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  1. Book ; Online ; Thesis: Post-transcriptional and translational mechanisms of cardiac growth

    Riechert, Eva [Verfasser] / Völkers, Mirko [Akademischer Betreuer]

    2021  

    Author's details Eva Riechert ; Betreuer: Mirko Völkers
    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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  2. Article: Corrigendum: A Multi-Network Comparative Analysis of Transcriptome and Translatome Identifies Novel Hub Genes in Cardiac Remodeling.

    Boileau, Etienne / Doroudgar, Shirin / Riechert, Eva / Jürgensen, Lonny / Ho, Thanh Cao / Katus, Hugo A / Völkers, Mirko / Dieterich, Christoph

    Frontiers in genetics

    2021  Volume 12, Page(s) 706542

    Abstract: This corrects the article DOI: 10.3389/fgene.2020.583124.]. ...

    Abstract [This corrects the article DOI: 10.3389/fgene.2020.583124.].
    Language English
    Publishing date 2021-06-17
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2021.706542
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: A Multi-Network Comparative Analysis of Transcriptome and Translatome Identifies Novel Hub Genes in Cardiac Remodeling.

    Boileau, Etienne / Doroudgar, Shirin / Riechert, Eva / Jürgensen, Lonny / Ho, Thanh Cao / Katus, Hugo A / Völkers, Mirko / Dieterich, Christoph

    Frontiers in genetics

    2020  Volume 11, Page(s) 583124

    Abstract: Our understanding of the transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on reductionist hypotheses. Here, we profiled the translatomes of 15 mouse hearts to provide a molecular blueprint of altered ... ...

    Abstract Our understanding of the transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on reductionist hypotheses. Here, we profiled the translatomes of 15 mouse hearts to provide a molecular blueprint of altered gene networks in early cardiac remodeling. Using co-expression analysis, we showed how sub-networks are orchestrated into functional modules associated with pathological phenotypes. We discovered unappreciated hub genes, many undocumented for their role in cardiac hypertrophy, and genes in the transcriptional network that were rewired in the translational network, and associated with semantically different subsets of enriched functional terms, such as
    Language English
    Publishing date 2020-11-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2020.583124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.

    Froese, Natali / Cordero, Julio / Abouissa, Aya / Trogisch, Felix A / Grein, Steve / Szaroszyk, Malgorzata / Wang, Yong / Gigina, Anna / Korf-Klingebiel, Mortimer / Bosnjak, Berislav / Davenport, Colin F / Wiehlmann, Lutz / Geffers, Robert / Riechert, Eva / Jürgensen, Lonny / Boileau, Etienne / Lin, Yanzhu / Dieterich, Christoph / Förster, Reinhold /
    Bauersachs, Johann / Ola, Roxana / Dobreva, Gergana / Völkers, Mirko / Heineke, Joerg

    iScience

    2022  Volume 25, Issue 3, Page(s) 103965

    Abstract: To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse ... ...

    Abstract To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse aortic constriction (TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication. Cardiomyocytes after TAC exerted an early and sustained upregulation of inflammatory and matrix genes and a concomitant suppression of metabolic and ion channel genes. Fibroblasts, in contrast, showed transient early upregulation of inflammatory and matrix genes and downregulation of angiogenesis genes, but sustained induction of cell cycle and ion channel genes during TAC. Endothelial cells transiently induced cell cycle and extracellular matrix genes early after TAC, but exerted a long-lasting upregulation of inflammatory genes. As we found that matrix production by multiple cell types triggers pathological cellular responses, it might serve as a future therapeutic target.
    Language English
    Publishing date 2022-02-23
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.103965
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Saraf-dependent activation of mTORC1 regulates cardiac growth.

    Sanlialp, Ayse / Schumacher, Dagmar / Kiper, Leon / Varma, Eshita / Riechert, Eva / Ho, Thanh Cao / Hofmann, Christoph / Kmietczyk, Vivien / Zimmermann, Frank / Dlugosz, Sascha / Wirth, Angela / Gorska, Agnieszka A / Burghaus, Jana / Camacho Londoño, Juan E / Katus, Hugo A / Doroudgar, Shirin / Freichel, Marc / Völkers, Mirko

    Journal of molecular and cellular cardiology

    2020  Volume 141, Page(s) 30–42

    Abstract: Pathological cardiac hypertrophy is an independent risk for heart failure (HF) and sudden death. Deciphering signaling pathways regulating intracellular ... ...

    Abstract Pathological cardiac hypertrophy is an independent risk for heart failure (HF) and sudden death. Deciphering signaling pathways regulating intracellular Ca
    MeSH term(s) Amino Acid Sequence ; Animals ; Animals, Newborn ; Base Sequence ; Calcium Signaling ; Calcium-Binding Proteins/chemistry ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Cell Proliferation ; Cell Size ; Electrocardiography ; Gene Knockdown Techniques ; Heart/growth & development ; Heart Function Tests ; Homeostasis ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/metabolism ; Rats
    Chemical Substances Calcium-Binding Proteins ; Saraf protein, mouse ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2020-03-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2020.03.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 426: 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)

    Order via subito

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  6. Book: Technologietransfer

    Riechert, Eva Christa

    rechtliche Aspekte der Unternehmenskooperation und -ausgründung unter Beteiligung außeruniversitärer Forschungseinrichtungen ; am Beispiel des Deutschen Zentrums für Luft- und Raumfahrt e.V

    (Management in Wissenschaft und Forschung ; 1)

    2000  

    Institution Deutsches Zentrum für Luft- und Raumfahrt
    Author's details von Eva Christa Riechert
    Series title Management in Wissenschaft und Forschung ; 1
    Keywords Cooperation/Research ; Joint ventures ; Science and state ; Technology transfer/Law and legislation ; Forschungskooperation ; Technologietransfer ; Recht
    Language German
    Size 259 S, 23 cm
    Publisher Lemmens
    Publishing place Bonn
    Document type Book
    Note Literaturverz. S. 241 - 253
    ISBN 3932306341 ; 9783932306341
    Database Former special subject collection: coastal and deep sea fishing

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    Inter-library loan at ZB MED

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  7. Book: Technologietransfer

    Riechert, Eva Christa

    rechtliche Aspekte der Unternehmenskooperation und -ausgründung unter Beteiligung außeruniversitärer Forschungseinrichtungen ; am Beispiel des Deutschen Zentrums für Luft- und Raumfahrt e.V

    (Management in Wissenschaft und Forschung ; 1)

    2000  

    Institution Deutsches Zentrum für Luft- und Raumfahrt
    Author's details von Eva Christa Riechert
    Series title Management in Wissenschaft und Forschung ; 1
    Keywords Cooperation/Research ; Joint ventures ; Science and state ; Technology transfer/Law and legislation ; Forschungskooperation ; Technologietransfer ; Recht
    Language German
    Size 259 S, 23 cm
    Document type Book
    Note Literaturverz. S. 241 - 253
    ISBN 3932306341 ; 9783932306341
    Database Leibniz Institute of Plant Genetics and Crop Plant Research

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  8. Article ; Online: Identification of dynamic RNA-binding proteins uncovers a Cpeb4-controlled regulatory cascade during pathological cell growth of cardiomyocytes.

    Riechert, Eva / Kmietczyk, Vivien / Stein, Frank / Schwarzl, Thomas / Sekaran, Thileepan / Jürgensen, Lonny / Kamuf-Schenk, Verena / Varma, Eshita / Hofmann, Christoph / Rettel, Mandy / Gür, Kira / Ölschläger, Julie / Kühl, Friederike / Martin, Judit / Ramirez-Pedraza, Marta / Fernandez, Mercedes / Doroudgar, Shirin / Méndez, Raúl / Katus, Hugo A /
    Hentze, Matthias W / Völkers, Mirko

    Cell reports

    2021  Volume 35, Issue 6, Page(s) 109100

    Abstract: RNA-binding proteins (RBPs) control critical aspects of cardiomyocyte function, but the repertoire of active RBPs in cardiomyocytes during the growth response is largely unknown. We define RBPs in healthy and diseased cardiomyocytes at a system-wide ... ...

    Abstract RNA-binding proteins (RBPs) control critical aspects of cardiomyocyte function, but the repertoire of active RBPs in cardiomyocytes during the growth response is largely unknown. We define RBPs in healthy and diseased cardiomyocytes at a system-wide level by RNA interactome capture. This identifies 67 cardiomyocyte-specific RBPs, including several contractile proteins. Furthermore, we identify the cytoplasmic polyadenylation element-binding protein 4 (Cpeb4) as a dynamic RBP, regulating cardiac growth both in vitro and in vivo. We identify mRNAs bound to and regulated by Cpeb4 in cardiomyocytes. Cpeb4 regulates cardiac remodeling by differential expression of transcription factors. Among Cpeb4 target mRNAs, two zinc finger transcription factors (Zeb1 and Zbtb20) are discovered. We show that Cpeb4 regulates the expression of these mRNAs and that Cpeb4 depletion increases their expression. Thus, Cpeb4 emerges as a critical regulator of cardiomyocyte function by differential binding to specific mRNAs in response to pathological growth stimulation.
    MeSH term(s) Animals ; Cell Proliferation ; Humans ; Mice ; Myocytes, Cardiac/metabolism ; RNA-Binding Proteins/metabolism
    Chemical Substances Cpeb4 protein, mouse ; RNA-Binding Proteins
    Language English
    Publishing date 2021-05-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.109100
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Muscle-specific Cand2 is translationally upregulated by mTORC1 and promotes adverse cardiac remodeling.

    Górska, Agnieszka A / Sandmann, Clara / Riechert, Eva / Hofmann, Christoph / Malovrh, Ellen / Varma, Eshita / Kmietczyk, Vivien / Ölschläger, Julie / Jürgensen, Lonny / Kamuf-Schenk, Verena / Stroh, Claudia / Furkel, Jennifer / Konstandin, Mathias H / Sticht, Carsten / Boileau, Etienne / Dieterich, Christoph / Frey, Norbert / Katus, Hugo A / Doroudgar, Shirin /
    Völkers, Mirko

    EMBO reports

    2021  Volume 22, Issue 12, Page(s) e52170

    Abstract: The mechanistic target of rapamycin (mTOR) promotes pathological remodeling in the heart by activating ribosomal biogenesis and mRNA translation. Inhibition of mTOR in cardiomyocytes is protective; however, a detailed role of mTOR in translational ... ...

    Abstract The mechanistic target of rapamycin (mTOR) promotes pathological remodeling in the heart by activating ribosomal biogenesis and mRNA translation. Inhibition of mTOR in cardiomyocytes is protective; however, a detailed role of mTOR in translational regulation of specific mRNA networks in the diseased heart is unknown. We performed cardiomyocyte genome-wide sequencing to define mTOR-dependent gene expression control at the level of mRNA translation. We identify the muscle-specific protein Cullin-associated NEDD8-dissociated protein 2 (Cand2) as a translationally upregulated gene, dependent on the activity of mTOR. Deletion of Cand2 protects the myocardium against pathological remodeling. Mechanistically, we show that Cand2 links mTOR signaling to pathological cell growth by increasing Grk5 protein expression. Our data suggest that cell-type-specific targeting of mTOR might have therapeutic value against pathological cardiac remodeling.
    MeSH term(s) Humans ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Muscle Proteins ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Signal Transduction ; Transcription Factors ; Up-Regulation ; Ventricular Remodeling/genetics
    Chemical Substances CAND2 protein, human ; Muscle Proteins ; Transcription Factors ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2021-10-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202052170
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5433: 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)
    Zs.MG 41: Show issues

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  10. Article ; Online: PRAS40 suppresses atherogenesis through inhibition of mTORC1-dependent pro-inflammatory signaling in endothelial cells.

    Zhang, Kevin Sun / Schecker, Johannes / Krull, Alexandros / Riechert, Eva / Jürgensen, Lonny / Kamuf-Schenk, Verena / Burghaus, Jana / Kiper, Leon / Cao Ho, Thanh / Wöltje, Kerstin / Stangl, Verena / Katus, Hugo A / Stangl, Karl / Völkers, Mirko / Althoff, Till F

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 16787

    Abstract: Endothelial pro-inflammatory activation plays a pivotal role in atherosclerosis, and many pro-inflammatory and atherogenic signals converge upon mechanistic target of rapamycin (mTOR). Inhibitors of mTOR complex 1 (mTORC1) reduced atherosclerosis in ... ...

    Abstract Endothelial pro-inflammatory activation plays a pivotal role in atherosclerosis, and many pro-inflammatory and atherogenic signals converge upon mechanistic target of rapamycin (mTOR). Inhibitors of mTOR complex 1 (mTORC1) reduced atherosclerosis in preclinical studies, but side effects including insulin resistance and dyslipidemia limit their clinical use in this context. Therefore, we investigated PRAS40, a cell type-specific endogenous modulator of mTORC1, as alternative target. Indeed, we previously found PRAS40 gene therapy to improve metabolic profile; however, its function in endothelial cells and its role in atherosclerosis remain unknown. Here we show that PRAS40 negatively regulates endothelial mTORC1 and pro-inflammatory signaling. Knockdown of PRAS40 in endothelial cells promoted TNFα-induced mTORC1 signaling, proliferation, upregulation of inflammatory markers and monocyte recruitment. In contrast, PRAS40-overexpression blocked mTORC1 and all measures of pro-inflammatory signaling. These effects were mimicked by pharmacological mTORC1-inhibition with torin1. In an in vivo model of atherogenic remodeling, mice with induced endothelium-specific PRAS40 deficiency showed enhanced endothelial pro-inflammatory activation as well as increased neointimal hyperplasia and atherosclerotic lesion formation. These data indicate that PRAS40 suppresses atherosclerosis via inhibition of endothelial mTORC1-mediated pro-inflammatory signaling. In conjunction with its favourable effects on metabolic homeostasis, this renders PRAS40 a potential target for the treatment of atherosclerosis.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Atherosclerosis/genetics ; Atherosclerosis/immunology ; Atherosclerosis/pathology ; Cell Proliferation ; Disease Models, Animal ; Endothelial Cells/metabolism ; Gain of Function Mutation ; Gene Knockout Techniques ; Human Umbilical Vein Endothelial Cells ; Humans ; Loss of Function Mutation ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances AKT1S1 protein, human ; Adaptor Proteins, Signal Transducing ; TNF protein, human ; Tumor Necrosis Factor-alpha ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2019-11-14
    Publishing country England
    Document type Journal Article ; 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/s41598-019-53098-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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