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1 ced fertility, although adult pex5-10 plants appear normal.
2 MET currents of heterozygous littermates appear normal.
3 xocytosis markers in rsd-2 and rsd-6 mutants appear normal.
4 tivation and arterial-venous differentiation appear normal.
5 cranial neural crest-derived enteric neurons appear normal.
6 eterozygous for the null allele, Sox2(EGFP), appear normal.
7 tor or the IGF-1 receptor plus one Ir allele appear normal.
8 mesenchymal transition (EMT) at gastrulation appear normal.
9 ough signaling, morphology, and cargo levels appear normal.
10 pe, whereas lamin, Ran, and tubulin staining appear normal.
11 membranes, although non-neuronal cell types appear normal.
12 e other populations of somatosensory neurons appear normal.
13 mice express OVA mRNA in the epidermis, and appear normal.
14 mice are born at the expected frequency and appear normal.
15 Lrat+/+ mice, whereas other neuronal layers appear normal.
16 At 1 year of age, CPLXII knockout (KO) mice appear normal.
17 ence of Itk, but the T cells that do develop appear normal.
18 eas the aerial part of the ABCG1-RNAi plants appear normal.
19 t presents focally; most renal tubular cells appear normal.
20 Other cell types in the immune system appear normal.
21 however, 53BP1 DSB responses in these cells appear normal.
22 Wild type and heterozygote mice appear normal.
23 movement is unaffected, and mitotic spindles appear normal.
24 ir follicle architecture and differentiation appear normal.
25 commitment in distal Runx1 knockout embryos appears normal.
26 mation and maintenance of adherens junctions appears normal.
27 of the dorsal FC whereas ventral/orbital FC appears normal.
28 hibited, whereas slow-muscle gene expression appears normal.
29 se stages, the synaptic physiology phenotype appears normal.
30 , nuclear transport of transcription factors appears normal.
31 obal systolic function of the left ventricle appears normal.
32 morphogenesis fails, although lens formation appears normal.
33 ugh the number of cell-surface Ca2+ channels appears normal.
34 ified by anaphase and chromosome segregation appears normal.
35 s and initial patterning of the hindlimb bud appears normal.
36 e marrow cells for T- and B-cell development appears normal.
37 Duct/gland development appears normal.
38 nvasion, and a compromised barrier; the lens appeared normal.
39 in allele yielding only wild-type prelamin A appeared normal.
40 level, and T-cell receptor (TCR) repertoire appeared normal.
41 t and malformed, whereas in renal cysts they appeared normal.
42 n these images, but the parts that were seen appeared normal.
43 ty was significantly diminished, but the ONL appeared normal.
44 For example, pstO cell differentiation appeared normal.
45 hR density on the remaining junctional folds appeared normal.
46 , moribund animals resumed linear growth and appeared normal.
47 erator and diaphragm neuromuscular junctions appeared normal.
48 tion, polarity, and photoreceptor morphology appeared normal.
49 n the shape and density of the cone pedicles appeared normal.
50 e ventral cord and peripheral nervous system appeared normal.
51 hereas single-transgenic littermate controls appeared normal.
52 The epithelium and Descemet's membrane appeared normal.
53 e initial generation of central 5-HT neurons appeared normal.
54 ntiation of the liver and endocrine pancreas appeared normal.
55 at the nevus margin, the choroid and sclera appeared normal.
56 orta and collagen fibrils in the aortic wall appeared normal.
57 and TH-IR amacrine cell somas and dendrites appeared normal.
58 d found that sensory neurons and motoneurons appeared normal.
59 oleus and quadriceps muscles from MGSKO mice appeared normal.
60 rin, c-kit, adaptin-3, and the HPS1 protein) appeared normal.
61 opaminergic amacrine cells, and Muller cells appeared normal.
62 In the newborn period, their joints appeared normal.
63 n particular, hematopoietic cell development appeared normal.
64 Retinas appeared normal.
65 The overall morphology of the hippocampus appeared normal.
66 ion in the parabrachial nucleus and amygdala appeared normal.
67 ction, the rate of collagen type I secretion appeared normal.
68 ponsive neurons for which responses to faces appeared normal.
69 horter body axis but cell fate specification appeared normal.
70 that decussate to more caudal brain segments appeared normal.
71 ation of viral replication compartments also appeared normal.
72 eir morphology, activation, and cargo levels appeared normal.
73 By week 6, the skin appeared normal.
74 er wild-type littermates) in all tissues and appeared normal.
75 eproductive organs and spermatozoid motility appeared normal.
76 tiation, whereas Th1 and Th2 differentiation appeared normal.
77 the podocyte markers GLEPP1 and synaptopodin appeared normal.
79 esis of CTSC and neutrophil serine proteases appeared normal along with initial processing and sortin
80 ponses of this mutant to nitrogen limitation appear normal, although the strain is also somewhat more
83 Surprisingly, homozygous Wisp3 mutant mice appear normal and do not recapitulate any of the morphol
84 ypoplastic, although their early progenitors appear normal and exhibit no premature differentiation o
85 ers of Lrat-/- mice upon histologic analysis appear normal and show no histological signs of liver fi
90 onditions, all stages of virus morphogenesis appeared normal and extracellular virions were detected
91 ertheless, all stages of virus morphogenesis appeared normal and extracellular virions were present o
92 The striatum as well as substantia nigra appeared normal and no loss of dopamine expressing cells
94 Unexpectedly, assembly and morphogenesis appeared normal and the noninfectious virus particles we
95 k or absent, although its adnexal expression appeared normal and the punctate membrane staining of Cx
97 in-1-deficient mice, podocyte ultrastructure appeared normal, and the podocyte proteins synaptopodin,
100 The dopaminergic system of LRRK2(-/-) mice appears normal, and numbers of dopaminergic neurons and
101 acellular signal-regulated kinase) signaling appears normal, and phosphoinositide 3-kinase (PI3K)-pro
103 Germinal centers and plasma cells in tonsils appeared normal, as were serum immunoglobulin levels.
104 ulation, axial patterning of the neural tube appears normal, as assessed by in situ hybridization for
105 Here, we report that alphaMHC-cyclin T1 mice appear normal at baseline yet suffer fulminant apoptotic
108 ufficiency of the Grb2 gene (Grb2(+/-) mice) appear normal at birth but have defective T cell signali
109 calcium, calciotropic hormones, and skeleton appear normal at birth in the offspring of mothers who a
110 disruption of the PURA gene in both alleles appear normal at birth, but at 2 weeks of age, they deve
111 ecifically in lung alveolar epithelial cells appear normal at the age of 6 weeks, when exposed to lon
115 BHD heterozygous knockout (BHDd(/+)) mice appeared normal at birth but developed kidney cysts and
120 sing an osteoprogenitor-specific Cre driver, appeared normal at birth; however, these mice showed sev
130 Mice heterozygous for a Tbx2 null mutation appear normal but homozygous embryos reveal a crucial ro
132 The MUV-E108Q meta I --> meta II transition appeared normal but the MUV-E108Q meta II decay to opsin
133 NA under the control of its native promoter, appeared normal but were male sterile due to delayed ant
135 neural responses in hyperplastic ICC tissues appeared normal but were up-regulated in the cecum, wher
137 Sp-nanos1 and 2 knockdown embryos initially appear normal, but do not develop adult rudiments; altho
138 ith later JHm treatments, extension programs appear normal, but retraction programs are maintained be
139 n 12-month-old knockout mice, photoreceptors appear normal, but the apical processes of the retinal p
140 atellite cell activation and myoblast fusion appear normal, but there is a reduction in early neutrop
141 cells in alpha9, alpha10, and alpha9/10 KOs appeared normal, but a quantitative analysis was not per
142 mon lymphoid progenitors and pre-pro-B cells appeared normal, but cells at subsequent stages of B lym
145 lls, from embryogenesis onwards, osteoblasts appeared normal, but haematopoietic stem and progenitor
146 PS treatment, quantitative parameters of URs appeared normal, but in the two MSG-treated hamsters tha
147 ent cardiomyocytes within the left ventricle appeared normal, but intercellular junctions were ill-fo
148 croRNA guide strand selection by ALG-1(anti) appeared normal, but microRNA* strand release was ineffi
149 ment of key midzone-stabilizing proteins all appeared normal, but microtubule polymerization was neve
150 of Lrp4, the organization of the hippocampus appeared normal, but the frequency of spontaneous releas
155 Cardiovascular and blood pressure regulation appears normal, but the integrity of sympathetic adrener
159 nstrated that quantitative TCR diversity can appear normal despite qualitative changes in repertoire
160 ain activations associated with movement may appear normal despite residual functional impairment.
166 mozygous targeted mutant (Stamp(tm/tm)) mice appear normal except for marked decreases in male fertil
168 have generated dube3a null mutants, and they appear normal externally, but display abnormal locomotiv
169 of conditioned and unconditioned stimuli but appear normal following a more robust five-pairing train
170 s equivalent to one endogenous allele (G0.5) appeared normal for a period of about 3-4 months, but at
171 he healing of serosal injury to intact bowel appeared normal given the reduced inflammatory response.
173 st of the surviving neurons in these animals appeared normal histologically, particularly motor neuro
176 rfollicular epidermis of Fntb-deficient mice appeared normal; however, keratinocytes from these mice
177 ture of corneodesmosomes and tight junctions appeared normal, immunohistochemistry for claudin 1 show
179 cell responses in two viral infection models appear normal in both magnitude and the hierarchy of ant
181 increased cone and rod spacing in areas that appear normal in conventional images, suggesting that ph
183 HSP) 40 at the spokehead-spokestalk juncture appear normal in length and composition but twitch activ
186 ma (Pip4k2c), the gene encoding PI5P4Kgamma, appear normal in regard to growth and viability but have
190 important for callosal axon midline crossing appear normal in the transgenic mice, suggesting that th
200 activation and the number of Ca(2+) channels appeared normal in Cabp2(LacZ/LacZ) mice, as were ribbon
205 the locomotor-stimulating effects of cocaine appeared normal in KOR(-/-) mutants, but was exaggerated
206 ic ganglia and innervation of target tissues appeared normal in mice lacking a core planar cell polar
207 1 foci formation and mitomycin C sensitivity appeared normal in MRG15-binding defective PALB2 mutants
208 omplexes, desmosomes, and basement membranes appeared normal in mutant embryos, indicating that proce
209 ugh thymocyte and splenic T-cell populations appeared normal in mutant mice, T-cell proliferation in
210 t occurs immediately after theta stimulation appeared normal in mutant slices but the newly formed po
213 PD-derived iPS cells containing the mutation appeared normal in phenotypes, karyotype, and pluripoten
220 r of oligodendrocyte progenitor cells (OPCs) appeared normal in the Erk2 conditional knock-out cortex
229 Although at birth the subventricular zone appears normal in mice lacking Hedgehog signaling, by po
236 Spermatogenesis up to and including meiosis appears normal in the absence of GLD2, but post-meiotic
238 e the development of immune cell populations appears normal in these animals, we show enhanced interl
239 the paradoxical picture of a person who may appear "normal" in some aspects, and yet hate himself an
245 Whereas lst-1 and sygl-1 single mutants appear normal, lst-1 sygl-1 double mutants are phenotypi
246 ctedly, that whereas blood vessel morphology appeared normal, lymphatic-blood vessel separation was i
247 ility of heterozygous NS-null (NS(+/-)) mice appeared normal, NS(+/-) mouse embryonic fibroblasts (ME
248 Zymogen granules in the GP2 knock-out mice appeared normal on electron microscopy and contained the
249 While the swimming pattern of mutant cells appeared normal, on swarm plates, mutant cells exhibited
251 cell specification in the anterior pituitary appears normal, patterning in the ventral diencephalon i
252 though light-/dark-adapted total cGMP levels appeared normal, Pde6b(H620Q) homozygotes exhibited depr
255 ed events in both Fyn-/- and Fyn/Lck-/- mice appear normal, reinforcing the theme of redundancy in th
257 the developing brain of MeHg-exposed embryos appeared normal, suggesting that the mechanism leading t
258 ans of null (-/-) mice, cholinergic staining appeared normal, suggesting that the overall gross devel
261 ion of activation-induced cytidine deaminase appear normal, the cell line does not hypermutate an ind
262 While adhesion to fibrinogen and collagen appeared normal, the platelets in thrombi from P2Y12-/-
263 ment of the inner ear and lateral-line organ appeared normal, the sensory epithelium showed progressi
264 Although collagen fibril assembly initially appeared normal, the tendons of Mkx(-/-) embryos express
265 though NFkappaB, c-Jun, and ATF-2 activation appears normal, the LPS-induced activation of IFNbeta re
266 and phenotype of MZ B cells in CD36-/- mice appeared normal, there was a minor block in the transiti
267 gene mutation alone, cerebellar histogenesis appears normal, thereby demonstrating functional redunda
268 hough cells from heterozygous DDB2(+/-) mice appeared normal, these mice had enhanced skin carcinogen
269 angential migration of immature interneurons appears normal, they develop dendritic and axonal proces
271 r alteration in lignin structure, the plants appear normal under standard conditions in the greenhous
273 required for survival, mice that lack RAMP3 appear normal until old age, at which point they have de
281 nd callus tissue produced from rescued seeds appeared normal when grown in the presence of His but ty
282 al white matter architecture and myelination appear normal, when crossed with an antioxidant response
283 vation and subsequent ubiquitination of EGFR appear normal, whereas downstream EGFR degradation is de
286 of recombination proteins AtRAD51 and AtMSH4 appears normal, whereas the numbers of AtMLH1 and AtMLH3
288 Cells transfected with pcDNA3.1 vector alone appeared normal, while cells expressing the PetS260A mut
290 The homozygous Cacng4-targeted mutant mouse appeared normal with no ataxic gait or absence seizures,
291 he NMU peptide-deficient mice, NMUR2 KO mice appeared normal with regard to stress, anxiety, body wei
292 r the engulfment stage, although sporulation appeared normal with the lower levels of gerA or gerK ov
294 the aortic structure of Nec-1s-treated mice appeared normal, with continuous and organized elastin l
295 he Apc-deficient crypts in Apc(CKO/CKO) mice appeared normal, with morphological transformation, incl
296 earts of hyperleptinemic ACS-transgenic mice appeared normal, with normal echocardiograms and cardiac
298 onic lethality, heterozygous ubc13(+/-) mice appeared normal, without alterations in immune cell popu
299 wever, the skin of untreated Cav-1 null mice appeared normal, without any evidence of epidermal hyper
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