Phenotype
|
Fish
|
Conditions
|
Figures
|
cell death increased occurrence, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Fig. 1
from Kaiser et al., 2012
|
whole organism necrotic, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Figure 4.
from Pollock et al., 2021
|
whole organism morphology, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Figure 4.
from Pollock et al., 2021
|
central nervous system development disrupted, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Fig. 1
from Kaiser et al., 2012
|
cranium edematous, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Fig. 1
from Kaiser et al., 2012
|
central nervous system morphology, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Fig. 1
from Kaiser et al., 2012
|
whole organism decreased size, abnormal
|
AB + MO1-prnpb
|
standard conditions
|
Fig. 1
from Kaiser et al., 2012
|
DEL increased accumulation DEL cytoplasmic vesicle, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 6
from Málaga-Trillo et al., 2009
|
EVL adherens junction disorganized, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 8
from Málaga-Trillo et al., 2009
|
DEL cell circular, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 4
from Málaga-Trillo et al., 2009
|
mediolateral intercalation disrupted, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 7
from Málaga-Trillo et al., 2009
|
adherens junction maintenance disrupted, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 8
from Málaga-Trillo et al., 2009
|
cell-cell adhesion disrupted, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 4
from Málaga-Trillo et al., 2009
|
calcium-independent cell-cell adhesion via plasma membrane cell-adhesion molecules disrupted, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 5
from Málaga-Trillo et al., 2009
|
DEL adherens junction disorganized, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 6
from Málaga-Trillo et al., 2009
|
DEL cell disorganized, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 4
from Málaga-Trillo et al., 2009
|
gastrulation arrested, abnormal
|
WT + MO1-prnpb
|
standard conditions
|
Fig. 2
from Málaga-Trillo et al., 2009
|
whole organism ab2-ctnnb labeling amount, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal
|
Fig. 1 ,
Fig. 4
from Sempou et al., 2016
|
DEL intracellular anatomical structure ab2-ctnnb labeling mislocalised, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
control
|
Fig. 1 ,
Fig. 3
from Sempou et al., 2016
|
epiboly arrested, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: dynasore
|
Fig. 1
from Sempou et al., 2016
|
epiboly arrested, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
standard conditions
|
Fig. 1 ,
Fig. 2
from Sempou et al., 2016
|
blastoderm thickness, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: ammonium chloride
|
Fig. 1
from Sempou et al., 2016
|
whole organism ab2-ctnnb labeling amount, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: chloroquine
|
Fig. 1 ,
Fig. 4
from Sempou et al., 2016
|
epiboly arrested, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: ammonium chloride
|
Fig. 1
from Sempou et al., 2016
|
endocytosis increased occurrence, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
control
|
Fig. 1
from Sempou et al., 2016
|
whole organism ab2-ctnnb labeling decreased amount, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
control
|
Fig. 1 ,
Fig. 4
from Sempou et al., 2016
|
epiboly arrested, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: chloroquine
|
Fig. 1
from Sempou et al., 2016
|
DEL cytosol ab2-ctnnb labeling mislocalised, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
control
|
Fig. 1 ,
Fig. 3
from Sempou et al., 2016
|
blastoderm thickness, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal
|
Fig. 1
from Sempou et al., 2016
|
blastoderm thickness, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: chloroquine
|
Fig. 1
from Sempou et al., 2016
|
DEL cell surface ab2-ctnnb labeling position, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: dynasore
|
Fig. 1
from Sempou et al., 2016
|
blastoderm thickness, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: dynasore
|
Fig. 1
from Sempou et al., 2016
|
blastoderm increased thickness, abnormal
|
WT + MO1-prnpb + MO2-prnpb
|
control
|
Fig. 1
from Sempou et al., 2016
|
epiboly arrested, ameliorated
|
WT + MO1-prnpb + MO2-prnpb
|
chemical treatment: N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal
|
Fig. 1
from Sempou et al., 2016
|
cell death increased occurrence, abnormal
|
AB + MO1-prnpb + MO2-appa
|
standard conditions
|
Fig. 3
from Kaiser et al., 2012
|
central nervous system malformed, abnormal
|
AB + MO1-prnpb + MO2-appa
|
standard conditions
|
Fig. 3
from Kaiser et al., 2012
|
peripheral nervous system malformed, abnormal
|
AB + MO1-prnpb + MO2-appa
|
standard conditions
|
Fig. 3
from Kaiser et al., 2012
|
activation of cysteine-type endopeptidase activity involved in apoptotic process increased occurrence, abnormal
|
AB + MO1-prnpb + MO2-appa
|
standard conditions
|
Fig. 4
from Kaiser et al., 2012
|
whole organism cell decreased adhesivity, abnormal
|
AB + MO1-prnpb + MO2-appa
|
standard conditions
|
Fig. 5
from Kaiser et al., 2012
|