Images |
Sources |
Experiment + Assay |
Phenotypes |
Human Diseases |
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Fig. 2 K-R
Kreis J et al. (2022)
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Xla Wt + rab7a MO
NF17 (in situ hybridization)
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Sup. Fig. 3 G I
Maerker M et al. (2021)
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Xla Wt + bicc1 MO
NF16 (in situ hybridization)
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Sup Fig. 3 G I
Maerker M et al. (2021)
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Xla Wt + bicc1 MO
NF16 (in situ hybridization)
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Fig. 3 D E
Maerker M et al. (2021)
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Xla Wt + bicc1 MO
NF20 (in situ hybridization)
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Fig. 4 D E
Maerker M et al. (2021)
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Xla Wt + bicc1 MO
NF20 (in situ hybridization)
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Sup. Fig. 4 A B
Maerker M et al. (2021)
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Xla Wt + gdf3 MO
NF20 (in situ hybridization)
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Fig.1.S1.D
Mukherjee S et al. (2020)
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Xtr Wt + sox17a MO + sox17b.1/b.2 MO
NF10.5 (in situ hybridization)
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Fig. 2 C
Sempou E et al. (2018)
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Xtr Wt + fgfr4 CRISPR
NF17 (in situ hybridization)
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congenital heart disease
visceral heterotaxy
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Fig. 2 D
Sempou E et al. (2018)
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Xtr Wt + fgfr4 CRISPR
NF19 (in situ hybridization)
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visceral heterotaxy
congenital heart disease
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Fig 10 E^1
Hooker LN et al. (2017)
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Xla Wt + pitx3 MO
NF28 (in situ hybridization)
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