Sasagawa et al., 2016 - Downregulation of GSTK1 Is a Common Mechanism Underlying Hypertrophic Cardiomyopathy. Frontiers in pharmacology   7:162 Full text @ Front Pharmacol

Fig. 4 ZFIN is incorporating published figure images and captions as part of an ongoing project. Figures from some publications have not yet been curated, or are not available for display because of copyright restrictions.

EXPRESSION / LABELING:
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Fish:
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Stage: Day 5
PHENOTYPE:
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Stage: Day 5

Fig. 5

gstk1 knockout decreases the cardiac end diastolic and systolic volumes in zebrafish. (A) In vivo imaging of the hearts of control and gstk1-knockout (KO) Tg (myl7:mRFP) zebrafish at 5 dpf. Zebrafish were placed on slides on their backs, and the heart was imaged under a fluorescence microscope at 100 frames/s for 10 s. Image stack projections and the M-mode imaging of ventricles are shown. Bar, 100 μm. (B) Quantitative analysis of the in vivo imaging of zebrafish heart. The end diastolic volume (EDV) of gstk1-KO zebrafish was significantly smaller than that of control zebrafish, whereas the end systolic volume (ESV) and ejection fraction (EF) were not significantly different. N = 13 and 7 for the control and gstk1-KO groups, respectively. *p < 0.05, ***p < 0.001 vs. control group.

PHENOTYPE:
Fish:
Knockdown Reagent:
Observed In:
Stage: Day 4
Acknowledgments:
ZFIN wishes to thank the journal Frontiers in pharmacology for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ Front Pharmacol