ZFIN ID: ZDB-FISH-150901-5739
Fish name: slc45a2b4/b4
Genotype: slc45a2b4/b4
Targeting Reagent: none
HUMAN DISEASE MODELED by slc45a2b4/b4
Human Disease Conditions Citations
cataract standard conditions Takamiya et al., 2016
retinal disease high light intensity Kawase et al., 2016
melanoma cancer xenotransplantation Saltari et al., 2016
bacterial infectious disease bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fehr et al., 2016
GENE EXPRESSION
Gene expression in slc45a2b4/b4
RNA expression
Expressed Gene Structure Conditions Figures
alkal1 standard conditions Fig. 2 with image from Fadeev et al., 2018
alkal2a standard conditions Fig. 2 with image from Fadeev et al., 2018
alkal2b standard conditions Fig. 2 with image from Fadeev et al., 2018
capn1a standard conditions Fig. S2 from Coomer et al., 2018
capn1b standard conditions Fig. S2 from Coomer et al., 2018
capn2a standard conditions Fig. S2 from Coomer et al., 2018
capn2b standard conditions Fig. S2 from Coomer et al., 2018
capn5a standard conditions Fig. 5 with image from Coomer et al., 2018
light damage: retina, constant light, high light intensity Fig. 5 with image from Coomer et al., 2018
capn5b standard conditions Fig. 5 with image from Coomer et al., 2018
light damage: retina, constant light, high light intensity Fig. 5 with image from Coomer et al., 2018
dct standard conditions Fig. 4 from Dooley et al., 2013
Fig. 3 from McNeill et al., 2007
text only from Kelsh et al., 2000
fads2 control Fig. 7 from Ashikawa et al., 2017
chemical treatment: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole Fig. 7 from Ashikawa et al., 2017
high light intensity Fig. 7 from Ashikawa et al., 2017
ltk standard conditions Fig. 2 with image from Fadeev et al., 2018
myo5b standard conditions Fig. 1 with image from Sonal et al., 2014
stat3 control Fig. 6 from Conner et al., 2014
chemical treatment: drug Fig. 6 from Conner et al., 2014
tnfa control Fig. 6 from Conner et al., 2014
chemical treatment: drug Fig. 6 from Conner et al., 2014
physical alteration: anatomical structure Fig. 6 from Conner et al., 2014
tyr standard conditions Fig. 4 from Dooley et al., 2013
tyrp1a standard conditions Fig. 2 from Krauss et al., 2014
tyrp1b standard conditions Fig. 2 from Krauss et al., 2014
Protein expression
Antibody Antigen Genes Structure Conditions Figures
zpr-3 control Fig. 5 with image from Kawase et al., 2016
zpr-3 chemical treatment: C646 Fig. 5 with image from Kawase et al., 2016
Ab1-capn5 light damage: retina, constant light, high light intensity Fig. 6 with imageFig. 7 with image from Coomer et al., 2018
Ab2-pcna light damage: retina, constant light, high light intensity Fig. 2 with imageFig. 8 with imageFig. 9 with imageFig. 10 with imageFig. 11 with image from Rajaram et al., 2014
zrf-1 standard conditions Fig. 7 with image from Coomer et al., 2018
Ab-4C12 light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
zpr-1 standard conditions Fig. 6 with image from Coomer et al., 2018
Ab1-capn5 standard conditions Fig. 6 with imageFig. 7 with image from Coomer et al., 2018
zrf-1 light damage: retina, constant light, high light intensity Fig. 7 with image from Coomer et al., 2018
zpr-3 high light intensity Fig. 5 with image from Kawase et al., 2016
Ab-4C12 standard conditions Fig. 6 with image from Coomer et al., 2018
zpr-1 light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
Ab3-stat3 stat3 control Fig. 6 from Conner et al., 2014
Ab3-stat3 chemical treatment: drug Fig. 6 from Conner et al., 2014
Ab1-tnfa tnfa control Fig. 6 from Conner et al., 2014
Ab1-tnfa chemical treatment: drug Fig. 6 from Conner et al., 2014
Ab1-tnfa physical alteration: anatomical structure Fig. 6 from Conner et al., 2014
Reporter gene expression No data available
PHENOTYPE
Phenotype in slc45a2b4/b4
Phenotype Conditions Figures
eye has normal numbers of parts of type iridophore, normal standard conditions Fig. 1 with image from Antinucci et al., 2016
iridophore present, normal standard conditions Fig. 1 from Dooley et al., 2013
larval melanophore stripe melanocyte absent, abnormal standard conditions Fig. 1 with image from Antinucci et al., 2016
larval melanophore stripe melanocyte decreased amount, abnormal standard conditions Fig. 1 with image from Antinucci et al., 2016
lens cellular oxidant detoxification disrupted, abnormal standard conditions Fig. 4 with image from Takamiya et al., 2016
lens radical increased amount, abnormal standard conditions Fig. 4 with image from Takamiya et al., 2016
melanocyte colorless, abnormal standard conditions Fig. 3 from McNeill et al., 2007
melanocyte decreased pigmentation, abnormal standard conditions Fig. 1 with imageFig. 2 with image from Irion et al., 2014
melanocyte unpigmented, abnormal standard conditions Fig. 1 from Dooley et al., 2013
text only from Kelsh et al., 2000
melanocyte melanosome decreased pigmentation, abnormal chemical treatment: bafilomycin A1 Fig. 6 from Dooley et al., 2013
melanocyte melanosome unpigmented, abnormal control Fig. 6 from Dooley et al., 2013
melanophore stripe absent, abnormal standard conditions Fig. 5 from Haffter et al., 1996
melanophore stripe melanocyte absent, abnormal standard conditions Fig. 1 with image from Antinucci et al., 2016
Muller cell zrf-1 labeling increased amount, abnormal light damage: retina, constant light, high light intensity Fig. 7 with image from Coomer et al., 2018
Muller cell proliferative, abnormal chemical treatment: drug Fig. 6 from Conner et al., 2014
Muller cell proliferative, abnormal heat shock, chemical treatment: purpurogallin Fig. 2 from Conner et al., 2014
Muller cell proliferative, abnormal physical alteration: anatomical structure Fig. 6 from Conner et al., 2014
Muller cell proliferative, normal chemical treatment: drug, chemical treatment: pharmaceutical Fig. 6 from Conner et al., 2014
Muller cell proliferative, normal chemical treatment: purpurogallin, chemical treatment: pharmaceutical Fig. 6 from Conner et al., 2014
Muller cell cell population proliferation increased occurrence, abnormal high light intensity, chemical treatment: C646 Fig. 6 with image from Kawase et al., 2016
pigmentation disrupted, abnormal standard conditions Fig. 1Fig. 6 from Dooley et al., 2013
pigmentation disrupted, abnormal chemical treatment: bafilomycin A1 Fig. 6 from Dooley et al., 2013
receptor signaling pathway via JAK-STAT increased occurrence, abnormal chemical treatment: drug Fig. 6 from Conner et al., 2014
receptor signaling pathway via JAK-STAT occurrence, normal chemical treatment: purpurogallin, chemical treatment: pharmaceutical Fig. 6 from Conner et al., 2014
response to light stimulus decreased strength, abnormal standard conditions Fig. 2 from Dooley et al., 2013
retina apoptotic, abnormal high light intensity Fig. 7 from Ashikawa et al., 2017
retina apoptotic, exacerbated high light intensity, chemical treatment: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole Fig. 7 from Ashikawa et al., 2017
retina zpr-3 labeling decreased distribution, abnormal high light intensity, chemical treatment: C646 Fig. 5 with image from Kawase et al., 2016
retina zpr-3 labeling decreased distribution, abnormal high light intensity Fig. 5 with image from Kawase et al., 2016
retina decreased pigmentation, abnormal standard conditions Fig. 3 with image from Wilk et al., 2017
retina capn5a expression increased amount, abnormal light damage: retina, constant light, high light intensity Fig. 5 with image from Coomer et al., 2018
retina structure, normal control Fig. 7 from Ashikawa et al., 2017
retina structure, normal chemical treatment: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole Fig. 7 from Ashikawa et al., 2017
retina apoptotic process increased occurrence, abnormal high light intensity Fig. 7 from Ashikawa et al., 2017
retina apoptotic process increased occurrence, abnormal high light intensity, chemical treatment: C646 Fig. 4 with image from Kawase et al., 2016
retina apoptotic process increased occurrence, abnormal high light intensity Fig. 4 with image from Kawase et al., 2016
retina apoptotic process increased occurrence, exacerbated high light intensity, chemical treatment: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole Fig. 7 from Ashikawa et al., 2017
retina dorsal side has fewer parts of type retinal cone cell, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retina dorsal side lacks all parts of type retinal rod cell, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retina ventral side has fewer parts of type retinal cone cell, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retina ventral side has fewer parts of type retinal rod cell, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retinal cone cell zpr-1 labeling decreased amount, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retinal cone cell Ab1-capn5 labeling increased amount, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retinal cone cell capn5a expression increased amount, abnormal light damage: retina, constant light, high light intensity Fig. 5 with image from Coomer et al., 2018
retinal cone cell photoreceptor outer segment decreased amount, abnormal high light intensity, chemical treatment: C646 Fig. 5 with image from Kawase et al., 2016
retinal cone cell photoreceptor outer segment decreased amount, abnormal high light intensity Fig. 5 with image from Kawase et al., 2016
retinal inner nuclear layer Ab1-capn5 labeling increased amount, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retinal inner nuclear layer cell population proliferation increased occurrence, abnormal chemical treatment: drug Fig. 6 from Conner et al., 2014
retinal inner nuclear layer cell population proliferation increased occurrence, abnormal physical alteration: anatomical structure Fig. 6 from Conner et al., 2014
retinal inner nuclear layer cell population proliferation increased occurrence, abnormal heat shock, chemical treatment: purpurogallin Fig. 2 from Conner et al., 2014
retinal inner nuclear layer cell population proliferation occurrence, normal chemical treatment: drug, chemical treatment: pharmaceutical Fig. 6 from Conner et al., 2014
retinal inner nuclear layer cell population proliferation occurrence, normal chemical treatment: purpurogallin, chemical treatment: pharmaceutical Fig. 6 from Conner et al., 2014
retinal outer nuclear layer morphology, abnormal light damage: retina, constant light, high light intensity Fig. 5 with image from Coomer et al., 2018
retinal pigmented epithelium decreased pigmentation, abnormal standard conditions Fig. 1 with image from Antinucci et al., 2016
retinal pigmented epithelium reflectivity, abnormal standard conditions Fig. 4 with image from Wilk et al., 2017
retinal pigmented epithelium unpigmented, abnormal standard conditions Fig. 1 with image from Antinucci et al., 2016
Fig. 1 from Dooley et al., 2013
text only from Kelsh et al., 2000
retinal pigmented epithelium melanosome amount, normal standard conditions Fig. 5 from Dooley et al., 2013
retinal pigmented epithelium melanosome decreased pigmentation, abnormal standard conditions Fig. 5 from Dooley et al., 2013
retinal rod cell ab-4c12 labeling decreased amount, abnormal light damage: retina, constant light, high light intensity Fig. 6 with image from Coomer et al., 2018
retinal rod cell photoreceptor outer segment decreased amount, abnormal high light intensity, chemical treatment: C646 Fig. 5 with image from Kawase et al., 2016
retinal rod cell photoreceptor outer segment decreased amount, abnormal high light intensity Fig. 5 with image from Kawase et al., 2016
swim bladder epithelial cell has extra parts of type neutrophil, abnormal bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 2 with image from Fehr et al., 2016
swim bladder epithelial cell morphology, abnormal bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 2 with image from Fehr et al., 2016
swim bladder epithelium increased thickness, abnormal bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 2 with image from Fehr et al., 2016
swim bladder epithelium surrounded by fibroblast, abnormal bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 2 with image from Fehr et al., 2016
visual system decreased functionality, abnormal standard conditions Fig. 2 from Dooley et al., 2013
whole organism fads2 expression decreased amount, abnormal high light intensity, chemical treatment: 4-(4-methylphenyl)-2-(2-propyl-4-pyridinyl)thiazole Fig. 7 from Ashikawa et al., 2017
whole organism decreased life span, abnormal chemical treatment by environment: ampicillin, bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 7 from Fehr et al., 2016
whole organism decreased life span, abnormal bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 3Fig. 7 from Fehr et al., 2016
whole organism decreased pigmentation, abnormal standard conditions Fig. 3 with image from Wilk et al., 2017
whole organism lacks all parts of type melanocyte, abnormal standard conditions Fig. 5 from Haffter et al., 1996
whole organism life span, ameliorated chemical treatment by environment: tetracycline, bacterial treatment by injection: Waddlia chondrophila WSU 86-1044 Fig. 7 from Fehr et al., 2016

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