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Article: p73 is regulated by phosphorylation at the G2/M transition.

Fulco, Marcella / Costanzo, Antonio / Merlo, Paola / Mangiacasale, Rosamaria / Strano, Sabrina / Blandino, Giovanni / Balsano, Clara / Lavia, Patrizia / Levrero, Massimo

The Journal of biological chemistry

2003 Volume 278, Issue 49, Page(s) 49196–49202

Abstract: ... these results indicate that M phase-specific phosphorylation of p73 by p34cdc2-cyclin B is associated ...

Abstract	p73 is a p53 paralog that encodes proapoptotic (transactivation-competent (TA)) and antiapoptotic (dominant negative) isoforms. TAp73 transcription factors mediate cell cycle arrest and/or apoptosis in response to DNA damage and are involved in developmental processes in the central nervous system and the immune system. p73 proteins may also play a role in the regulation of cell growth. Indeed, p73 expression is itself modulated during the cell cycle and TAp73 proteins accumulate in S phase cells. In addition, the function of p73 proteins is also regulated by post-translational modifications and protein-protein interactions in different cellular and pathophysiological contexts. Here we show that p73 is a physiological target of the p34cdc2-cyclin B mitotic kinase complex in vivo. Both p73beta and p73alpha isoforms are hyperphosphorylated in normal mitotic cells and during mitotic arrest induced by microtubule-targeting drugs. p34cdc2-cyclin B phosphorylates and associates with p73 in vivo, which results in a decreased ability of p73 to both bind DNA and activate transcription in mitotic cells. Indeed, p73 is excluded from condensed chromosomes in meta- and anaphase, redistributes throughout the mitotic cytoplasm, and unlike p53, shows no association with centrosomes. Together these results indicate that M phase-specific phosphorylation of p73 by p34cdc2-cyclin B is associated with negative regulation of its transcriptional activating function.
MeSH term(s)	Cell Line, Tumor ; Cyclin B/metabolism ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/physiology ; G2 Phase ; Genes, Tumor Suppressor ; Humans ; Mitosis ; Nuclear Proteins/physiology ; Phosphorylation ; Proto-Oncogene Proteins ; Tumor Protein p73 ; Tumor Suppressor Proteins
Chemical Substances	Cyclin B ; DNA-Binding Proteins ; Nuclear Proteins ; Proto-Oncogene Proteins ; TP73 protein, human ; Tumor Protein p73 ; Tumor Suppressor Proteins ; CDK4 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2003-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M304921200
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Article ; Online: Monocyte phenotypic liquid biopsy for NASH and liver fibrosis diagnosis: a new kid on the block.

Chouik, Yasmina / Levrero, Massimo

Gut

2023 Volume 73, Issue 1, Page(s) 10–11

MeSH term(s)	Humans ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/pathology ; Monocytes/pathology ; Liver Cirrhosis/diagnosis ; Liver Cirrhosis/pathology ; Liver/pathology ; Liquid Biopsy ; Biopsy ; Fibrosis
Language	English
Publishing date	2023-12-07
Publishing country	England
Document type	Journal Article
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2022-328189
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Zs.A 160: Show issues

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Article ; Online: HBV, mitochondrial stress, and liver fibrosis: chicken or the egg.

Guerrieri, Francesca / Levrero, Massimo

Hepatology (Baltimore, Md.)

2023 Volume 77, Issue 4, Page(s) 1088–1089

MeSH term(s)	Humans ; Hepatitis B virus ; Liver Cirrhosis
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1097/HEP.0000000000000031
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Article ; Online: Combination of heterozygous APOB gene mutation with PNPLA3 and TM6SF2 variants promotes steatotic liver disease, cirrhosis and HCC development.

Chouik, Yasmina / Di Filippo, Mathilde / Radenne, Sylvie / Dumortier, Jérôme / Moulin, Philippe / Levrero, Massimo

Liver international : official journal of the International Association for the Study of the Liver

2024

Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Letter
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.15837
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Article ; Online: miRNA-27a-3p is involved in the plasticity of differentiated hepatocytes.

Salerno, Debora / Peruzzi, Giovanna / Giuseppe Rubens Pascucci / Levrero, Massimo / Belloni, Laura / Pediconi, Natalia

Gene

2024 Volume 913, Page(s) 148387

Abstract: Background: Epigenetic mechanisms, including DNA methylation, histone modifications, and chromatin remodeling, are highly involved in the regulation of hepatocyte viability, proliferation, and plasticity. We have previously demonstrated that repression ... ...

Abstract	Background: Epigenetic mechanisms, including DNA methylation, histone modifications, and chromatin remodeling, are highly involved in the regulation of hepatocyte viability, proliferation, and plasticity. We have previously demonstrated that repression of H3K27 methylation in differentiated hepatic HepaRG cells by treatment with GSK-J4, an inhibitor of JMJD3 and UTX H3K27 demethylase activity, changed their phenotype, inducing differentiated hepatocytes to proliferate. In addition to the epigenetic enzymatic role in the regulation of the retro-differentiation process, emerging evidence indicate that microRNAs (miRNAs) are involved in controlling hepatocyte proliferation during liver regeneration. Hence, the aim of this work is to investigate the impact of H3K27 methylation on miRNAs expression profile and its role in the regulation of the differentiation status of human hepatic progenitors HepaRG cells. Methods: A miRNA-sequencing was carried out in differentiated HepaRG cells treated or not with GSK-J4. Target searching and Gene Ontology analysis were performed to identify the molecular processes modulated by differentially expressed miRNAs. The biological functions of selected miRNAs was further investigated by transfection of miRNAs inhibitors or mimics in differentiated HepaRG cells followed by qPCR analysis, albumin ELISA assay, CD49a FACS analysis and EdU staining. Results: We identified 12 miRNAs modulated by GSK-J4; among these, miR-27a-3p and miR- 423-5p influenced the expression of several proliferation genes in differentiated HepaRG cells. MiR-27a-3p overexpression increased the number of hepatic cells reentering proliferation. Interestingly, both miR-27a-3p and miR-423-5p did not affect the expression levels of genes involved in the differentiation of progenitors HepaRG cells. Conclusions: Modulation of H3K27me3 methylation in differentiated HepaRG cells, by GSK-J4 treatment, influenced miRNA' s expression profile pushing liver cells towards a proliferating phenotype. We demonstrated the involvement of miR-27a-3p in reinducing proliferation of differentiated hepatocytes suggesting a potential role in liver plasticity.
MeSH term(s)	Humans ; Hepatocytes/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Liver/metabolism ; Cell Differentiation/genetics ; Epigenesis, Genetic
Chemical Substances	MicroRNAs
Language	English
Publishing date	2024-03-17
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2024.148387
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Zs.A 1357: Show issues

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Article: Host Epigenetic Alterations and Hepatitis B Virus-Associated Hepatocellular Carcinoma.

Zeisel, Mirjam B / Guerrieri, Francesca / Levrero, Massimo

Journal of clinical medicine

2021 Volume 10, Issue 8

Abstract: Hepatocellular carcinoma (HCC) is the most frequent primary malignancy of the liver and a leading cause of cancer-related deaths worldwide. Although much progress has been made in HCC drug development in recent years, treatment options remain limited. ... ...

Abstract	Hepatocellular carcinoma (HCC) is the most frequent primary malignancy of the liver and a leading cause of cancer-related deaths worldwide. Although much progress has been made in HCC drug development in recent years, treatment options remain limited. The major cause of HCC is chronic hepatitis B virus (HBV) infection. Despite the existence of a vaccine, more than 250 million individuals are chronically infected by HBV. Current antiviral therapies can repress viral replication but to date there is no cure for chronic hepatitis B. Of note, inhibition of viral replication reduces but does not eliminate the risk of HCC development. HBV contributes to liver carcinogenesis by direct and indirect effects. This review summarizes the current knowledge of HBV-induced host epigenetic alterations and their association with HCC, with an emphasis on the interactions between HBV proteins and the host cell epigenetic machinery leading to modulation of gene expression.
Language	English
Publishing date	2021-04-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm10081715
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Article ; Online: Prise en charge des toxicités hépatiques sous immunothérapie anticancéreuse.

Lebossé, Fanny / Bancel, Brigitte / Levrero, Massimo / Merle, Philippe

Bulletin du cancer

2020 Volume 107, Issue 10, Page(s) 1056–1068

Abstract: Pharmacological immune checkpoint inhibitors (ICI) restore the anti-tumor properties of T-lymphocytes, but unfortunately can engender auto-immune-like disorders. Those, frequent and of variable severity, sometimes target the liver parenchyma. Liver ... ...

Title translation	Management of immune checkpoint inhibitors-induced liver toxicity in cancer.
Abstract	Pharmacological immune checkpoint inhibitors (ICI) restore the anti-tumor properties of T-lymphocytes, but unfortunately can engender auto-immune-like disorders. Those, frequent and of variable severity, sometimes target the liver parenchyma. Liver toxicity of ICI firstly leads to alteration of liver function tests (ALFT) with a risk of clinical decompensation. The appearance of ALFT should lead the clinician to exclude a non-immunological injury or a tumoral invasion of the liver parenchyma. In case of high grade ALFT, liver biopsy is necessary for diagnosis purpose. In ICI-induced hepatoxicity, histology examination shows most frequently a lobular acute hepatitis associated with lymphocytic infiltrates, but with different features than those encountered in primary auto-immune hepatitis. The management of ICI-related ALFT depends of their severity. Discontinuation of ICI is recommended for ALFT≥grade 2, and corticosteroid therapy for ALFT≥grade 3, or grade 2 without any improvement after ICI discontinuation. Addition of mycophenolate may be indicated whether corticosteroid inefficiency. Reintroduction of ICI is inadvisable for the most severe toxicities. The management of ALFT occurring on underlying chronic hepatopathy has not got consensual guidelines so far, but they should take account of the basal grade of ALFT and their worsening level under ICI therapy. The situation becomes more complex with associations between ICI and anti-angiogenic agents or cytotoxic chemotherapies where each of the drugs can be hepatotoxic. Thus, liver biopsy is primordial to figure out the mechanism of liver toxicity.
MeSH term(s)	Antineoplastic Agents, Immunological/adverse effects ; Antineoplastic Agents, Immunological/therapeutic use ; Chemical and Drug Induced Liver Injury/diagnosis ; Chemical and Drug Induced Liver Injury/epidemiology ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/therapy ; Humans ; Incidence ; Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents, Immunological
Language	French
Publishing date	2020-09-17
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	213270-9
ISSN	1769-6917 ; 0007-4551
ISSN (online)	1769-6917
ISSN	0007-4551
DOI	10.1016/j.bulcan.2020.06.011
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Article ; Online: Social pressure drives "conversational rules" in great apes.

Pougnault, Loïc / Levréro, Florence / Leroux, Maël / Paulet, Julien / Bombani, Pablo / Dentressangle, Fabrice / Deruti, Laure / Mulot, Baptiste / Lemasson, Alban

Biological reviews of the Cambridge Philosophical Society

2021 Volume 97, Issue 2, Page(s) 749–765

Abstract: In the last decade, two hypotheses, one on the evolution of animal vocal communication in general and the other on the origins of human language, have gained ground. The first hypothesis argues that the complexity of communication co-evolved with the ... ...

Abstract	In the last decade, two hypotheses, one on the evolution of animal vocal communication in general and the other on the origins of human language, have gained ground. The first hypothesis argues that the complexity of communication co-evolved with the complexity of sociality. Species forming larger groups with complex social networks have more elaborate vocal repertoires. The second hypothesis posits that the core of communication is represented not only by what can be expressed by an isolated caller, but also by the way that vocal interactions are structured, language being above all a social act. Primitive forms of conversational rules based on a vocal turn-taking principle are thought to exist in primates. To support and bring together these hypotheses, more comparative studies of socially diverse species at different levels of the primate phylogeny are needed. However, the majority of available studies focus on monkeys, primates that are distant from the human lineage. Great apes represent excellent candidates for such comparative studies because of their phylogenetic proximity to humans and their varied social lives. We propose that studying vocal turn-taking in apes could address several major gaps regarding the social relevance of vocal turn-taking and the evolutionary trajectory of this behaviour among anthropoids. Indeed, how the social structure of a species may influence the vocal interaction patterns observed among group members remains an open question. We gathered data from the literature as well as original unpublished data (where absent in the literature) on four great ape species: chimpanzees Pan troglodytes, bonobos Pan paniscus, western lowland gorillas Gorilla gorilla gorilla and Bornean orang-utans Pongo pygmaeus. We found no clear-cut relationship between classical social complexity metrics (e.g. number of group members, interaction rates) and vocal complexity parameters (e.g. repertoire size, call rates). Nevertheless, the nature of the society (i.e. group composition, diversity and valence of social bonds) and the type of vocal interaction patterns (isolated calling, call overlap, turn-taking-based vocal exchanges) do appear to be related. Isolated calling is the main vocal pattern found in the species with the smallest social networks (orang-utan), while the other species show vocal interactions that are structured according to temporal rules. A high proportion of overlapping vocalisations is found in the most competitive species (chimpanzee), while vocal turn-taking predominates in more tolerant bonobos and gorillas. Also, preferentially interacting individuals and call types used to interact are not randomly distributed. Vocal overlap ('chorusing') and vocal exchange ('conversing') appear as possible social strategies used to advertise/strengthen social bonds. Our analyses highlight that: (i) vocal turn-taking is also observed in non-human great apes, revealing universal rules for conversing that may be deeply rooted in the primate lineage; (ii) vocal interaction patterns match the species' social lifestyle; (iii) although limited to four species here, adopting a targeted comparative approach could help to identify the multiple and subtle factors underlying social and vocal complexity. We believe that vocal interaction patterns form the basis of a promising field of investigation that may ultimately improve our understanding of the socially driven evolution of communication.
MeSH term(s)	Animal Communication ; Animals ; Gorilla gorilla ; Hominidae/psychology ; Pan troglodytes ; Phylogeny ; Pongo pygmaeus ; Social Behavior
Language	English
Publishing date	2021-12-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1423558-4
ISSN	1469-185X ; 0006-3231 ; 1464-7931
ISSN (online)	1469-185X
ISSN	0006-3231 ; 1464-7931
DOI	10.1111/brv.12821
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Article: The lncRNAs in HBV-Related HCCs: Targeting Chromatin Dynamics and Beyond.

Alfano, Vincenzo / Zeisel, Mirjam B / Levrero, Massimo / Guerrieri, Francesca

Cancers

2021 Volume 13, Issue 13

Abstract: Hepatocellular carcinoma (HCC) represents the fourth leading and fastest rising cause of cancer death (841,000 new cases and 782,000 deaths annually), and hepatitis B (HBV), with 250 million people chronically infected at risk of developing HCC, accounts ...

Abstract	Hepatocellular carcinoma (HCC) represents the fourth leading and fastest rising cause of cancer death (841,000 new cases and 782,000 deaths annually), and hepatitis B (HBV), with 250 million people chronically infected at risk of developing HCC, accounts for >50% of the cases worldwide. Long non-coding RNAs (lncRNAs), untranslated transcripts longer than 200 nucleotides, are implicated in gene regulation at the transcriptional and post-transcriptional levels, exerting their activities both in the nuclear and cytoplasmic compartments. Thanks to high-throughput sequencing techniques, several lncRNAs have been shown to favor the establishment of chronic HBV infection, to change the host transcriptome to establish a pro-carcinogenic environment, and to directly participate in HCC development and progression. In this review, we summarize current knowledge on the role of lncRNAs in HBV infection and HBV-related liver carcinogenesis and discuss the potential of lncRNAs as predictive or diagnostic biomarkers.
Language	English
Publishing date	2021-06-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13133115
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Article ; Online: The grade of obesity affects the noninvasive diagnosis of advanced fibrosis in individuals with MASLD.

Chouik, Yasmina / Aubin, Adrien / Maynard-Muet, Marianne / Segrestin, Bérénice / Milot, Laurent / Hervieu, Valérie / Zoulim, Fabien / Disse, Emmanuel / Levrero, Massimo / Caussy, Cyrielle

Obesity (Silver Spring, Md.)

2024

Abstract: ... Results: The median BMI was 35.0 kg/m: Conclusions: The grade of obesity affects the detection ...

Abstract	Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely associated with obesity. We aimed to assess the impact of obesity on the performance of different noninvasive tests, including liver stiffness measurement (LSM) and Agile3+ (A3+), to detect advanced fibrosis (AF) in a population of patients with MASLD encompassing a wide range of BMI values. Methods: A total of 479 patients with MASLD were consecutively included (Lyon Hepatology Institute). Clinical data and noninvasive tests, including FibroTest, LSM, A3+, Fibrosis-4 (FIB-4), magnetic resonance elastography, and liver biopsies, were collected. AF was determined by a composite endpoint, i.e., histological stage ≥ F3, overt diagnosis of cirrhosis by magnetic resonance elastography, or concordant LSM ≥ 9.6 kPa and FibroTest ≥ F3. Results: The median BMI was 35.0 kg/m Conclusions: The grade of obesity affects the detection of MASLD-related AF. A sequential use of LSM/A3
Language	English
Publishing date	2024-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.24033
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