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1 GFR2 signaling or using a vascular deficient zebrafish mutant.
2 epileptic activities observed in a mind bomb zebrafish mutant.
3 nt mutant ARL13B rescued the Arl13b scorpion zebrafish mutant.
4 opment necessary for the characterization of zebrafish mutants.
5 examine cmlc2 and vmhc expression in several zebrafish mutants.
6 ge of defects similar to those of dorsalized zebrafish mutants.
7 drocyte number and myelinated axons in gpr56 zebrafish mutants.
8                     Here, we discuss work on zebrafish mutants affecting gastrulation and patterning
9                     Here we analyse a set of zebrafish mutants and arrive at a different interpretati
10                                        Using zebrafish mutants and in vivo imaging, we identified the
11 the exocyst complex, by analyzing both exoc5 zebrafish mutants, and photoreceptor-specific Exoc5 knoc
12 zygous kcnh2 mutations and expand the use of zebrafish mutants as a model system to study human arrhy
13 on in somite measurements across a number of zebrafish mutants; (b) the delayed formation of somites
14 ral patterns of gene expression in different zebrafish mutant backgrounds allow further quantitative
15 netic analyses of a recessive, larval lethal zebrafish mutant, bal(a69), characterized by severe eye
16 cterized the ocular defects in the recessive zebrafish mutant blowout that presents with a variably p
17 , the study was focused on a reduced melanin zebrafish mutant, brass.
18 roadly rescue morphology and motility in the zebrafish mutant, but alter motor axon morphology, demon
19  those of phenotypic rescue of headless/tcf3 zebrafish mutants by mouse Six3, demonstrate that region
20                   Here, we describe a unique zebrafish mutant, caliban (clbn), with arrested developm
21                          A homozygous lethal zebrafish mutant, cassiopeia (csp), was identified by a
22 sible for the cell cycle defects seen in the zebrafish mutant, cease&desist (cds).
23                   We previously identified a zebrafish mutant ceylon (cey) that has a severe reductio
24 ellular, and electrophysiological basis of a zebrafish mutant characterized by ventricular asystole.
25  We performed a deep characterization of the zebrafish mutant Chihuahua, that carries a G574D (p.G736
26                                       In the zebrafish mutant cloche (clo), SCL expression is nearly
27 t hematopoietic and vascular deficits in the zebrafish mutant cloche.
28                                          The zebrafish mutant colgate (col)/histone deacetylase1 (hda
29                                  We utilized zebrafish mutant combinations that disrupt Chordin and m
30                           Here we describe a zebrafish mutant crimsonless (crs) with a developmental
31                                       In the zebrafish mutant cyclops (Cyc(b16)), most embryos have t
32 alling pathway, such as those mutated in the zebrafish mutants cyclops, squint and one-eyed pinhead (
33                            We characterize a zebrafish mutant defective in definitive haematopoiesis
34       From a genetic screen, we identified a zebrafish mutant defective in the leo1 gene.
35 ovel genes for congenital muscle diseases, a zebrafish mutant, designated patchytail, was identified
36                               The corneas of zebrafish mutants display severe abnormalities of the ep
37 2) knockdown in these cells or its loss in a zebrafish mutant disrupted cell extrusion.
38 Moreover, when expressed in mfsd2aa-morphant zebrafish, mutants failed to rescue microcephaly, BBB br
39 ectron microscopy to evaluate the corneas of zebrafish mutant for a crumbs locus oko meduzy (ome) and
40 enetic screen yielded malbec (mlb(bw306)), a zebrafish mutant for cdh5, with normal embryonic and def
41                                              Zebrafish mutant for foxp3a displayed excess T lymphocyt
42                                        Using zebrafish mutants for cav1, cav3, and cavin1b, we show t
43        To address this question, we utilized zebrafish mutants for ewsa and tp53.
44 sidedness to organ chirality, we examined 12 zebrafish mutants for initial heart tube position and la
45                                 We generated zebrafish mutants for pkd1 and noted cystic kidney and m
46        Here, we report the identification of zebrafish mutants for the gene encoding Structure specif
47                           Here we describe a zebrafish mutant, frascati (frs), that shows profound hy
48 polarity in vertebrates, we have studied the zebrafish mutant fused somites (fss), because its paraxi
49                                  Analyses of zebrafish mutants have confirmed the action of chordin (
50                                         Many zebrafish mutants have specific defects in axon guidance
51 ies using in vitro chick models and systemic zebrafish mutants have suggested that FGF signaling is r
52                                              Zebrafish mutants have traditionally been obtained by us
53      Here, we report the identification of a zebrafish mutant, heart and mind, which exhibits multipl
54 , we find that the lama5 mutant is the first zebrafish mutant identified in which the pectoral fins f
55                We identified an adult-viable zebrafish mutant in which the negative feedback on the s
56 zer coordinates morphogenetic movements, and zebrafish mutants in T-box mesoderm-specific genes help
57                                 We show that zebrafish mutants in uhrf1 and dnmt1 have defects in len
58 ucted to characterize ocular defects in five zebrafish mutants in which core components of the v-ATPa
59                                        Using zebrafish mutants in which OPCs migrate out of the spina
60  mechanosensory neurons of touch-insensitive zebrafish mutants indicates that in three mutant lines t
61 that the hypochromic anaemia in shiraz (sir) zebrafish mutants is caused by deficiency of glutaredoxi
62  (vlt(m651)) is one of only five "bloodless" zebrafish mutants isolated through large-scale chemical
63  is capable of rescuing hypomyelination in a zebrafish mutant lacking BACE1.
64                  In this study, we generated zebrafish mutants lacking all four zebrafish Mesp genes
65                        Here, we show that in zebrafish mutants lacking ErbB3 function, neural crest c
66                                  Analysis of zebrafish mutants lacking functional Pten revealed that
67                      Here, we report that in zebrafish mutants lacking Schwann cells in peripheral ne
68                             We have cloned a zebrafish mutant, lauscher (lau), identified by its swol
69               Here, we present analysis of a zebrafish mutant line carrying a truncation mutation, W8
70 activated HIF transcriptional responses in a zebrafish mutant line harboring a point mutation in the
71                         We have identified a zebrafish mutant line in which deficient emi1 gene expre
72 d genetic screen, we previously identified a zebrafish mutant line, tgct, which develops spontaneous
73                                          The zebrafish mutant line, twister, models SCS in terms of a
74 aB-crystallin, we generated loss-of-function zebrafish mutant lines by utilizing the CRISPR/Cas9 syst
75                            However, managing zebrafish mutant lines derived from mutagenesis screens
76 ion, we screened a collection of insertional zebrafish mutant lines for expression of the HSC marker,
77 suitable for large-scale deep-phenotyping of zebrafish mutant lines, which uses optical projection to
78 quencing and mRNA rescue that the dorsalized zebrafish mutant lost-a-fin (laf) is defective in the ge
79               Furthermore, we found that the zebrafish mutants mariner (myo7aa) and sputnik (cad23) t
80 ificant risk factor for glaucoma, the bugeye zebrafish mutant may be a model organism for the disease
81                                          The zebrafish mutants merlot (mot) and chablis (cha) exhibit
82 decreased cilia) in a CRISPR/Cas9-engineered zebrafish mutant model provide additional support for AR
83                                           In zebrafish, mutant MYL4 leads to disruption of sarcomeric
84 e as a screening assay, we have identified a zebrafish mutant named fantasma (fan), which displays re
85 imary and secondary hindbrain neurons in the zebrafish mutant neckless (nls), which disrupts retinald
86  we identified a homolog of the Stil gene in zebrafish mutant (night blindness b, nbb), which showed
87                           Here we describe a zebrafish mutant, no optokinetic response f(w21) (nof),
88                             Studies with the zebrafish mutant nrc have revealed that loss of SynJ1 al
89                                          The zebrafish mutant nrc is a possible model for human retin
90  Here we present crystal, an optically clear zebrafish mutant obtained by combining different viable
91                                          The zebrafish mutants of CCTbeta are known to exhibit the ey
92                                          The zebrafish mutant, partial optokinetic response b (pob),
93                                  A red-blind zebrafish mutant, partial optokinetic response b (pob),
94 irst identified as the locus affected in the zebrafish mutant pescadillo, which exhibits severe defec
95                   The striking similarity of zebrafish mutant phenotypes and human diseases emphasize
96 approach is based on the rescue of embryonic zebrafish mutant phenotypes by "humanized" zebrafish ort
97              In comparing mouse knockout and zebrafish mutant phenotypes, we propose a pathway for er
98                     A recent analysis of the zebrafish mutant prometheus points to a previously unkno
99                                        A new zebrafish mutant provides further insight into how the a
100                                          The zebrafish mutant rapunzel has heterozygous defects in bo
101                          Here, we identify a zebrafish mutant, redhead (rhd(mi149)), that exhibits em
102                                          The zebrafish mutant represents the first genetically 'accur
103                       Here we characterize a zebrafish mutant, retsina (ret), that exhibits an erythr
104                                            A zebrafish mutant (s434 mutation) was identified that dis
105                                          The zebrafish mutant sauternes (sau) has a microcytic, hypoc
106                                          Our zebrafish mutant serves as a model for developing therap
107 ion of chordin in D-V patterning, dorsalized zebrafish mutants showed expanded domains of chordin exp
108                 Genetic screening identifies zebrafish mutants, such as fat free, that show normal di
109 mutant phenotype of the strongest dorsalized zebrafish mutant swirl/bmp2b, revealing equivalent genet
110 ns of positional cloning, we reveal that the zebrafish mutant tennismatch is a hypomorphic allele of
111                           Here, we present a zebrafish mutant that ceases mitosis at the beginning of
112 ified split top, a recessive maternal-effect zebrafish mutant that disrupts embryonic patterning upst
113 e identified brambleberry, a maternal-effect zebrafish mutant that disrupts karyomere fusion, resulti
114             Using a novel hypomorphic hnf1ba zebrafish mutant that exhibits pancreas hypoplasia, as o
115 ycat from the deletion interval of cloche, a zebrafish mutant that has dramatically reduced hematopoi
116                  A recent report describes a zebrafish mutant that provides us with some enticing clu
117 ered expression patterns of lft1 and lft2 in zebrafish mutants that affect midline development sugges
118 ssues, we analyzed otic placode induction in zebrafish mutants that are deficient in prospective otic
119                                      Work on zebrafish mutants that develop supernumerary neuromasts
120                                 By analyzing zebrafish mutants that disrupt sonic hedgehog (shh) expr
121                                          Two zebrafish mutants that do not develop brain ventricles a
122 o rescues retinal axon pathfinding errors in zebrafish mutants that have a partial functional loss of
123                                  Analysis of zebrafish mutants that have defects in motor behavior ca
124  primary motoneuron specification in several zebrafish mutants that have distinct effects on paraxial
125  in one-eyed pinhead (oep) and cyclops (cyc) zebrafish mutants, the pattern is altered.
126    Here, we use a temperature-sensitive mitf zebrafish mutant to conditionally control endogenous MIT
127                                  To identify zebrafish mutants to serve as models for hepatic patholo
128                      Here we characterized a zebrafish mutant--too few (tof)--that develops hindbrain
129 its C terminus, cause the touch-unresponsive zebrafish mutant touchdown.
130                                       In the zebrafish mutant unplugged, two of the three segmental m
131  Here we quantifiy four eye movements in the zebrafish mutant valentino and hox3 knockdowns, and find
132                                          The zebrafish mutant violet beauregarde (vbg) can be identif
133 e describe the positional cloning of a blind zebrafish mutant, wait until dark (wud), which encodes a
134                                  Because the zebrafish mutant was a global knockout, we also observed
135 pproach we mapped each of the five different zebrafish mutants we sequenced and identified likely cau
136                                        Using zebrafish mutants we show here that in the zebrafish gbx
137 ession studies and the analysis of different zebrafish mutants, we have assembled a molecular pathway
138                        Using pax7a and pax7b zebrafish mutants, we identified a previously unknown re
139 sponsible for the hypochromic anaemia of the zebrafish mutant weissherbst.
140                       yquem (yqe(tp61)) is a zebrafish mutant with a photosensitive porphyria syndrom
141 dx4 as the locus mutated in kugelig (kgg), a zebrafish mutant with an early defect in haematopoiesis
142 esis screen to identify no blastema (nbl), a zebrafish mutant with an early fin regeneration defect.
143                            Here we isolate a zebrafish mutant with heart malformations, called 34c.
144 terized the phenotype of chardonnay (cdy), a zebrafish mutant with hypochromic, microcytic anemia, an
145 l ATPase inhibitory factor 1 (atpif1) from a zebrafish mutant with profound anaemia, pinotage (pnt (t
146                   We have identified a blind zebrafish mutant with rapid degeneration of cone photore
147 e cellular bases of heart development and on zebrafish mutants with cardiac abnormalities whose study
148 left-right asymmetry defects, reminiscent of zebrafish mutants with defective cilia.
149                            Today, studies of zebrafish mutants with defective heart function are prov
150  reagents, future studies of Hb switching in zebrafish mutants with defective hematopoiesis will be p
151                          We identified three zebrafish mutants with defects in biliary development.
152 s screens for developmental mutants, several zebrafish mutants with defects in blood development have
153 ide a useful molecular probe for identifying zebrafish mutants with defects in granulopoiesis.
154  and will ultimately be useful in evaluating zebrafish mutants with defects in hemoglobin production
155 n important framework for future analyses of zebrafish mutants with defects in this process.
156 s epilepsy and autism, we determined whether zebrafish mutants with grossly abnormal brain structure
157 ipid mass, we performed a genetic screen for zebrafish mutants with hepatic steatosis, a pathological
158 unc45b, hsp90aa1.1 and smyd1b is specific to zebrafish mutants with myosin folding defects, and is no
159 nt and myelination, we undertook a screen of zebrafish mutants with previously characterized neural d
160  Behavioral screens have uncovered dozens of zebrafish mutants with striking visual defects.

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