Orai1 and Stim1 regulate normal and hypertrophic growth in cardiomyocytes
Cardiac hypertrophy is an independent risk for heart failure (HF) and sudden death. Deciphering signalling pathways dependent on extracellular calcium (Ca2+) influx that control normal and pathological cardiac growth may enable identification of novel therapeutic targets. The objective of the presen...
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| Hauptverfasser: | , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
6 February 2010
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| In: |
Journal of molecular and cellular cardiology
Year: 2010, Jahrgang: 48, Heft: 6, Pages: 1329-1334 |
| ISSN: | 1095-8584 |
| DOI: | 10.1016/j.yjmcc.2010.01.020 |
| Online-Zugang: | Resolving-System, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.yjmcc.2010.01.020 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0022282810000337 
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| Verfasserangaben: | Mirko Voelkers, Mareen Salz, Nicole Herzog, Derk Frank, Nima Dolatabadi, Norbert Frey, Natalie Gude, Oliver Friedrich, Walter J. Koch, Hugo A. Katus, Mark A. Sussman, Patrick Most |
MARC
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| 520 | |a Cardiac hypertrophy is an independent risk for heart failure (HF) and sudden death. Deciphering signalling pathways dependent on extracellular calcium (Ca2+) influx that control normal and pathological cardiac growth may enable identification of novel therapeutic targets. The objective of the present study is to determine the role of the Ca2+ release-activated Ca2+ (CRAC) channel Orai1 and stromal interaction molecule 1 (Stim1) in postnatal cardiomyocyte store operated Ca2+ entry (SOCE) and impact on normal and hypertrophic postnatal cardiomyocyte growth. | ||
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