Phenotype
|
Fish
|
Conditions
|
Figures
|
whole organism ins expression decreased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 5
from Lou et al., 2020
|
determination of digestive tract left/right asymmetry process quality, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
pancreatic B cell decreased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Kimmel et al., 2011
|
determination of liver left/right asymmetry process quality, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
whole organism aldh7a1 expression decreased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. S6
from Lou et al., 2020
|
acinar cell decreased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
endocrine pancreas development disrupted, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Kimmel et al., 2011
|
exocrine pancreas hypoplastic, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
endocrine pancreas decreased size, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
whole organism aldh1l2 expression increased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. S6
from Lou et al., 2020
|
digestive system positional polarity, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
posterior pancreatic bud decreased size, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Kimmel et al., 2011
|
whole organism glucose increased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 7
from Lou et al., 2020
Fig. 9
from Schmöhl et al., 2019
|
endocrine pancreas decreased functionality, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
determination of pancreatic left/right asymmetry process quality, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 1
from Yee et al., 2001
|
whole organism aldh1a3 expression increased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. S6
from Lou et al., 2020
|
whole organism aldh3a1 expression increased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. S6
from Lou et al., 2020
|
whole organism aldh3b1 expression increased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. S6
from Lou et al., 2020
|
whole organism ADP decreased amount, abnormal
|
WT + MO1-pdx1
|
standard conditions
|
Fig. 7
from Lou et al., 2020
|
pronephric tubule length, ameliorated
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Meclizine
|
Fig. 4
from Wiggenhauser et al., 2022
|
pronephric tubule decreased length, abnormal
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Z-Val-Ala-Asp(OMe)-CH2F
|
Fig. 6
from Sharma et al., 2016
|
pronephric glomerulus increased length, abnormal
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Meclizine
|
Fig. 4
from Wiggenhauser et al., 2022
|
pronephros morphogenesis decreased process quality, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3 ,
Fig. 6
from Sharma et al., 2016
|
pronephric glomerulus increased size, abnormal
|
li1Tg + MO1-pdx1
|
control
|
Fig. 7
from She et al., 2017
|
pronephros renal filtration decreased occurrence, abnormal
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Z-Val-Ala-Asp(OMe)-CH2F
|
Fig. 6
from Sharma et al., 2016
|
pronephric podocyte podocyte foot dystrophic, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 5
from Sharma et al., 2016
|
pronephric glomerulus increased width, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3 ,
Fig. 6
from Sharma et al., 2016
|
pronephros renal filtration decreased occurrence, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 7
from She et al., 2017
Fig. 6
from Sharma et al., 2016
|
pronephric glomerulus length, ameliorated
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: thiosulfate
|
Fig. 2
from Al-Dahmani et al., 2022
|
pronephric podocyte podocyte development decreased process quality, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 5
from Sharma et al., 2016
|
pronephric tubule decreased length, abnormal
|
li1Tg + MO1-pdx1
|
control
|
Fig. 2
from Al-Dahmani et al., 2022
Fig. 4
from Wiggenhauser et al., 2022
Fig. 7
from She et al., 2017
Fig. 3 ,
Fig. 6
from Sharma et al., 2016
|
pronephric glomerulus increased width, abnormal
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Z-Val-Ala-Asp(OMe)-CH2F
|
Fig. 6
from Sharma et al., 2016
|
pronephric tubule length, ameliorated
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: thiosulfate
|
Fig. 2
from Al-Dahmani et al., 2022
|
pronephric glomerulus increased length, abnormal
|
li1Tg + MO1-pdx1
|
control
|
Fig. 2
from Al-Dahmani et al., 2022
Fig. 4
from Wiggenhauser et al., 2022
|
pronephros morphogenesis decreased process quality, abnormal
|
li1Tg + MO1-pdx1
|
chemical treatment by environment: Z-Val-Ala-Asp(OMe)-CH2F
|
Fig. 6
from Sharma et al., 2016
|
pronephric podocyte podocyte foot malformed, abnormal
|
li1Tg + MO1-pdx1
|
standard conditions
|
Fig. 5
from Sharma et al., 2016
|
pancreas decreased size, abnormal
|
ml2Tg + MO1-pdx1
|
standard conditions
|
Fig. 5
from Lou et al., 2020
|
endocrine pancreas EGFP expression decreased distribution, abnormal
|
nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. S10
from O'Hare et al., 2016
|
endocrine pancreas decreased size, abnormal
|
nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. S10
from O'Hare et al., 2016
|
enteroendocrine cell differentiation disrupted, abnormal
|
nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. S10
from O'Hare et al., 2016
|
endocrine pancreas development disrupted, abnormal
|
nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. S10
from O'Hare et al., 2016
|
ocular blood vessel has extra parts of type hyaloid vessel nucleus, abnormal
|
ubs1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Wiggenhauser et al., 2020
|
intersegmental vessel increased branchiness, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Lou et al., 2020
|
intersegmental vessel morphology, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Lou et al., 2020
|
pronephric tubule decreased length, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
renal glomerulus increased length, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
ocular blood vessel sprouting angiogenesis increased process quality, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 4
from Lou et al., 2020
|
vasculature morphology, abnormal
|
y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
intersegmental vessel morphology, abnormal
|
y1Tg + MO1-pdx1 + MO4-tp53
|
standard conditions
|
Fig. 2
from Jörgens et al., 2015
|
intersegmental vessel structure, abnormal
|
y1Tg + MO1-pdx1 + MO4-tp53
|
standard conditions
|
Fig. 2
from Jörgens et al., 2015
|
blood vessel increased branchiness, abnormal
|
y1Tg + MO1-pdx1 + MO4-tp53
|
standard conditions
|
Fig. 2
from Jörgens et al., 2015
|
blood vessel morphology, abnormal
|
y1Tg + MO1-pdx1 + MO4-tp53
|
standard conditions
|
Fig. 2
from Jörgens et al., 2015
|
endocrine pancreas hypoplastic, abnormal
|
zf5Tg + MO1-pdx1
|
standard conditions
|
Fig. 6
from Jurczyk et al., 2011
|
glucose metabolic process disrupted, abnormal
|
zf5Tg + MO1-pdx1
|
standard conditions
|
Fig. 6
from Jurczyk et al., 2011
|
glucose homeostasis disrupted, abnormal
|
jh1Tg; jh2Tg + MO1-pdx1
|
chemical treatment by environment: glucose
|
Fig. S15
from O'Hare et al., 2016
|
glucose homeostasis disrupted, abnormal
|
jh1Tg; jh2Tg + MO1-pdx1
|
control
|
Fig. S15
from O'Hare et al., 2016
|
pancreatic B cell decreased amount, abnormal
|
jh1Tg; jh2Tg + MO1-pdx1
|
standard conditions
|
Fig. 2
from O'Hare et al., 2016
|
response to glucose decreased process quality, abnormal
|
jh1Tg; jh2Tg + MO1-pdx1
|
chemical treatment by environment: glucose
|
Fig. 4
from O'Hare et al., 2016
|
pancreatic B cell decreased amount, abnormal
|
jh1Tg; jh2Tg + MO1-pdx1
|
chemical treatment by environment: glucose
|
Fig. 4
from O'Hare et al., 2016
|
pancreatic B cell decreased amount, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
endocrine pancreas decreased size, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
endocrine pancreas has fewer parts of type endodermal cell, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
endocrine pancreas development disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
type B pancreatic cell differentiation disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
type B pancreatic cell proliferation disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
whole organism ADP decreased amount, abnormal
|
aldh3a1zf3260/zf3260 + MO1-pdx1
|
standard conditions
|
Fig. 7
from Lou et al., 2020
|
whole organism ATP decreased amount, abnormal
|
aldh3a1zf3260/zf3260 + MO1-pdx1
|
standard conditions
|
Fig. 7
from Lou et al., 2020
|
whole organism glucose increased amount, exacerbated
|
aldh3a1zf3260/zf3260 + MO1-pdx1
|
standard conditions
|
Fig. 7
from Lou et al., 2020
|
whole organism glucose increased amount, abnormal
|
cndp1zf3241/zf3241 + MO1-pdx1
|
standard conditions
|
Fig. 9
from Schmöhl et al., 2019
|
whole organism glucose increased amount, abnormal
|
cndp1zf3242/zf3242 + MO1-pdx1
|
standard conditions
|
Fig. 9
from Schmöhl et al., 2019
|
whole organism glucose increased amount, abnormal
|
cndp1zf3243/zf3243 + MO1-pdx1
|
standard conditions
|
Fig. 9
from Schmöhl et al., 2019
|
pancreatic B cell absent, abnormal
|
WT + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 1
from Kimmel et al., 2011
|
endocrine pancreas development disrupted, abnormal
|
WT + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 1
from Kimmel et al., 2011
|
pancreatic B cell decreased amount, abnormal
|
jh4Tg + MO1-pdx1
|
standard conditions
|
Fig. 5
from Lou et al., 2020
|
pronephros renal filtration occurrence, ameliorated
|
li1Tg + MO1-epoa + MO1-pdx1
|
control
|
Fig. 7
from She et al., 2017
|
pronephric tubule decreased length, exacerbated
|
li1Tg + MO1-epoa + MO1-pdx1
|
control
|
Fig. 7
from She et al., 2017
|
pronephric glomerulus increased size, exacerbated
|
li1Tg + MO1-epoa + MO1-pdx1
|
control
|
Fig. 7
from She et al., 2017
|
endocrine pancreas development disrupted, abnormal
|
nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2
from Kimmel et al., 2011
|
posterior pancreatic bud elongated, abnormal
|
nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2
from Kimmel et al., 2011
|
posterior pancreatic bud cellular motility, abnormal
|
nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2
from Kimmel et al., 2011
|
ocular blood vessel sprouting angiogenesis increased process quality, exacerbated
|
aldh3a1zf3260/zf3260; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 4
from Lou et al., 2020
|
ocular blood vessel increased diameter, abnormal
|
aldh3a1zf3260/zf3260; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 4
from Lou et al., 2020
|
intersegmental vessel morphology, exacerbated
|
aldh3a1zf3260/zf3260; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Lou et al., 2020
|
intersegmental vessel increased branchiness, exacerbated
|
aldh3a1zf3260/zf3260; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 3
from Lou et al., 2020
|
vasculature morphology, abnormal
|
cndp1zf3241/zf3241; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
pronephric tubule decreased length, abnormal
|
cndp1zf3241/zf3241; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
renal glomerulus increased length, abnormal
|
cndp1zf3241/zf3241; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
vasculature morphology, abnormal
|
cndp1zf3242/zf3242; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
pronephric tubule decreased length, abnormal
|
cndp1zf3242/zf3242; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
renal glomerulus increased length, abnormal
|
cndp1zf3242/zf3242; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
pronephric tubule decreased length, abnormal
|
cndp1zf3243/zf3243; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
renal glomerulus increased length, abnormal
|
cndp1zf3243/zf3243; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
vasculature morphology, abnormal
|
cndp1zf3243/zf3243; y1Tg + MO1-pdx1
|
standard conditions
|
Fig. 10
from Schmöhl et al., 2019
|
type B pancreatic cell differentiation absent, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2
from Kimmel et al., 2011
|
endocrine pancreas has fewer parts of type endodermal cell, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
endocrine pancreas development disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2
from Kimmel et al., 2011
|
type B pancreatic cell differentiation disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
endocrine pancreas decreased size, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
type B pancreatic cell proliferation disrupted, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 3
from Kimmel et al., 2011
|
pancreatic B cell absent, abnormal
|
m1018Tg; nl1Tg + MO1-pdx1 + MO2-mnx1
|
standard conditions
|
Fig. 2 ,
Fig. 3
from Kimmel et al., 2011
|