Phenotype
|
Fish
|
Conditions
|
Figures
|
habenula axon misrouted, abnormal
|
AB + MO2-nrp1a
|
standard conditions
|
Fig. 3
from Kuan et al., 2007
|
axon guidance disrupted, abnormal
|
AB + MO2-nrp1a
|
standard conditions
|
Fig. 3
from Kuan et al., 2007
|
CaP motoneuron axon decreased length, abnormal
|
AB + MO2-nrp1a
|
standard conditions
|
text only
from Cantu et al., 2013
|
interpeduncular nucleus tegmentum structure, abnormal
|
AB + MO2-nrp1a
|
standard conditions
|
Fig. 3
from Kuan et al., 2007
|
postoptic commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
postoptic commissure axon decreased distribution, abnormal
|
RW + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon decreased distribution, abnormal
|
RW + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
axon extension process quality, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 9
from Chitramuthu et al., 2010
|
whole organism curved ventral, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 6
from Hillman et al., 2011
|
somite U-shaped, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 6
from Hillman et al., 2011
|
motor neuron axon branchiness, abnormal
|
WT + MO2-nrp1a
|
control
|
Fig. 3
from Balastik et al., 2015
|
motor neuron axon truncated, abnormal
|
WT + MO2-nrp1a
|
control
|
Fig. 3
from Balastik et al., 2015
|
CaP motoneuron axon branched, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 9
from Chitramuthu et al., 2010
|
motor neuron axon guidance process quality, abnormal
|
WT + MO2-nrp1a
|
control
|
Fig. 3
from Balastik et al., 2015
|
retinal neural layer axon guidance disrupted, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Liu et al., 2018
|
retinal neural layer axon mislocalised, abnormal
|
WT + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Liu et al., 2018
|
brain vasculature development process quality, abnormal
|
WT + MO2-nrp1a + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
brain vasculature broken, abnormal
|
WT + MO2-nrp1a + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
brain hemorrhagic, abnormal
|
WT + MO2-nrp1a + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
common cardinal vein actin filament bundle organization decreased process quality, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 7 ,
Fig. 8
from Hamm et al., 2016
|
common cardinal vein actin filament bundle disoriented, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 7 ,
Fig. 8
from Hamm et al., 2016
|
common cardinal vein blood vessel endothelial cell structure, cavities, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 8
from Hamm et al., 2016
|
common cardinal vein blood vessel endothelium patchy, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 7
from Hamm et al., 2016
|
venous blood vessel morphogenesis decreased process quality, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 7 ,
Fig. 8
from Hamm et al., 2016
|
common cardinal vein cell-cell junction decreased length, abnormal
|
mu240Tg + MO2-nrp1a
|
standard conditions
|
Fig. 7 ,
Fig. 8
from Hamm et al., 2016
|
retina axon ipsilateral to optic tectum, abnormal
|
AB + MO1-plxnb3 + MO2-nrp1a
|
control
|
FIGURE 3
from Liu et al., 2024
|
axon guidance disrupted, abnormal
|
AB + MO1-sema3d + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Kuan et al., 2007
|
interpeduncular nucleus tegmentum structure, abnormal
|
AB + MO1-sema3d + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Kuan et al., 2007
|
habenula axon misrouted, abnormal
|
AB + MO1-sema3d + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Kuan et al., 2007
|
postoptic commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-dpysl3 + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon spatial pattern, exacerbated
|
RW + MO2-dpysl3 + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-dpysl3 + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
postoptic commissure axon spatial pattern, exacerbated
|
RW + MO2-dpysl3 + MO2-nrp1a
|
control
|
Fig. 6
from Guo et al., 2022
|
postoptic commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-nrp1a + MO3-dpysl2b
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon spatial pattern, exacerbated
|
RW + MO2-nrp1a + MO3-dpysl2b
|
control
|
Fig. 6
from Guo et al., 2022
|
anterior commissure axon ab1-tuba labeling spatial pattern, abnormal
|
RW + MO2-nrp1a + MO3-dpysl2b
|
control
|
Fig. 6
from Guo et al., 2022
|
postoptic commissure axon spatial pattern, exacerbated
|
RW + MO2-nrp1a + MO3-dpysl2b
|
control
|
Fig. 6
from Guo et al., 2022
|
retinal neural layer axon guidance disrupted, abnormal
|
WT + MO1-dpysl3 + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Liu et al., 2018
|
retinal neural layer axon mislocalised, abnormal
|
WT + MO1-dpysl3 + MO2-nrp1a
|
standard conditions
|
Fig. 4
from Liu et al., 2018
|
motor neuron axon guidance process quality, ameliorated
|
WT + MO2-nrp1a + MO2-pin1
|
control
|
Fig. 3
from Balastik et al., 2015
|
motor neuron axon branchiness, ameliorated
|
WT + MO2-nrp1a + MO2-pin1
|
control
|
Fig. 3
from Balastik et al., 2015
|
motor neuron axon truncated, ameliorated
|
WT + MO2-nrp1a + MO2-pin1
|
control
|
Fig. 3
from Balastik et al., 2015
|
brain hemorrhagic, abnormal
|
WT + MO2-nrp1a + MO3-itgb8 + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
brain vasculature broken, abnormal
|
WT + MO2-nrp1a + MO3-itgb8 + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
brain vasculature development process quality, abnormal
|
WT + MO2-nrp1a + MO3-itgb8 + MO4-tp53
|
control
|
Fig. 4
from Hirota et al., 2015
|
blood circulation absent, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
angiogenesis process quality, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
intersegmental vessel angiogenesis process quality, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
intersegmental vessel malformed, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
dorsal longitudinal anastomotic vessel aplastic, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
dorsal longitudinal anastomotic vessel malformed, abnormal
|
zf565Tg + MO2-nrp1a + MO4-nrp1b
|
standard conditions
|
Fig. 3
from Delcourt et al., 2015
|
dorsomedial optic tract morphology, ameliorated
|
cu2Tg + MO1-rbpms2a + MO1-rbpms2b + MO2-nrp1a
|
control
|
Fig. 4
from Hörnberg et al., 2016
|
dorsomedial optic tract axon mislocalised, ameliorated
|
cu2Tg + MO1-rbpms2a + MO1-rbpms2b + MO2-nrp1a
|
control
|
Fig. 4
from Hörnberg et al., 2016
|