Sumoylation-independent activation of Calcineurin-NFAT-signaling via SUMO2 mediates cardiomyocyte hypertrophy
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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In: Scientific Reports 6:35758 (2016). DOI: 10.1038/srep35758
- Event
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Veröffentlichung
- (where)
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Würzburg
- (who)
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Universität Würzburg
- (when)
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2019
- URN
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urn:nbn:de:bvb:20-opus-167525
- Rights
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Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
25.03.2025, 1:51 PM CET
Data provider
This object is provided by:
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Bernt, Alexander
- Rangrez, Ashraf Y.
- Eden, Matthias
- Jungmann, Andreas
- Katz, Sylvia
- Rohr, Claudia
- Müller, Oliver J.
- Katus, Hugo
- Sossalla, Samuel Tobias
- Williams, Tatjana
- Ritter, Oliver
- Frank, Derk
- Frey, Norbert
- Universität Würzburg
Time of origin
- 2019
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Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies
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Calcineurin-independent NFATc1 signaling is essential for survival of Burkitt lymphoma cells
Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions
The acute phase protein alpha-2-macroglobulin induces rat ventricular cardiomyocyte hypertrophy via ERK1, 2 and PI3 kinase, akt pathways
Sumoylation-independent activation of calcineurin-NFAT-signaling via SUMO2 causes cardiomyocyte hypertrophy
Inhibition of cardiomyocyte hypertrophy by heterocyclic thiourylenes in vitro
Inhibition of Nuclear Import of Calcineurin Prevents the Development of Myocardial Hypertrophy
Three-dimensional human pluripotent stem cell-derived cardiomyocyte models for investigating cardiac hypertrophy
Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies
Altered cellular protein quality control system modulates cardiomyocyte function in volume overload-induced hypertrophy
Amlexanox and forskolin prevents isoproterenol-induced cardiomyopathy by subduing cardiomyocyte hypertrophy and maladaptive inflammatory responses
Angiotensin-(1-9) prevents cardiomyocyte hypertrophy via miR-129-3p/PKIA/PKA signaling pathway
Using iPSC-CMs to develop a new, 2D in vitro culture-based model for cardiomyocyte hypertrophy
Calcineurin-independent NFATc1 signaling is essential for survival of Burkitt lymphoma cells
Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions
The acute phase protein alpha-2-macroglobulin induces rat ventricular cardiomyocyte hypertrophy via ERK1, 2 and PI3 kinase, akt pathways
Sumoylation-independent activation of calcineurin-NFAT-signaling via SUMO2 causes cardiomyocyte hypertrophy
Inhibition of cardiomyocyte hypertrophy by heterocyclic thiourylenes in vitro
Inhibition of Nuclear Import of Calcineurin Prevents the Development of Myocardial Hypertrophy
Three-dimensional human pluripotent stem cell-derived cardiomyocyte models for investigating cardiac hypertrophy
Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies
Altered cellular protein quality control system modulates cardiomyocyte function in volume overload-induced hypertrophy
Amlexanox and forskolin prevents isoproterenol-induced cardiomyopathy by subduing cardiomyocyte hypertrophy and maladaptive inflammatory responses
Angiotensin-(1-9) prevents cardiomyocyte hypertrophy via miR-129-3p/PKIA/PKA signaling pathway
Using iPSC-CMs to develop a new, 2D in vitro culture-based model for cardiomyocyte hypertrophy
Calcineurin-independent NFATc1 signaling is essential for survival of Burkitt lymphoma cells
Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions