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  1. Article: ncRNAs Orchestrate Chemosensitivity Induction by Neddylation Blockades.

    Pérez-González, Andrea / Ramírez-Díaz, Ivonne / Guzmán-Linares, Josué / Sarvari, Pouya / Sarvari, Pourya / Rubio, Karla

    Cancers

    2024  Volume 16, Issue 4

    Abstract: We performed an integrative transcriptomic in silico analysis using lung adenocarcinoma A549 cells treated with the neddylation inhibitor MLN4924 and the gefitinib-resistant PC9 cell line (PC9GR). We focused on the transcriptional effects of the top ... ...

    Abstract We performed an integrative transcriptomic in silico analysis using lung adenocarcinoma A549 cells treated with the neddylation inhibitor MLN4924 and the gefitinib-resistant PC9 cell line (PC9GR). We focused on the transcriptional effects of the top differentially expressed ncRNA biotypes and their correlating stemness factors. Interestingly, MLN4924-treated cells showed a significant upregulation of mRNAs involved in carcinogenesis, cell attachment, and differentiation pathways, as well as a parallel downregulation of stemness maintenance and survival signaling pathways, an effect that was inversely observed in PC9GR cells. Moreover, we found that stemness factor expression could be contrasted by selected up-regulated ncRNAs upon MLN4924 treatment in a dose and time-independent manner. Furthermore, upregulated miRNAs and lncRNA-targeted mRNAs showed an evident enrichment of proliferation, differentiation, and apoptosis pathways, while downregulated ncRNA-targeted mRNAs were implicated in stem cell maintenance. Finally, our results proved that stemness (
    Language English
    Publishing date 2024-02-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16040825
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Advances of Epigenetic Biomarkers and Epigenome Editing for Early Diagnosis in Breast Cancer.

    Sarvari, Pourya / Sarvari, Pouya / Ramírez-Díaz, Ivonne / Mahjoubi, Frouzandeh / Rubio, Karla

    International journal of molecular sciences

    2022  Volume 23, Issue 17

    Abstract: Epigenetic modifications are known to regulate cell phenotype during cancer progression, including breast cancer. Unlike genetic alterations, changes in the epigenome are reversible, thus potentially reversed by epi-drugs. Breast cancer, the most common ... ...

    Abstract Epigenetic modifications are known to regulate cell phenotype during cancer progression, including breast cancer. Unlike genetic alterations, changes in the epigenome are reversible, thus potentially reversed by epi-drugs. Breast cancer, the most common cause of cancer death worldwide in women, encompasses multiple histopathological and molecular subtypes. Several lines of evidence demonstrated distortion of the epigenetic landscape in breast cancer. Interestingly, mammary cells isolated from breast cancer patients and cultured ex vivo maintained the tumorigenic phenotype and exhibited aberrant epigenetic modifications. Recent studies indicated that the therapeutic efficiency for breast cancer regimens has increased over time, resulting in reduced mortality. Future medical treatment for breast cancer patients, however, will likely depend upon a better understanding of epigenetic modifications. The present review aims to outline different epigenetic mechanisms including DNA methylation, histone modifications, and ncRNAs with their impact on breast cancer, as well as to discuss studies highlighting the central role of epigenetic mechanisms in breast cancer pathogenesis. We propose new research areas that may facilitate locus-specific epigenome editing as breast cancer therapeutics.
    MeSH term(s) Biomarkers ; Breast Neoplasms/diagnosis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; DNA Methylation ; Early Detection of Cancer ; Epigenesis, Genetic ; Epigenome ; Female ; Humans
    Chemical Substances Biomarkers
    Language English
    Publishing date 2022-08-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23179521
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The E3 ubiquitin-protein ligase Rbx1 regulates cardiac wall morphogenesis in zebrafish.

    Sarvari, Pourya / Rasouli, S Javad / Allanki, Srinivas / Stone, Oliver A / Sokol, Anna M / Graumann, Johannes / Stainier, Didier Y R

    Developmental biology

    2021  Volume 480, Page(s) 1–12

    Abstract: Cardiac trabeculae are muscular ridge-like structures within the ventricular wall that are crucial for cardiac function. In zebrafish, these structures first form primarily through the delamination of compact wall cardiomyocytes (CMs). Although defects ... ...

    Abstract Cardiac trabeculae are muscular ridge-like structures within the ventricular wall that are crucial for cardiac function. In zebrafish, these structures first form primarily through the delamination of compact wall cardiomyocytes (CMs). Although defects in proteasomal degradation have been associated with decreased cardiac function, whether they also affect cardiac development has not been extensively analyzed. Here we report a role during cardiac wall morphogenesis in zebrafish for the E3 ubiquitin-protein ligase Rbx1, which has been shown to regulate the degradation of key signaling molecules. Although development is largely unperturbed in zebrafish rbx1 mutant larvae, they exhibit CM multi-layering. This phenotype is not affected by blocking ErbB signaling, but fails to manifest itself in the absence of blood flow/cardiac contractility. Surprisingly, rbx1 mutants display ErbB independent Notch reporter expression in the myocardium. We generated tissue-specific rbx1 overexpression lines and found that endothelial, but not myocardial, specific rbx1 expression normalizes the cardiac wall morphogenesis phenotype. In addition, we found that pharmacological activation of Hedgehog signaling ameliorates the multi-layered myocardial wall phenotype in rbx1 mutants. Collectively, our data indicate that endocardial activity of Rbx1 is essential for cardiac wall morphogenesis.
    MeSH term(s) Animals ; Cell Proliferation/genetics ; Endocardium/metabolism ; Endothelium/metabolism ; Gene Expression/genetics ; Gene Expression Regulation/genetics ; Genes, erbB/genetics ; Heart/physiology ; Heart Ventricles/metabolism ; Hedgehog Proteins/metabolism ; Morphogenesis/genetics ; Myocardial Contraction ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Organogenesis/genetics ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances Hedgehog Proteins ; Receptors, Notch ; Zebrafish Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2021-08-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2021.07.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 508: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: The E3 ubiquitin-protein ligase Rbx1 regulates cardiac wall morphogenesis in zebrafish

    Sarvari, Pourya / Rasouli, S. Javad / Allanki, Srinivas / Stone, Oliver A. / Sokol, Anna M. / Graumann, Johannes / Stainier, Didier Y.R.

    Developmental biology. 2021 Dec., v. 480

    2021  

    Abstract: Cardiac trabeculae are muscular ridge-like structures within the ventricular wall that are crucial for cardiac function. In zebrafish, these structures first form primarily through the delamination of compact wall cardiomyocytes (CMs). Although defects ... ...

    Abstract Cardiac trabeculae are muscular ridge-like structures within the ventricular wall that are crucial for cardiac function. In zebrafish, these structures first form primarily through the delamination of compact wall cardiomyocytes (CMs). Although defects in proteasomal degradation have been associated with decreased cardiac function, whether they also affect cardiac development has not been extensively analyzed. Here we report a role during cardiac wall morphogenesis in zebrafish for the E3 ubiquitin-protein ligase Rbx1, which has been shown to regulate the degradation of key signaling molecules. Although development is largely unperturbed in zebrafish rbx1 mutant larvae, they exhibit CM multi-layering. This phenotype is not affected by blocking ErbB signaling, but fails to manifest itself in the absence of blood flow/cardiac contractility. Surprisingly, rbx1 mutants display ErbB independent Notch reporter expression in the myocardium. We generated tissue-specific rbx1 overexpression lines and found that endothelial, but not myocardial, specific rbx1 expression normalizes the cardiac wall morphogenesis phenotype. In addition, we found that pharmacological activation of Hedgehog signaling ameliorates the multi-layered myocardial wall phenotype in rbx1 mutants. Collectively, our data indicate that endocardial activity of Rbx1 is essential for cardiac wall morphogenesis.
    Keywords Danio rerio ; Erinaceidae ; blood flow ; cardiac output ; cardiomyocytes ; delamination ; morphogenesis ; mutants ; phenotype ; ubiquitin-protein ligase
    Language English
    Dates of publication 2021-12
    Size p. 1-12.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2021.07.019
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    In stock of ZB MED Bonn / Germany

    Z 76/715: Show issues

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  5. Article: Secondary dormancy in Brassica napus is correlated with enhanced BnaDOG1 transcript levels

    Née, Guillaume / Nakabayashi, Kazumi / Obeng-Hinneh, Evelyn / Sarvari, Pourya / Soppe, Wim J.J

    Seed science research. 2015 June, v. 25, no. 2

    2015  

    Abstract: Dormancy has evolved in plants to restrict germination to favourable growth seasons. Seeds from most crop plants have low dormancy levels due to selection for immediate germination during domestication. Seed dormancy is usually not completely lost and ... ...

    Abstract Dormancy has evolved in plants to restrict germination to favourable growth seasons. Seeds from most crop plants have low dormancy levels due to selection for immediate germination during domestication. Seed dormancy is usually not completely lost and low levels are required to maintain sufficient seed quality. Brassica napus cultivars show low levels of primary seed dormancy. However, B. napus seeds are prone to the induction of secondary dormancy, which can lead to the occurrence of volunteers in the field in subsequent years after cultivation. The DELAY OF GERMINATION 1 (DOG1) gene has been identified as a major dormancy gene in the model plant Arabidopsis thaliana. DOG1 is a conserved gene and has been shown to be required for seed dormancy in various monocot and dicot plant species. We have identified three B. napus genes with high homology to AtDOG1, which we named BnaA.DOG1.a, BnaC.DOG1.a and BnaC.DOG1.b. The transcripts of these genes could only be detected in seeds and showed a similar expression pattern during seed maturation as AtDOG1. In addition, the BnaDOG1 genes showed enhanced transcript levels after the induction of secondary dormancy. These results suggest a role for DOG1 in the induction of secondary dormancy in B. napus.
    Keywords Arabidopsis thaliana ; Brassica napus ; crops ; cultivars ; domestication ; genes ; germination ; Liliopsida ; seed dormancy ; seed maturation ; seed quality ; seeds ; volunteers
    Language English
    Dates of publication 2015-06
    Size p. 221-229.
    Publishing place Cambridge University Press
    Document type Article
    ZDB-ID 1102085-4
    ISSN 1475-2735 ; 0960-2585
    ISSN (online) 1475-2735
    ISSN 0960-2585
    DOI 10.1017/S0960258514000427
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    In stock of ZB MED Bonn / Germany

    Z 5472: Show issues

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  6. Article ; Online: Dimethyl fumarate and 4-octyl itaconate are anticoagulants that suppress Tissue Factor in macrophages via inhibition of Type I Interferon.

    Ryan, Tristram A J / Hooftman, Alexander / Rehill, Aisling M / Johansen, Matt D / Brien, Eóin C O' / Toller-Kawahisa, Juliana E / Wilk, Mieszko M / Day, Emily A / Weiss, Hauke J / Sarvari, Pourya / Vozza, Emilio G / Schramm, Fabian / Peace, Christian G / Zotta, Alessia / Miemczyk, Stefan / Nalkurthi, Christina / Hansbro, Nicole G / McManus, Gavin / O'Doherty, Laura /
    Gargan, Siobhan / Long, Aideen / Dunne, Jean / Cheallaigh, Clíona Ní / Conlon, Niall / Carty, Michael / Fallon, Padraic G / Mills, Kingston H G / Creagh, Emma M / Donnell, James S O' / Hertzog, Paul J / Hansbro, Philip M / McLoughlin, Rachel M / Wygrecka, Małgorzata / Preston, Roger J S / Zasłona, Zbigniew / O'Neill, Luke A J

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 3513

    Abstract: Excessive inflammation-associated coagulation is a feature of infectious diseases, occurring in such conditions as bacterial sepsis and COVID-19. It can lead to disseminated intravascular coagulation, one of the leading causes of mortality worldwide. ... ...

    Abstract Excessive inflammation-associated coagulation is a feature of infectious diseases, occurring in such conditions as bacterial sepsis and COVID-19. It can lead to disseminated intravascular coagulation, one of the leading causes of mortality worldwide. Recently, type I interferon (IFN) signaling has been shown to be required for tissue factor (TF; gene name F3) release from macrophages, a critical initiator of coagulation, providing an important mechanistic link between innate immunity and coagulation. The mechanism of release involves type I IFN-induced caspase-11 which promotes macrophage pyroptosis. Here we find that F3 is a type I IFN-stimulated gene. Furthermore, F3 induction by lipopolysaccharide (LPS) is inhibited by the anti-inflammatory agents dimethyl fumarate (DMF) and 4-octyl itaconate (4-OI). Mechanistically, inhibition of F3 by DMF and 4-OI involves suppression of Ifnb1 expression. Additionally, they block type I IFN- and caspase-11-mediated macrophage pyroptosis, and subsequent TF release. Thereby, DMF and 4-OI inhibit TF-dependent thrombin generation. In vivo, DMF and 4-OI suppress TF-dependent thrombin generation, pulmonary thromboinflammation, and lethality induced by LPS, E. coli, and S. aureus, with 4-OI additionally attenuating inflammation-associated coagulation in a model of SARS-CoV-2 infection. Our results identify the clinically approved drug DMF and the pre-clinical tool compound 4-OI as anticoagulants that inhibit TF-mediated coagulopathy via inhibition of the macrophage type I IFN-TF axis.
    MeSH term(s) Humans ; Anticoagulants ; Thromboplastin ; Dimethyl Fumarate/pharmacology ; Dimethyl Fumarate/therapeutic use ; Escherichia coli ; Inflammation ; Lipopolysaccharides ; Staphylococcus aureus ; Thrombin ; COVID-19 ; SARS-CoV-2 ; Thrombosis ; Macrophages ; Caspases ; Interferon Type I
    Chemical Substances Anticoagulants ; 4-octyl itaconate ; Thromboplastin (9035-58-9) ; Dimethyl Fumarate (FO2303MNI2) ; Lipopolysaccharides ; Thrombin (EC 3.4.21.5) ; Caspases (EC 3.4.22.-) ; Interferon Type I
    Language English
    Publishing date 2023-06-14
    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/s41467-023-39174-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Publisher Correction: Dimethyl fumarate and 4-octyl itaconate are anticoagulants that suppress Tissue Factor in macrophages via inhibition of Type I Interferon.

    Ryan, Tristram A J / Hooftman, Alexander / Rehill, Aisling M / Johansen, Matt D / O' Brien, Eóin C / Toller-Kawahisa, Juliana E / Wilk, Mieszko M / Day, Emily A / Weiss, Hauke J / Sarvari, Pourya / Vozza, Emilio G / Schramm, Fabian / Peace, Christian G / Zotta, Alessia / Miemczyk, Stefan / Nalkurthi, Christina / Hansbro, Nicole G / McManus, Gavin / O'Doherty, Laura /
    Gargan, Siobhan / Long, Aideen / Dunne, Jean / Cheallaigh, Clíona Ní / Conlon, Niall / Carty, Michael / Fallon, Padraic G / Mills, Kingston H G / Creagh, Emma M / O' Donnell, James S / Hertzog, Paul J / Hansbro, Philip M / McLoughlin, Rachel M / Wygrecka, Małgorzata / Preston, Roger J S / Zasłona, Zbigniew / O'Neill, Luke A J

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 4374

    Language English
    Publishing date 2023-07-20
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-40034-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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