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1 ate published Morpholino-induced phenotypes (morphants).
2 endothelial Notch and HSC formations in evi1 morphants.
3 ring early primitive hematopoiesis in scube1 morphants.
4 mber of Rohon-Beard sensory neurons in cdk10 morphants.
5 biliary defects similar to those of the gpc1 morphants.
6 redicted roles in biomineralization in vegf3 morphants.
7 he cell junctions had disintegrated in zBves morphants.
8 ic acid are significantly decreased in rdhe2 morphants.
9 ntuated by L-leucine in both Rps19 and Rps14 morphants.
10 trated significant impairment of C-E in Zic3 morphants.
11 ants, rescues the growth retardation of orc1 morphants.
12 prematurely and rescues retraction in slit1b morphants.
13 ewer or truncated cilia are observed in Rfx2 morphants.
14 d body size, mirroring the phenotype of orc1 morphants.
15  and (c) pSmad2 levels were reduced in rbms3 morphants.
16 sylation and LLO levels were reduced in pmm2 morphants.
17 ally rescue the small eye phenotype of ZFRP2 morphants.
18 I restores pronephric duct formation in pkd2 morphants.
19 mbly is defective and disorganized in double morphants.
20 pitulated the laterality phenotype of alphaV morphants.
21 t partially overlap with those seen in ecscr morphants.
22 inding activity of alpha-dystroglycan in the morphants.
23 nockdown rescued neurogenesis defects in g9a morphants.
24 ectopic cytosolic CaMK-II expression in tbx5 morphants.
25 at is demethylated and up-regulated in dnmt3 morphants.
26 ly rescued the branching phenotype in sema5A morphants.
27  severely shortened or fail to form in Foxj1 morphants.
28 Lim3 and Pit1 expression in hypomorphic FGF3 morphants.
29 e number of cardiomyocyte was reduced in the morphants.
30 d signaling is significantly reduced in EGAP morphants.
31  mechanism for the vascular defects in magp1 morphants.
32  the bloodless phenotype in ZBP-89 zebrafish morphants.
33 while overexpressing notch rescues angptl1/2 morphants.
34 factor, are significantly reduced in elavl1a morphants.
35 ture and kidney cystogenesis in polycystin 2 morphants.
36 opic tubule gene expression in prkciota/zeta morphants.
37 bers, even in mild or intermediate phenotype morphants.
38 vinolin phenocopied the defects seen in scp2 morphants.
39 ns from slb/wnt11 mutants or wnt11 knockdown morphants.
40 h arch tissue can rescue cell death in foxi1 morphants.
41 cAMPS, partially rescued phenotypes of pde1a morphants.
42 tores spinal cord marker expression in Sall4 morphants.
43 scle myosin was markedly decreased in scube3 morphants.
44  ganglion cells was also diminished in cdk10 morphants.
45 nt extension movement was defective in Dhrs3 morphants.
46 ular morphogenesis appeared normal in scube1 morphants.
47 67 null mouse (bpck) and in zebrafish tmem67 morphants.
48 ion in a manner similar to that seen in lef1 morphants.
49 red sox2 and ngn1 transcript levels in cdk10 morphants.
50 enin and PCP activities is able to mimic the morphant accelerated cell motility phenotype.
51                                   In tmem88a morphants, activation of the WNT pathway exacerbates the
52                        Cav-1alpha and -1beta morphants also exhibited disruption in the actin cytoske
53 trikingly, BMP misregulation seen in 3-OST-7 morphants also occurs in multiple cardiac noncontraction
54 were still able to rescue motor axons in smn morphants, although not as well as full-length PLS3.
55     Here, we use a combination of mutant and morphant analysis to ablate the function of each of the
56           Elevating Nodal levels in aplnra/b morphant and double mutant embryos is sufficient to resc
57 t this expression is diminished in both tbx5 morphant and hst embryos.
58                                          The morphant and overexpression phenotype represent a conver
59 entered the cell cycle relative to the stat3 morphant and significantly decreased the number and inte
60 sal axis curvature formation in polycystin 2 morphants and curly up polycystin 2 mutants.
61 e neurovascular characterization of mutants, morphants and drug-treated embryos.
62 own, but not Suv39h1 loss, phenocopied dnmt3 morphants and G9a overexpression provided a striking res
63                    Similarly, zebrafish tbx5 morphants and mutants (heartstrings; hst) lack pectoral
64 synthesis and rRNA production in the cohesin morphants and partially restored phosphorylation of RPS6
65 are elevated in Na,K-ATPase alpha2 and Ncx4a morphants and that the defects in ciliary motility, KV f
66 idance is specifically disrupted in Lv-vegf3 morphants and these embryos fail to form skeletal elemen
67 ression, adcy8 and nrp1a morphants, or nrp1a morphants and transgenic DNGalpha(S) expression.
68 oc5 mutant zebrafish lines phenocopied exoc5 morphants and, strikingly, exhibited a virtual absence o
69 ranscripts are incorrectly spliced in Eif4a3 morphants, and demonstrate that inhibition of Xenopus Ry
70            Exogenous VEGFA rescues Tel1/ETV6 morphants, and depletion of VEGFA or its receptor, Flk1,
71  promoter were reduced in both dnmt3 and g9a morphants, and its knockdown rescued neurogenesis defect
72 rescue the body curvature phenotype of ZFRP2 morphants, and the eye size of the resultant morphants w
73 ervation of hair cells was reduced in ribeye morphants, and the reduction was correlated with depleti
74 d the developmental phenotypes of ciliopathy morphants, and this effect was rescued by human XPNPEP3
75 vacuolar protein sorting) family mutants and morphants, and we report here that knockdown of atp6ap2
76 rast, PMC migration is unaffected in Lv-fgfa morphants, and well-patterned but shortened skeletal ele
77            Low-dose Lgi1a MO knockdown fish (morphants) appear morphologically normal but are sensiti
78                ast (robo2) mutant and slit1a morphant arbors had more branch tips and greater arbor a
79 e-lapse imaging revealed that ast and slit1a morphant arbors stabilized earlier than wild-type, sugge
80          Ipsilateral misprojections in adcy8 morphants are corrected by the expression of an nrp1a re
81 e phenotypes observed in both Dhx34 and Nbas morphants are similar to defects in Upf1, Smg-5- or Smg-
82 he convergent extension defects in zebrafish morphants are similar to those found in planar cell pola
83                    Lastly, CE defects in mcc morphants are suppressed by downstream activation of Rho
84 oretinograms (ERGs) were performed on dynein morphants at 5 to 6 days after fertilization (dpf).
85 ature was distorted in both fukutin and FKRP morphants, but not in dystroglycan morphants or control
86 escued the development of rad21 and nipbla/b morphants by boosting mTOR-dependent translation.
87 V cilia length, and KV morphogenesis in sdc2 morphants can be rescued by expression of fgf2 mRNA.
88      Knockdown of the ANLN gene in zebrafish morphants caused a loss of glomerular filtration barrier
89 etion of PDE1A aggravated phenotypes in pkd2 morphants, causing more severe body curvature, and human
90                By contrast, mesodermal Mypt1 morphant cells transplanted into wild-type hosts undergo
91                           However, in CCDC78 morphants, Cep152 fails to localize to the deuterosome a
92           We also demonstrate that in CEP120 morphants, cilia are shortened in the neural tube and di
93 utonomous to CNC tissue, as the migration of morphant CNC can only be rescued by ADAM13 expression in
94 pended on Dnmt1 catalytic activity, as Dnmt1 morphants could be rescued by active zebra fish or human
95      Consistently, a comparison of published morphant defects with the Sanger Zebrafish Mutation Proj
96 m2 overexpression can partially rescue ccm2l morphant defects.
97  and ciliary organization analysis in tmem67 morphants did not support a global loss of planar polari
98                                              Morphants display a moderate decrease in the numbers of
99                                      decorin morphants displayed a pronounced shortening of the head-
100  Surprisingly, tubule cells in prkciota/zeta morphants displayed ectopic expression of the transcript
101                                          The morphants displayed shortened and abnormally branched mo
102                              Although alphaV morphants displayed vascular defects, they also exhibite
103 at cultured muscle cells derived from Eif4a3 morphants do not contract, and fail to undergo calcium-d
104 RNA production were decreased in the cohesin morphant embryo cells.
105                                    The SmyD1 morphant embryos (embryos injected with morpholino oligo
106  proliferation and cartilage defects in chd7 morphant embryos and can lead to complete rescue of the
107      Conditional expression of Otx2 in these morphant embryos cell-autonomously rescues the formation
108                                              Morphant embryos displayed both cardiac and left/right p
109                                              Morphant embryos displayed cardiac abnormalities, includ
110                            Single and double morphant embryos exhibited changes in splicing of overla
111                                              Morphant embryos had developmental abnormalities consist
112 enic DNGalpha(S)-expressing embryos or adcy8 morphant embryos have decreased levels of nrp1a and nrp1
113 ion of gene expression suggests that the APP morphant embryos have defective convergent-extension mov
114                                         Dvr1 morphant embryos have normal KV morphology and function,
115 his regard, laminin isolated from beta4GalT1 morphant embryos is poorly galactosylated, which may con
116                      Cardiac myocytes in the morphant embryos lacked the intercalated disks that were
117                                              Morphant embryos manifest craniofacial defects, impaired
118 the developmental processes affected in FKRP morphant embryos may lead to a better understanding of t
119                                         FKRP morphant embryos showed a spectrum of phenotypic severit
120  and the retinal neuroblasts observed in the morphant embryos suggests that obscurin A-mediated small
121                Myofibril organization in the morphant embryos was severely disrupted.
122         Morphology and development of single morphant embryos were strikingly normal; however, muscle
123 BP1) was reduced in nipbla/b, rad21 and smc3-morphant embryos, a pattern indicating reduced translati
124 ns in adcy1, adcy8, nrp1a, sema3D, or sema3E morphant embryos, as well as in sema3D mutant embryos.
125                                      In tag1 morphant embryos, FBMN migration is specifically blocked
126    Integrin function is compromised in magp1 morphant embryos, suggesting that reduced integrin-matri
127 s are affected similarly in all three single morphant embryos, with an inability to extend protrusion
128 onses to, mesoderm-inducing signals in lin28 morphant embryos.
129  OR111-7 transgene-expressing neurons in DCC morphant embryos.
130 ecreased glut1 transcript expression in akt2 morphant embryos.
131 he inhibition of apoptosis and rescue of the morphant embryos.
132 ingly similar defects to those seen in disc1 morphant embryos.
133 erm is severely abnormal in lin28 knockdown (morphant) embryos.
134 rexpression was sufficient to rescue Swap70b morphants, establishing Swap70b as a novel member of the
135 naffected in mitf mutants, as well as in otx morphants, even in regions lacking RPE.
136 pondin repeat (TSR) domain alone into sema5A morphants exclusively rescued delay in ventral motor axo
137                    Late gastrula-stage FoxH1 morphants exhibit delayed mesoderm and endoderm marker g
138 arch osteochondrogenic progenitors, and that morphants exhibit diminished and dysmorphic arch cartila
139                              Moreover, cdk10 morphants exhibited a marked loss of huC-positive neuron
140                                      Swap70b morphants exhibited broader and shorter body axis but ce
141                                   The Lrrc10 morphants exhibited cardiac functional defects as eviden
142 hants had similar brain abnormalities, kdm6a morphants exhibited craniofacial phenotypes, whereas kdm
143                                    The kmt2d morphants exhibited severe abnormalities in all tissues
144                                  The dnajb1a morphants exhibited underdeveloped cataractous lenses wi
145 th reduced expression of the cftr gene (Cftr morphants) exhibited reduced respiratory burst response
146 ependent hair-cell loss occurred in neurog1a morphants exposed to either agonist, and the loss was co
147                                       In Zic morphants expression of roof plate markers, including lm
148 d less stable protrusions, and those in myh6 morphants extended fewer protrusions per cell.
149 nscription analysis revealed that nanog-like morphants fail to develop the extraembryonic yolk syncyt
150                   Within the retina of lmx1b morphants, Fgf activity is transiently up-regulated and
151               Analysis of rx3 chk mutant/rx3 morphant fish and EdU pulse-chase studies reveal that rx
152 monstrate atp1b2b levels are reduced in eya4 morphant fish and that morpholino oligonucleotides targe
153 re viable, and by 4 days post-fertilization, morphant fish display multiple defects in organ systems
154                      Consequently, tgfbeta1a morphant fish displayed phenotypical similarities with p
155                                         eya4 morphant fish embryos had reduced numbers of hair cells
156                      In general, the fukutin morphant fish had the most severe skeletal muscle and ey
157                         Interestingly, these morphant fish having human FKRP mutations showed a wide
158 r some of the effects of PINK1 knockdown, as morphant fish show elevated GSK3beta activity and their
159                                          All morphant fish showed muscle damage and vascular abnormal
160 hout the central nervous system of high-dose morphant fish, accounting for the size reduction of neur
161 sregulation of pax2 in the developing eye of morphant fish, suggesting that Nlz1 and Nlz2 act upstrea
162                                     In actn2 morphant fish, the Z-disc defect sequentially affects ca
163 rexpression rescued these phenotypes in eya4 morphant fish.
164 e to innervating neurons, I exposed neurog1a morphants-fish whose hair-cell organs are devoid of affe
165 afish paralogs kdm6a and kdm6al, we analyzed morphants for developmental abnormalities in tissues tha
166                                    Zebrafish morphants for either gene develop pigmentary defects and
167                                              Morphants for rbms3 displayed reduced proliferation of p
168                                    Zebrafish morphants for snx14 showed dramatic loss of cerebellar p
169  likely to form protrusions, those in tnnt2a morphants formed less stable protrusions, and those in m
170                             Zebrafish adcy1b morphants had no FM1-43 dye uptake and lacked startle re
171 ited craniofacial phenotypes, whereas kdm6al morphants had prominent defects in heart development.
172                Although the kdm6a and kdm6al morphants had similar brain abnormalities, kdm6a morphan
173                           Further, otoferlin morphants had uninflated swim bladders.
174 pparently not in the neural crest, and nrp1A morphants have cardiac development defects.
175                                         Chd7 morphants have impaired migration of neural crest cells
176                              High-dose Lgi1a morphants have morphological defects which persist into
177                                       Sema3D morphants have subsequent complex congenital heart defec
178 uced fluorescence intensity from NADH in the morphant heart was observed in live zebrafish embryos as
179                                              Morphant hearts were hypoplastic and dysmorphic and exhi
180 genetic interaction between arl13b and sec10 morphants in cilia-dependent phenotypes.
181 nts was significantly increased over that of morphants in which ZFRP2 had been depleted.
182  of two cardiac genes was deregulated in the morphants including an increase in atrial natriuretic fa
183 ions of hepatoblasts are detectable in rargb morphants, indicating Rargb acts during hepatic specific
184 ICD), rescued the expansion of MCCs in mecom morphants, indicating that mecom acts upstream to induce
185  embryos is abnormally widened in beta4GalT1 morphants, indicative of abnormal convergent extension.
186 protein accumulates in hair cells of CaMK-II morphants, indicative of defective recycling and/or exoc
187                     Bacterial burden in Cftr morphants infected with a P. aeruginosa DeltaLasR mutant
188    Similar to what was observed in the glut1 morphants, inhibiting the expression of the proapoptotic
189                Here we show that mutants and morphants involving other V-H(+)-ATPase subunits also de
190  Decreased hepatocyte proliferation in copeb morphants is accompanied by upregulation of the cell cyc
191          The motility phenotype found in the morphants is not observed in embryos in which the Wnt/be
192  failure to form the PAC in netrin 1a or dcc morphants is phenocopied by laser ablation of motoneuron
193 o rescue motor neuron pathology in zebrafish morphants lacking Gle1.
194 -gamma) or IFN-alpha signaling and zebrafish morphants lacking IFN-gamma and IFN-varphi activity had
195 ryos shows defective calcium release in bin1 morphants, linking the presence of abnormal triads to im
196 veral lysosomal glycosidases was observed in morphant lysates, consistent with the reduction in phosp
197 lin 2 and alpha-actinin 1 did not affect smn morphant motor axon outgrowth.
198 sed embryonic skeletal muscle paralysis, and morphant motor neurons had aberrant morphology including
199 ypomorphs and isoform-specific (medium/long) morphants not only recapitulate this phenotype but also
200                                              Morphants of beta2 CaMK-II (camk2b2), but not the beta1
201  death of the periocular mesenchyme in Lmx1b morphants, optic vesicle morphogenesis is largely restor
202  and FKRP morphants, but not in dystroglycan morphants or control fish.
203 ignature and myc overexpression in angptl1/2 morphants or mib restored HSPCs formation.
204 ding domain mutations, FoxH1 splice-blocking morphants or other Nodal pathway mutants, and it cannot
205             Noninvasive live imaging of Rac2 morphants or Rac2D57N zebrafish larvae demonstrates an e
206 enic DNGalpha(S) expression, adcy8 and nrp1a morphants, or nrp1a morphants and transgenic DNGalpha(S)
207  if the first hair cells are missing (atoh1b morphant), otolith formation is severely disrupted and d
208 l matrix formation and calcium deposition in morphant otoliths.
209                                    The FoxH1 morphant phenotype is much more severe than that of zebr
210                                 However, the morphant phenotype observed following specific depletion
211                         Similar NBP and Numb morphant phenotype such as impaired convergence and exte
212                                  The overall morphant phenotype was also obtained by co-injecting sub
213                                    This Grk5 morphant phenotype was associated with an overall decrea
214                                          The morphant phenotype was efficiently rescued by zebrafish
215                                          The morphant phenotype was rescued when mRNA encoding murine
216 of TGF-beta signalling phenocopies the ltbp3-morphant phenotype whereas expression of a constitutivel
217 F1A2 wild-type mRNA successfully rescued the morphant phenotype, but mutant RNA did not.
218 so show that wild-type human APP rescues the morphant phenotype, but the Swedish mutant APP, which ca
219 nhibition of Bmp signaling rescues the rargb morphant phenotype, indicating Rargb functions upstream
220 sulted in a failure to rescue the cav-1alpha morphant phenotype, verifying an essential role for Cav-
221 sion of vhnf1 mRNA led to rescue of the pk1a morphant phenotype.
222 s with a mixture of MOs reproduces the FoxH1 morphant phenotype.
223 n analysis of Cby's embryonic expression and morphant phenotypes in Xenopus laevis.
224 n Project revealed that approximately 80% of morphant phenotypes were not observed in mutant embryos,
225                                              Morphant phenotypes were rescued by injection of homotyp
226                           Many, but not all, morphant phenotypes were significantly reversed by the W
227  hands were essential for PLS3 rescue of smn morphant phenotypes, and mutation of the Ca(2+)-binding
228 , and human PDE1A RNA partially rescued pkd2 morphant phenotypes, pronephric cysts, hydrocephalus, an
229 bitor) resulted in a partial rescue of smad7 morphant phenotypes, suggesting scl2a10/glut10 functions
230 pression provided a striking rescue of dnmt3 morphant phenotypes, whereas Suv39h1 overexpression fail
231                                              Morphant photoreceptor connecting cilia were swollen, bu
232 3 inhibits normal PMC ingression and foxN2/3 morphant PMCs do not organize in the blastocoel and fail
233 rystallin isoform mRNAs lost from the eif3ha morphant polysomes, revealing a mechanism by which lens
234     We establish that, in FoxA2-FoxA3 double morphants, precursors of axial tissues are correctly ind
235                              In the perlecan morphants, primary intersegmental vessel sprouts, which
236                        In zebrafish, tbc1d23 morphants replicated the human phenotype showing hindbra
237 lasts, activation of Notch signaling in hey2 morphants rescues HSC formation in zebrafish embryos.
238                                Def6a/Swap70b morphants resemble Ppt/Slb double mutant embryos suggest
239             The increased OPC numbers in nf1 morphants resulted from increased proliferation, as dete
240  Microarray analyses of apc mutants and Rdh5 morphants revealed a profound overlap in the transcripti
241 ic Swap70b expression robustly rescued Wnt11 morphants, RhoA overexpression was sufficient to rescue
242                                Probing FoxH1 morphant RNA by microarray, we identified a cohort of fi
243                                 The perlecan morphants show a severe myopathy characterized by abnorm
244 tivity is transiently up-regulated and these morphants show defective naso-temporal patterning.
245                Danio rerio (Zebrafish) tbx20 morphants show defects in the migration patterns of moto
246                                     The chd7 morphants show elevated expression of several potent cel
247                              These zebrafish morphants show Rac hyperactivation and progress faster t
248        Characterization of the gne knockdown morphants showed a significantly reduced locomotor activ
249       Consistent with these results, slc2a10 morphants showed decreased respiration and reduced TGFbe
250 racked in real-time, individual DFCs of both morphants showed defects in DFC migration, preventing th
251                                     The FKRP morphants showed phenotypes involving alterations in som
252 and, accordingly, tuba start and splice site morphants showed various ciliary mutant phenotypes in th
253 nd enhanced phenotypic aberrations in double morphants suggest that the genes interact genetically.
254 nd that the sarcomere remains intact in tcap morphants, suggest that defective sarcomere assembly doe
255 ved in fast muscle fibers of pgam2 zebrafish morphants, suggesting affected myoblast fusion.
256 idline and gut looping is perturbed in rargb morphants, suggesting Rargb affects lateral plate mesode
257 is abolished in Na,K-ATPase alpha2 and Ncx4a morphants, suggesting their essential role in KV ciliary
258 on of constitutively active TOR rescued EGAP morphants, suggesting TOR is a direct or indirect endoge
259 d Notch signalling [mindbomb mutant or Su(H) morphant], supernumerary hair cells develop and otolith
260 stand the in vivo function of Pen-2, we used morphant technology available in zebrafish and transient
261 to be significantly higher in zebrafish Cftr morphants than in controls, but this phenomenon was not
262                          In Zic1 and/or Zic4 morphants the ventricle does not open properly, but rema
263                        Consequently, in Wnt1 morphants, the blastopore is located at the border of th
264                                      In pmm2 morphants, the free glycan by-products of LLO cleavage i
265 re present in muscle fibers of rbfox1l/rbox2 morphants, they are substantially reduced in number and
266                         Exposure of the gpc1 morphants to cyclopamine, a Hedgehog antagonist, partial
267 stigation of the craniofacial defects in the morphants uncovered striking changes in the timing and l
268 splayed phenotypical similarities with pcsk7 morphants, underscoring the importance of this cytokine
269    Knockdown of Lrrc10 in zebrafish embryos (morphants) using morpholinos caused severe cardiac morph
270                                   In 3-OST-7 morphants, ventricular contraction can be rescued by ove
271 guingly, overexpression of glut1 in the akt2 morphants was also able to rescue these embryos.
272             The phenotype of ZFRP2 knockdown morphants was characterized by immunohistology and histo
273 ormal; however, muscle development in double morphants was severely disrupted.
274 morphants, and the eye size of the resultant morphants was significantly increased over that of morph
275 etinas and ciliated cells of these zebrafish morphants were analyzed by immunohistochemistry and tran
276                                     When the morphants were exposed to several drugs with antioxidant
277                                         Cftr morphants were infected with P. aeruginosa or other bact
278 of tfpi, and hematopoietic defects in adtrp1 morphants were rescued by tfpi overexpression.
279                  Both gonzo mutants and scap morphants were resistant to steatosis in response to 2%
280 ted after knockdown of Bves, and these zBves morphants were sensitive to osmotic stress.
281 ize was also smaller in the fukutin and FKRP morphants when compared with dystroglycan knockdown fish
282 d size and neuroanatomical defects of kctd13 morphants, whereas suppression or overexpression of CEP2
283 lack cardiac contractions and flow, and myh6 morphants, which lack atrial contraction and exhibit red
284 ent animals, including erbb2 mutants, tnnt2a morphants, which lack cardiac contractions and flow, and
285 Dnmt1p target genes can be reimposed in xDMO morphants with an mRNA encoding a catalytically inactive
286 tterning defects at later stages, since Zic3 morphants with moderate to severe C-E defects exhibited
287                      Second, co-injection of morphants with the long human TMEM260 mRNA rescued CNS p
288                                              Morphant zebrafish also exhibited elevated levels of apo
289     In addition, Mmp21-mutant mice and mmp21-morphant zebrafish displayed heterotaxy and abnormal car
290                                         toe1-morphant zebrafish displayed midbrain and hindbrain dege
291                                              Morphant zebrafish embryos also exhibited increased apop
292 ts in cells lacking BBS1, BBS4, and OFD1, in morphant zebrafish embryos, and in induced neurons from
293 g strategy using stage-matched WT and eif3ha morphant zebrafish embryos.
294 fy motor axon outgrowth phenotypes in an smn morphant zebrafish model of SMA.
295                       Confocal microscopy of morphant zebrafish revealed olfactory placodes with defe
296          Moreover, when expressed in mfsd2aa-morphant zebrafish, mutants failed to rescue microcephal
297     In contrast to what has been reported in morphant zebrafish, zap70(y442) homozygous mutant zebraf
298  defects were seen in both knockout mice and morphant zebrafish.
299 ion and mineralization were delayed in panx3 morphant zebrafish.
300 nd examined the skeletal phenotypes of panx3 morphant zebrafish.

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