LIVIVO - Search results -

Search results

Result 1 - 10 of total 21

Search options

Article: Rarγ -Foxa1 signaling promotes luminal identity in prostate progenitors and is disrupted in prostate cancer.

bioRxiv : the preprint server for biology

2024

Abstract: Retinoic acid (RA) signaling is a master regulator of vertebrate development with crucial roles in directing body axis orientation and tissue differentiation, including in the reproductive system. However, a mechanistic understanding of how RA signaling ... ...

Abstract	Retinoic acid (RA) signaling is a master regulator of vertebrate development with crucial roles in directing body axis orientation and tissue differentiation, including in the reproductive system. However, a mechanistic understanding of how RA signaling promotes cell lineage identity in different tissues is often missing. Here, leveraging prostate organoid technology, we demonstrated that RA signaling orchestrates the commitment of adult mouse prostate progenitors to glandular identity, epithelial barrier integrity, and ultimately, proper specification of the prostatic lumen. Mechanistically, RA-dependent RARγ activation promotes the expression of the pioneer factor Foxa1, which synergizes with the androgen pathway for proper luminal expansion, cytoarchitecture and function.
Language	English
Publishing date	2024-03-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.06.583256
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: Sleep fragmentation affects glymphatic system through the different expression of AQP4 in wild type and 5xFAD mouse models.

Vasciaveo, Valeria / Iadarola, Antonella / Casile, Antonino / Dante, Davide / Morello, Giulia / Minotta, Lorenzo / Tamagno, Elena / Cicolin, Alessandro / Guglielmotto, Michela

Acta neuropathologica communications

2023 Volume 11, Issue 1, Page(s) 16

Abstract: Alzheimer's disease (AD) is characterized by genetic and multifactorial risk factors. Many studies correlate AD to sleep disorders. In this study, we performed and validated a mouse model of AD and sleep fragmentation, which properly mimics a real ... ...

Abstract	Alzheimer's disease (AD) is characterized by genetic and multifactorial risk factors. Many studies correlate AD to sleep disorders. In this study, we performed and validated a mouse model of AD and sleep fragmentation, which properly mimics a real condition of intermittent awakening. We noticed that sleep fragmentation induces a general acceleration of AD progression in 5xFAD mice, while in wild type mice it affects cognitive behaviors in particular learning and memory. Both these events may be correlated to aquaporin-4 (AQP4) modulation, a crucial player of the glymphatic system activity. In particular, sleep fragmentation differentially affects aquaporin-4 channel (AQP4) expression according to the stage of the disease, with an up-regulation in younger animals, while such change cannot be detected in older ones. Moreover, in wild type mice sleep fragmentation affects cognitive behaviors, in particular learning and memory, by compromising the glymphatic system through the decrease of AQP4. Nevertheless, an in-depth study is needed to better understand the mechanism by which AQP4 is modulated and whether it could be considered a risk factor for the disease development in wild type mice. If our hypotheses are going to be confirmed, AQP4 modulation may represent the convergence point between AD and sleep disorder pathogenic mechanisms.
MeSH term(s)	Animals ; Mice ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Aquaporin 4/genetics ; Aquaporin 4/metabolism ; Brain/pathology ; Disease Models, Animal ; Glymphatic System/pathology ; Mice, Transgenic ; Sleep Deprivation/metabolism ; Sleep Wake Disorders/genetics
Chemical Substances	Amyloid beta-Peptides ; Aquaporin 4 ; Aqp4 protein, mouse
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-022-01498-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- Full text online
- Order with fees

Article ; Online: Subtype-selective prenylated isoflavonoids disrupt regulatory drivers of MYCN-amplified cancers.

Stokes, Michael E / Vasciaveo, Alessandro / Small, Jonnell Candice / Zask, Arie / Reznik, Eduard / Smith, Nailah / Wang, Qian / Daniels, Jacob / Forouhar, Farhad / Rajbhandari, Presha / Califano, Andrea / Stockwell, Brent R

Cell chemical biology

2023 Volume 31, Issue 4, Page(s) 805–819.e9

Abstract: Transcription factors have proven difficult to target with small molecules because they lack pockets necessary for potent binding. Disruption of protein expression can suppress targets and enable therapeutic intervention. To this end, we developed a drug ...

Abstract	Transcription factors have proven difficult to target with small molecules because they lack pockets necessary for potent binding. Disruption of protein expression can suppress targets and enable therapeutic intervention. To this end, we developed a drug discovery workflow that incorporates cell-line-selective screening and high-throughput expression profiling followed by regulatory network analysis to identify compounds that suppress regulatory drivers of disease. Applying this approach to neuroblastoma (NBL), we screened bioactive molecules in cell lines representing its MYC-dependent (MYCNA) and mesenchymal (MES) subtypes to identify selective compounds, followed by PLATESeq profiling of treated cells. This revealed compounds that disrupt a sub-network of MYCNA-specific regulatory proteins, resulting in MYCN degradation in vivo. The top hit was isopomiferin, a prenylated isoflavonoid that inhibited casein kinase 2 (CK2) in cells. Isopomiferin and its structural analogs inhibited MYC and MYCN in NBL and lung cancer cells, highlighting the general MYC-inhibiting potential of this unique scaffold.
MeSH term(s)	Humans ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; N-Myc Proto-Oncogene Protein/genetics ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/drug therapy ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Transcription Factors/metabolism
Chemical Substances	MYCN protein, human ; N-Myc Proto-Oncogene Protein ; Nuclear Proteins ; Oncogene Proteins ; Transcription Factors
Language	English
Publishing date	2023-12-06
Publishing country	United States
Document type	Journal Article
ISSN	2451-9448
ISSN (online)	2451-9448
DOI	10.1016/j.chembiol.2023.11.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: NSD2 maintains lineage plasticity and castration-resistance in neuroendocrine prostate cancer.

bioRxiv : the preprint server for biology

2023

Abstract: The clinical use of potent androgen receptor (AR) inhibitors has promoted the emergence of novel subtypes of metastatic castration-resistant prostate cancer (mCRPC), including neuroendocrine prostate cancer (CRPC-NE), which is highly aggressive and ... ...

Abstract	The clinical use of potent androgen receptor (AR) inhibitors has promoted the emergence of novel subtypes of metastatic castration-resistant prostate cancer (mCRPC), including neuroendocrine prostate cancer (CRPC-NE), which is highly aggressive and lethal
Language	English
Publishing date	2023-07-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.18.549585
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article: A Graph Based Framework to Model Virus Integration Sites.

Fronza, Raffaele / Vasciaveo, Alessandro / Benso, Alfredo / Schmidt, Manfred

Computational and structural biotechnology journal

2015 Volume 14, Page(s) 69–77

Abstract: With next generation sequencing thousands of virus and viral vector integration genome targets are now under investigation to uncover specific integration preferences and to define clusters of integration, termed common integration sites (CIS), that may ... ...

Abstract	With next generation sequencing thousands of virus and viral vector integration genome targets are now under investigation to uncover specific integration preferences and to define clusters of integration, termed common integration sites (CIS), that may allow to assess gene therapy safety or to detect disease related genomic features such as oncogenes. Here, we addressed the challenge to: 1) define the notion of CIS on graph models, 2) demonstrate that the structure of CIS enters in the category of scale-free networks and 3) show that our network approach analyzes CIS dynamically in an integrated systems biology framework using the Retroviral Transposon Tagged Cancer Gene Database (RTCGD) as a testing dataset.
Language	English
Publishing date	2015-11-30
Publishing country	Netherlands
Document type	Journal Article
ISSN	2001-0370
ISSN	2001-0370
DOI	10.1016/j.csbj.2015.10.006
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: SMARCAL1 is a dual regulator of innate immune signaling and PD-L1 expression that promotes tumor immune evasion.

Leuzzi, Giuseppe / Vasciaveo, Alessandro / Taglialatela, Angelo / Chen, Xiao / Firestone, Tessa M / Hickman, Allison R / Mao, Wendy / Thakar, Tanay / Vaitsiankova, Alina / Huang, Jen-Wei / Cuella-Martin, Raquel / Hayward, Samuel B / Kesner, Jordan S / Ghasemzadeh, Ali / Nambiar, Tarun S / Ho, Patricia / Rialdi, Alexander / Hebrard, Maxime / Li, Yinglu /

Gao, Jinmei / Gopinath, Saarang / Adeleke, Oluwatobi A / Venters, Bryan J / Drake, Charles G / Baer, Richard / Izar, Benjamin / Guccione, Ernesto / Keogh, Michael-Christopher / Guerois, Raphael / Sun, Lu / Lu, Chao / Califano, Andrea / Ciccia, Alberto

Cell

2024 Volume 187, Issue 4, Page(s) 861–881.e32

Abstract: Genomic instability can trigger cancer-intrinsic innate immune responses that promote tumor rejection. However, cancer cells often evade these responses by overexpressing immune checkpoint regulators, such as PD-L1. Here, we identify the SNF2-family DNA ... ...

Abstract	Genomic instability can trigger cancer-intrinsic innate immune responses that promote tumor rejection. However, cancer cells often evade these responses by overexpressing immune checkpoint regulators, such as PD-L1. Here, we identify the SNF2-family DNA translocase SMARCAL1 as a factor that favors tumor immune evasion by a dual mechanism involving both the suppression of innate immune signaling and the induction of PD-L1-mediated immune checkpoint responses. Mechanistically, SMARCAL1 limits endogenous DNA damage, thereby suppressing cGAS-STING-dependent signaling during cancer cell growth. Simultaneously, it cooperates with the AP-1 family member JUN to maintain chromatin accessibility at a PD-L1 transcriptional regulatory element, thereby promoting PD-L1 expression in cancer cells. SMARCAL1 loss hinders the ability of tumor cells to induce PD-L1 in response to genomic instability, enhances anti-tumor immune responses and sensitizes tumors to immune checkpoint blockade in a mouse melanoma model. Collectively, these studies uncover SMARCAL1 as a promising target for cancer immunotherapy.
MeSH term(s)	Animals ; Mice ; B7-H1 Antigen/metabolism ; Genomic Instability ; Immunity, Innate ; Melanoma/immunology ; Melanoma/metabolism ; Tumor Escape ; DNA Helicases/metabolism
Chemical Substances	B7-H1 Antigen ; Smarcal1 protein, mouse (EC 2.7.7.-) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2024.01.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1167: 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.MG 58: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Mesenchymal subtype neuroblastomas are addicted to TGF-βR2/HMGCR-driven protein geranylgeranylation.

Stokes, Michael E / Small, Jonnell Candice / Vasciaveo, Alessandro / Shimada, Kenichi / Hirschhorn, Tal / Califano, Andrea / Stockwell, Brent R

Scientific reports

2020 Volume 10, Issue 1, Page(s) 10748

Abstract: The identification of targeted agents with high therapeutic index is a major challenge for cancer drug discovery. We found that screening chemical libraries across neuroblastoma (NBL) tumor subtypes for selectively-lethal compounds revealed metabolic ... ...

Abstract	The identification of targeted agents with high therapeutic index is a major challenge for cancer drug discovery. We found that screening chemical libraries across neuroblastoma (NBL) tumor subtypes for selectively-lethal compounds revealed metabolic dependencies that defined each subtype. Bioactive compounds were screened across cell models of mesenchymal (MESN) and MYCN-amplified (MYCNA) NBL subtypes, which revealed the mevalonate and folate biosynthetic pathways as MESN-selective dependencies. Treatment with lovastatin, a mevalonate biosynthesis inhibitor, selectively inhibited protein prenylation and induced apoptosis in MESN cells, while having little effect in MYCNA lines. Statin sensitivity was driven by HMGCR expression, the rate-limiting enzyme for cholesterol synthesis, which correlated with statin sensitivity across NBL cell lines, thus providing a drug sensitivity biomarker. Comparing expression profiles from sensitive and resistant cell lines revealed a TGFBR2 signaling axis that regulates HMGCR, defining an actionable addiction in that leads to MESN-subtype-dependent apoptotic cell death.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Fluvastatin/pharmacology ; Humans ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lipids/chemistry ; Lovastatin/pharmacology ; Methotrexate/pharmacology ; N-Myc Proto-Oncogene Protein/metabolism ; Neuroblastoma/metabolism ; Protein Prenylation ; RNA, Small Interfering/metabolism ; Receptor, Transforming Growth Factor-beta Type II/metabolism ; Signal Transduction ; Triamterene/pharmacology
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipids ; MYCN protein, human ; N-Myc Proto-Oncogene Protein ; RNA, Small Interfering ; Fluvastatin (4L066368AS) ; Lovastatin (9LHU78OQFD) ; HMGCR protein, human (EC 1.1.1.-) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; Receptor, Transforming Growth Factor-beta Type II (EC 2.7.11.30) ; TGFBR2 protein, human (EC 2.7.11.30) ; Triamterene (WS821Z52LQ) ; Methotrexate (YL5FZ2Y5U1)
Language	English
Publishing date	2020-07-01
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/s41598-020-67310-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A Graph Based Framework to Model Virus Integration Sites

Raffaele Fronza / Alessandro Vasciaveo / Alfredo Benso / Manfred Schmidt

Computational and Structural Biotechnology Journal, Vol 14, Iss C, Pp 69-

2016 Volume 77

Abstract	With next generation sequencing thousands of virus and viral vector integration genome targets are now under investigation to uncover specific integration preferences and to define clusters of integration, termed common integration sites (CIS), that may allow to assess gene therapy safety or to detect disease related genomic features such as oncogenes. Here, we addressed the challenge to: 1) define the notion of CIS on graph models, 2) demonstrate that the structure of CIS enters in the category of scale-free networks and 3) show that our network approach analyzes CIS dynamically in an integrated systems biology framework using the Retroviral Transposon Tagged Cancer Gene Database (RTCGD) as a testing dataset.
Keywords	Gene therapy ; Systems biology ; Genomics ; Insertional mutagenesis ; Biotechnology ; TP248.13-248.65
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: A modular master regulator landscape controls cancer transcriptional identity.

Paull, Evan O / Aytes, Alvaro / Jones, Sunny J / Subramaniam, Prem S / Giorgi, Federico M / Douglass, Eugene F / Tagore, Somnath / Chu, Brennan / Vasciaveo, Alessandro / Zheng, Siyuan / Verhaak, Roel / Abate-Shen, Cory / Alvarez, Mariano J / Califano, Andrea

Cell

2021 Volume 184, Issue 2, Page(s) 334–351.e20

Abstract: Despite considerable efforts, the mechanisms linking genomic alterations to the transcriptional identity of cancer cells remain elusive. Integrative genomic analysis, using a network-based approach, identified 407 master regulator (MR) proteins ... ...

Abstract	Despite considerable efforts, the mechanisms linking genomic alterations to the transcriptional identity of cancer cells remain elusive. Integrative genomic analysis, using a network-based approach, identified 407 master regulator (MR) proteins responsible for canalizing the genetics of individual samples from 20 cohorts in The Cancer Genome Atlas (TCGA) into 112 transcriptionally distinct tumor subtypes. MR proteins could be further organized into 24 pan-cancer, master regulator block modules (MRBs), each regulating key cancer hallmarks and predictive of patient outcome in multiple cohorts. Of all somatic alterations detected in each individual sample, >50% were predicted to induce aberrant MR activity, yielding insight into mechanisms linking tumor genetics and transcriptional identity and establishing non-oncogene dependencies. Genetic and pharmacological validation assays confirmed the predicted effect of upstream mutations and MR activity on downstream cellular identity and phenotype. Thus, co-analysis of mutational and gene expression profiles identified elusive subtypes and provided testable hypothesis for mechanisms mediating the effect of genetic alterations.
MeSH term(s)	Adenocarcinoma/genetics ; Animals ; Cell Line, Tumor ; Colonic Neoplasms/genetics ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genome, Human ; HEK293 Cells ; Humans ; Mice, Nude ; Mutation/genetics ; Neoplasms/genetics ; Reproducibility of Results ; Transcription, Genetic ; Mice
Language	English
Publishing date	2021-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2020.11.045
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1167: 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.MG 58: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Measuring risk culture in banks

Arnaboldi, Fabio / Carretta, Alessandro / Schwizer, Paola / Vasciaveo, Caterina

The Italian banks : which will be the "new normal"? : industrial, institutional and behavioural economics , p. 325-344

how can behavioural auditing make the impossible possible

2016 , Page(s) 325–344

Author's details	Fabio Arnaboldi, Alessandro Carretta, Paola Schwizer and Caterina Vasciaveo
Keywords	Bankrisiko ; Unternehmenskultur ; Risikomanagement ; Italien
Language	English
Publisher	Edibank
Publishing place	Roma
Document type	Article
ISBN	978-88-449-1106-5 ; 88-449-1106-X
Database	ECONomics Information System

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED