid biosynthesis and adipogenesis by controlling the expression of several enzymes required for cholesterol, fatty acid, triacylglycerol and ... ...

Abstract	Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid biosynthesis and adipogenesis by controlling the expression of several enzymes required for cholesterol, fatty acid, triacylglycerol and phospholipid synthesis. In vertebrates, SREBP activation is mainly controlled by a complex and well-characterized feedback mechanism mediated by cholesterol, a crucial bio-product of the SREBP-activated mevalonate pathway. In this work, we identified acto-myosin contractility and mechanical forces imposed by the extracellular matrix (ECM) as SREBP1 regulators. SREBP1 control by mechanical cues depends on geranylgeranyl pyrophosphate, another key bio-product of the mevalonate pathway, and impacts on stem cell fate in mouse and on fat storage in Drosophila. Mechanistically, we show that activation of AMP-activated protein kinase (AMPK) by ECM stiffening and geranylgeranylated RhoA-dependent acto-myosin contraction inhibits SREBP1 activation. Our results unveil an unpredicted and evolutionary conserved role of SREBP1 in rewiring cell metabolism in response to mechanical cues.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Actins/metabolism ; Adipogenesis ; Animals ; Cell Line, Tumor ; Cytoskeleton/metabolism ; Drosophila melanogaster/metabolism ; Evolution, Molecular ; Extracellular Matrix/metabolism ; Humans ; Lipid Metabolism ; Lipids/biosynthesis ; Mechanotransduction, Cellular ; Mice ; Myosins/metabolism ; Protein Prenylation ; Sterol Regulatory Element Binding Protein 1/metabolism ; Transcription, Genetic ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	Actins ; Lipids ; Sterol Regulatory Element Binding Protein 1 ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Myosins (EC 3.6.4.1) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2019-03-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-09152-7
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Article ; Online: Regulation of mitochondrial apoptosis by Pin1 in cancer and neurodegeneration.

Sorrentino, Giovanni / Comel, Anna / Mantovani, Fiamma / Del Sal, Giannino

Mitochondrion

2014 Volume 19 Pt A, Page(s) 88–96

Abstract: Mitochondria are sensitive and efficient organelles that regulate essential biological processes including: energy metabolism, decoding and transduction of intracellular signals, and balance between cell death and survival. Of note, dysfunctions in ... ...

Abstract	Mitochondria are sensitive and efficient organelles that regulate essential biological processes including: energy metabolism, decoding and transduction of intracellular signals, and balance between cell death and survival. Of note, dysfunctions in mitochondrial physiology are a general hallmark of cancer cells, leading to transformation-related features such as altered cellular metabolism, survival under stress conditions and reduced apoptotic response to chemotherapy. Mitochondrial apoptosis is a finely regulated process that derives from activation of multiple signaling networks. A crucial biochemical requirement for transducing pro-apoptotic stimuli is represented by kinase-dependent phosphorylation cascades. In this context a pivotal role is played by the prolyl-isomerase Pin1, which translates Ser/Thr-Pro phosphorylation into conformational changes able to modify the activities of its substrates. In this review we will discuss the impact of Pin1 in regulating various aspects of apoptosis in different biological contexts with particular emphasis on cancer and neurodegenerative diseases.
MeSH term(s)	Apoptosis/physiology ; Gene Expression Regulation/physiology ; Humans ; Mitochondria/physiology ; NIMA-Interacting Peptidylprolyl Isomerase ; Neoplasms/metabolism ; Neurodegenerative Diseases/metabolism ; Peptidylprolyl Isomerase/genetics ; Peptidylprolyl Isomerase/metabolism
Chemical Substances	NIMA-Interacting Peptidylprolyl Isomerase ; PIN1 protein, human (EC 5.2.1.8) ; Peptidylprolyl Isomerase (EC 5.2.1.8)
Language	English
Publishing date	2014-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2014.08.003
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Article ; Online: The cytoplasmic side of p53's oncosuppressive activities.

Comel, Anna / Sorrentino, Giovanni / Capaci, Valeria / Del Sal, Giannino

FEBS letters

2014 Volume 588, Issue 16, Page(s) 2600–2609

Abstract: The tumor suppressor p53 is a transcription factor that in response to a plethora of stress stimuli activates a complex and context-dependent cellular response ultimately protecting genome integrity. In the last two decades, the discovery of cytoplasmic ... ...

Abstract	The tumor suppressor p53 is a transcription factor that in response to a plethora of stress stimuli activates a complex and context-dependent cellular response ultimately protecting genome integrity. In the last two decades, the discovery of cytoplasmic p53 localization has driven an intense research on its extra-nuclear functions. The ability to induce apoptosis acting directly at mitochondria and the related mechanisms of p53 localization and translocation in the cytoplasm and mitochondria have been dissected. However, recent works indicate the involvement of cytoplasmic p53 also in biological processes such as autophagy, metabolism, oxidative stress and drug response. This review will focus on the mechanisms of cytoplasmic p53 activation and the pathophysiological role of p53's transcription-independent functions, highlighting possible therapeutic implications.
MeSH term(s)	Animals ; Cell Death ; Cytoplasm/metabolism ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/physiopathology ; Oxidative Stress ; Protein Transport ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2014-08-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2014.04.015
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Article ; Online: L-Cell Differentiation Is Induced by Bile Acids Through GPBAR1 and Paracrine GLP-1 and Serotonin Signaling.

Lund, Mari Lilith / Sorrentino, Giovanni / Egerod, Kristoffer Lihme / Kroone, Chantal / Mortensen, Brynjulf / Knop, Filip Krag / Reimann, Frank / Gribble, Fiona M / Drucker, Daniel J / de Koning, Eelco J P / Schoonjans, Kristina / Bäckhed, Fredrik / Schwartz, Thue W / Petersen, Natalia

Diabetes

2020 Volume 69, Issue 4, Page(s) 614–623

Abstract: Glucagon-like peptide 1 (GLP-1) mimetics are effective drugs for treatment of type 2 diabetes, and there is consequently extensive interest in increasing endogenous GLP-1 secretion and L-cell abundance. Here we identify G-protein-coupled bile acid ... ...

Abstract	Glucagon-like peptide 1 (GLP-1) mimetics are effective drugs for treatment of type 2 diabetes, and there is consequently extensive interest in increasing endogenous GLP-1 secretion and L-cell abundance. Here we identify G-protein-coupled bile acid receptor 1 (GPBAR1) as a selective regulator of intestinal L-cell differentiation. Lithocholic acid and the synthetic GPBAR1 agonist, L3740, selectively increased L-cell density in mouse and human intestinal organoids and elevated GLP-1 secretory capacity. L3740 induced expression of
MeSH term(s)	Animals ; Bile Acids and Salts/pharmacology ; Cell Differentiation/drug effects ; Enteroendocrine Cells/drug effects ; Enteroendocrine Cells/physiology ; Female ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/metabolism ; Humans ; Jejunum/drug effects ; Jejunum/metabolism ; Male ; Mice ; Paracrine Communication/drug effects ; Paracrine Communication/physiology ; Receptors, G-Protein-Coupled/metabolism ; Serotonin/metabolism ; Signal Transduction/drug effects
Chemical Substances	Bile Acids and Salts ; GPBAR1 protein, human ; Glucagon-Like Peptide-1 Receptor ; Receptors, G-Protein-Coupled ; Serotonin (333DO1RDJY) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2020-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db19-0764
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