Phenotype
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Fish
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Conditions
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Figures
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heart edematous, abnormal
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WT + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. S2
from Rydeen et al., 2014
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hindbrain edematous, abnormal
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WT + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. S2
from Rydeen et al., 2014
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whole organism mmp9 expression increased amount, abnormal
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WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 5
from Rydeen et al., 2016
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whole organism fgf8a expression decreased amount, abnormal
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WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 4
from Rydeen et al., 2016
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heart fgf8a expression decreased amount, abnormal
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WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 4
from Rydeen et al., 2016
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heart mmp9 expression increased amount, abnormal
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WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 5
from Rydeen et al., 2016
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hindbrain edematous, abnormal
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WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. S2
from Rydeen et al., 2014
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atrium has fewer parts of type cardiac muscle cell, abnormal
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WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 2
from Rydeen et al., 2014
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heart edematous, abnormal
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WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. S2
from Rydeen et al., 2014
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midbrain hindbrain boundary absent, abnormal
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WT + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1
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standard conditions
|
Fig. 5 ,
Fig. 6
from D'Aniello et al., 2013
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caudal fin shortened, abnormal
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WT + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1
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standard conditions
|
Fig. 5
from D'Aniello et al., 2013
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ventricular myocardium cardiac muscle cell mislocalised, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
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cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
|
Fig. 5
from Rydeen et al., 2016
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cardiac ventricle has number of cardiac muscle cell, ameliorated
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE
|
Fig. 5
from Rydeen et al., 2016
|
whole organism myl7 expression decreased amount, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 1
from Rydeen et al., 2016
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cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
control
|
Fig. 1 ,
Fig. 5
from Rydeen et al., 2016
|
cardiac ventricle decreased size, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
|
Fig. 1
from Rydeen et al., 2016
|
cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac muscle cell external to heart, abnormal
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f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac ventricle cardiac ventricle morphogenesis process quality, ameliorated
|
f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE
|
Fig. 5
from Rydeen et al., 2016
|
whole organism myh7 expression decreased amount, abnormal
|
f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
|
Fig. 1
from Rydeen et al., 2016
|
cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal
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f2Tg + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1
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standard conditions
|
Fig. 5
from D'Aniello et al., 2013
|
heart has fewer parts of type cardiac muscle cell, abnormal
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f2Tg + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1
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standard conditions
|
Fig. 5
from D'Aniello et al., 2013
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presumptive bulbus arteriosus ripply3 expression increased amount, abnormal
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fb7Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1
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standard conditions
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Fig 7
from Song et al., 2019
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cell migration involved in heart formation process quality, abnormal
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fb7Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 2
from Rydeen et al., 2016
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cardiac ventricle cell migration involved in heart formation decreased process quality, abnormal
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fb9Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 2
from Rydeen et al., 2016
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aortic arch has extra parts of type blood vessel endothelial cell, abnormal
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fb9Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 2
from Rydeen et al., 2016
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bulbus arteriosus outflow tract morphogenesis decreased process quality, abnormal
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sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
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bulbus arteriosus outflow tract morphogenesis process quality, ameliorated
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sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE
|
Fig. 5
from Rydeen et al., 2016
|
cardiac muscle cell external to heart, abnormal
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sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 1
from Rydeen et al., 2016
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cardiac muscle cell mislocalised, abnormal
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sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 1
from Rydeen et al., 2016
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bulbus arteriosus outflow tract morphogenesis decreased process quality, abnormal
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sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 1 ,
Fig. 5
from Rydeen et al., 2016
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ventricular myocardium cardiac muscle cell mislocalised, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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cardiac ventricle cardiac muscle cell circular, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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ventricular myocardium cell-cell junction ab1-ctnnb labeling spatial pattern, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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ventricular myocardium bicellular tight junction ab1-tjp1 labeling spatial pattern, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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cardiac ventricle establishment of cell polarity decreased process quality, abnormal
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twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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endocardium has fewer parts of type endothelial cell, abnormal
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ubs1Tg + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 7
from Rydeen et al., 2014
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cranial vasculature has fewer parts of type endothelial cell, abnormal
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ubs1Tg + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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standard conditions
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Fig. 7
from Rydeen et al., 2014
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ventricular myocardium increased distance ventricular endocardium, abnormal
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ci5Tg; twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal
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ci5Tg; twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 3
from Rydeen et al., 2016
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aortic arch 4 has extra parts of type blood vessel endothelial cell, abnormal
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fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 2
from Rydeen et al., 2016
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cardiac ventricle cell migration involved in heart formation decreased process quality, abnormal
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fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 2
from Rydeen et al., 2016
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aortic arch 3 has extra parts of type blood vessel endothelial cell, abnormal
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fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
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control
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Fig. 2
from Rydeen et al., 2016
|
ventricular myocardium cardiac muscle cell mislocalised, abnormal
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f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal
|
f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac ventricle has number of cardiac muscle cell, ameliorated
|
f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac muscle cell external to heart, abnormal
|
f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal
|
f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|
bulbus arteriosus outflow tract morphogenesis process quality, ameliorated
|
pd3Tg; sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1
|
heat shock
|
Fig. 4
from Rydeen et al., 2016
|