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1 d aberrant collagen fibers in tibiae of seal homozygous mice.
2 ed by 19% in heterozygous mice and by 69% in homozygous mice.
3 thdrawal (FPW) in wild type mice, but not in homozygous mice.
4 tion of paw withdrawal in both wild type and homozygous mice.
5 ygous mice, but had no significant effect in homozygous mice.
6  no translocation occurred in deltaF508 Cftr homozygous mice.
7 gous mice but the increase was attenuated in homozygous mice.
8  increased in Cx50D47A lenses, especially in homozygous mice.
9 sporters were not significantly decreased in homozygous mice.
10 r of wild-type mice was completely absent in homozygous mice.
11 ficant differences with Zn treatment in male homozygous mice.
12 owed that both cause edema and are lethal in homozygous mice.
13  loss of cerebellar Purkinje neurons in aged homozygous mice.
14 -BP1 and S6 in muscle and adipose tissues of homozygous mice.
15  otoacoustic emissions (SOAEs) in 70% of the homozygous mice.
16  increased in vivo thrombosis, in Pro32Pro33 homozygous mice.
17 gnificantly smaller and less frequent in the homozygous mice.
18 can be used to distinguish heterozygous from homozygous mice.
19 us with more severe deficits detected in the homozygous mice.
20 e of NDUFS4 protein in all tissues tested of homozygous mice.
21 d forkhead box A2 (Foxa2), were decreased in homozygous mice.
22 kidney (but not the brain or fibroblasts) of homozygous mice.
23 d by the early embryonic lethality of HMG-17 homozygous mice.
24 s was not affected by the lack of Arc in GFP homozygous mice.
25 nked with phenotypes of Er-heterozygous and -homozygous mice.
26 activities were significantly reduced in the homozygous mice.
27  weeks of age, the time of seizure onset for homozygous mice.
28 ance in most WT and CF heterozygous, but not homozygous mice.
29 o be essential as has been observed in ERCC1 homozygous -/- mice.
30 d (3H-U69,593) binding were abolished in the homozygous (-/-) mice.
31 ere evaluated in wild-type, heterozygous and homozygous mice 1 week following TBI.
32                                Surprisingly, homozygous mice also displayed threefold enlargement by
33               Eyes of adult heterozygous and homozygous mice also were evaluated histologically.
34  cultures from adult ears and kidneys of Atm homozygous mice and found that these cultures immortaliz
35 recessive trait causing a dwarf phenotype in homozygous mice and has been mapped to the distal region
36 alters inner and outer retinal layers in cbs homozygous mice and older cbs heterozygous mice, and it
37 MYCN) extended tumor latency and survival in homozygous mice and prevented oncogenesis in hemizygous
38 l of PR mRNA in ovariectomized wild-type and homozygous mice, and a marked increase in expression aft
39                  H67D homozygous mice, C294Y homozygous mice, and H67D/C294Y compound heterozygous mi
40        These changes were more severe in the homozygous mice, and were associated with decreased rod
41                  In the cerebella of cdf/cdf homozygous mice, approximately 40% of Purkinje cells are
42                            Nevertheless, the homozygous mice are fertile and are normal in gross appe
43                                              Homozygous mice are hypersusceptible to Staphylococcus a
44                  Cones from PDE6alpha'DeltaC homozygous mice are less sensitive to light, and their r
45 e known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and d
46 served in older homozygous animals, although homozygous mice are smaller than wild type littermates t
47                                              Homozygous mice are viable and fertile and have grossly
48                           The FAT10 knockout homozygous mice are viable and fertile.
49                               However, these homozygous mice are viable, but growth-retarded and infe
50 20(DeltaRRM)mice with a further reduction in homozygous (-/-) mice at only the intact myocyte level.
51 loping GI tract of Ret null heterozygous and homozygous mice at embryonic day (E)12.5 and E14.5.
52                                              Homozygous mice bearing mutated MyBP-C alleles are viabl
53 -V2475F mutation appears embryonic-lethal in homozygous mice, but heterozygous mice have no alteratio
54                                         H67D homozygous mice, C294Y homozygous mice, and H67D/C294Y c
55  in wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice carrying a null mutation of c-fos.
56                                              Homozygous mice carrying a null mutation for the DARPP-3
57                                  Remarkably, homozygous mice carrying the alphaA-R49C mutant exhibit
58  delay, and early-onset cerebellar ataxia in homozygous mice carrying the bi-allelic variant.
59 t dendrite complexity is severely reduced in homozygous mice deficient in Reelin signaling both in vi
60                                              Homozygous mice demonstrate variable expression of abnor
61                    Although normal at birth, homozygous mice develop hindlimb paralysis from Day 13,
62 he uncharacterized L4a domain of LAMA5 where homozygous mice develop nephrotic syndrome with severe p
63                                              Homozygous mice (-/-) develop normally and suffer mild c
64 d onto the PL/J inbred strain, virtually all homozygous mice developed a chronic inflammatory skin di
65                                    JAK2V617F-homozygous mice developed a severe hematopoietic stem ce
66 ted hypertrophic cardiomyopathy (HCM), while homozygous mice developed both HCM and dilated cardiomyo
67                                              Homozygous mice developed severe cataracts early, and he
68                                              Homozygous mice die at embryonic day 14.5 in cardiac fai
69                                         Most homozygous mice die by 3 months.
70                                              Homozygous mice die in utero at embryonic days 11.5-12.5
71                                           As homozygous mice die in utero, we generated FADD-/- embry
72  no death in utero occurred, the majority of homozygous mice die within two weeks after birth.
73 re phenotypically normal, but 50- 85% of the homozygous (-/-) mice died in utero at embryonic day 11.
74                                         Most homozygous mice died during gastrulation and organogenes
75  The majority ( approximately 90%) of double-homozygous mice died during the neonatal period.
76                                      All the homozygous mice died perinatally.
77                                              Homozygous mice died within 12 h of birth.
78                                              Homozygous mice display defects consistent with HGPS, in
79                     The Tmprss3(A306T/A306T) homozygous mice display delayed onset progressive hearin
80                                              Homozygous mice displayed a stem cell-intrinsic defect i
81              Lens fiber cells of alphaA-R49C homozygous mice displayed an increase in cell death by a
82                                          The homozygous mice displayed elevated islet hA that correla
83 n CD18 was generated by gene targeting, with homozygous mice displaying increased circulating neutrop
84 n an embryonic failure of NMJ formation, and homozygous mice do not survive postpartum.
85                                   Ed deleted homozygous mice (Ed-/-) have moderately reduced numbers
86                                In the normal homozygous mice, electrical field stimulation caused a b
87                                Unexpectedly, homozygous mice (Elovl4(del/del)) display scaly, wrinkle
88 nsive defects were found in the brain of the homozygous mice, especially in the ventral region of the
89                                 Pde6b(H620Q) homozygous mice exhibit a hypomorphic phenotype with par
90                                   Pudgy (pu) homozygous mice exhibit clear patterning defects at the
91 al and do not develop brachydactyly, whereas homozygous mice exhibit features resembling RRS.
92                                   RAG1-S723C homozygous mice exhibit impaired lymphocyte development
93                                        R249Q homozygous mice exhibited cardiac conduction abnormaliti
94                                     However, homozygous mice exhibited complete deafness, as well as
95 did not exhibit retinal degeneration whereas homozygous mice exhibited progressive retinal degenerati
96                               Ets1(DeltaVII) homozygous mice express no p51-Ets1 and elevated levels
97  transmission were bred to homozygosity, the homozygous mice expressed no GUS enzyme activity but exp
98 e of congenital hypothyroid goiter; further, homozygous mice expressing two cog/cog alleles (linked t
99 formation and bone mass in both F508del-Cftr homozygous mice (F508del Cftr(tm1Eur)) and Cftr(+/+) lit
100                                        Clock homozygous mice failed to show the dramatic increase in
101                                              Homozygous mice for all three mutations were fetal letha
102            The supermodel mutation protected homozygous mice from high fat diet-induced obesity, like
103                 Microphthalmic eyes of adult homozygous mice had a poorly developed cornea, and the a
104                             Furthermore, the homozygous mice had no thyroid gland but had a normal pa
105  and cell size is also found in hypomorphic, homozygous mice harboring a single amino acid mutation (
106                                  Remarkably, homozygous mice harbouring the cyclin B1 mitosis degrada
107 f these viable Fli1(DeltaCTA)/Fli1(DeltaCTA) homozygous mice has reduced platelet numbers.
108                                       Double homozygous mice have characteristic defects of the crani
109                                     Affected homozygous mice have no detectable GALNS enzyme activity
110                                              Homozygous mice have PCD characterized by hydrocephalus,
111 zygous Fli1(DeltaCTA) mice are viable, while homozygous mice have reduced viability.
112                                              Homozygous mice have significantly smaller spleens and t
113                                           No homozygous mice however were identified at birth, consis
114 ect along the anterior-posterior axis in all homozygous mice identified.
115 stablished with wild-type, heterozygous, and homozygous mice in a Mendelian ratio.
116 R activity in the nasal airways of DeltaF508 homozygous mice in vivo.
117                            The defect in tlt homozygous mice is limited to the utricle and saccule of
118 t the defect in development in CD8 transgene homozygous mice is the result of a reduction in secondar
119                             However, 100% of homozygous mice lack most or all of their corpus callosu
120                                        c-Fos homozygous mice lack osteoclasts with a failure of the t
121 a3 gene by deletion of exon 5 and found that homozygous (-/-) mice lacked detectable mRNA on Northern
122 se oligonucleotides and in the skin of Acra7 homozygous mice lacking alpha7 nAChR channels.
123                                              Homozygous mice lacking D3 receptors display increased l
124 e observed alterations of eye development in homozygous mice leading to severe anatomical and morphol
125 he accumulation of H2B-GFP in the nucleus of homozygous mice led to apoptosis within 2 weeks.
126 genesis in AFB1-treated p53 heterozygous and homozygous mice not expressing HBsAg.
127       We assessed the phenotypic spectrum of homozygous mice (Nphs1(tm1Rkl)/Nphs1(tm1Rkl)) compared t
128                                The number of homozygous mice observed was lower than expected under m
129                                              Homozygous mice of both sexes also lack preputial glands
130 as found to be concentration dependent, with homozygous mice presenting extremely high toxicity, whil
131 IL-4Ralpha-/-, beta2-microglobulin-/- double homozygous mice produced less IL-4 than did either IL-4R
132                                      NMJs in homozygous mice progressively degrade postnataly.
133 173Q mice were embryonic lethal, while R167Q homozygous mice (R167Q+/+) had ~5% of normal HMBS activi
134                                    When L9'A homozygous mice received a 10 mg/kg nicotine injection,
135 on of cartilage link protein gene (Crtl1) in homozygous mice resulted in a severe chondrodysplasia an
136                                 In contrast, homozygous mice (RLC-/-) had no RLC-f mRNA or protein an
137                                              Homozygous mice show large reductions in brain tissue mo
138                                 Themis(I23N) homozygous mice show reduced CD4(+) and CD8(+) T lymphoc
139 nloaded cardiomyocytes from heterozygous and homozygous mice showed reduced basal sarcomere length wi
140                  Islets from RIPCre;KD-mTOR (Homozygous) mice showed reduced mTORC1 and mTORC2 signal
141 in a gene dosage-dependent fashion, with the homozygous mice showing the greatest protection.
142 ss IA Pi3k catalytic subunits; nevertheless, homozygous mice still displayed hypoglycaemia, lower ins
143 enylalanine, or succinylacetone-increased in homozygous mice, suggesting that swst mutants provide a
144 ular damage beginning at 3 weeks of age, and homozygous mice supported up to 97% parenchymal repopula
145                                           No homozygous mice survive postnatally.
146                           Tbx5 deficiency in homozygous mice (Tbx5(del/del)) decreased expression of
147 sis of ALS and FTLD-TDP, we generated TDP-25 homozygous mice (TgTDP-25(+/+)), thereby further increas
148 roexcitatory changes were more pronounced in homozygous mice than in heterozygotes, consistent with t
149  spontaneous null allele of Ednrb results in homozygous mice that are predominantly white and die as
150                                              Homozygous mice that do not express K4 develop a spectru
151 uman osteocalcin promoter, were crossed with homozygous mice that express loxP-flanked Cnb1 (Cnb1(f/f
152  Med30 causing progressive cardiomyopathy in homozygous mice that, although viable during lactation,
153                                           In homozygous mice, the extent of anemia generally correlat
154 the most severe phenotype is observed in the homozygous mice, this model will still provide a test-be
155  therefore used the skin of heterozygous and homozygous mice to create a cDNA library, and we report
156        In contrast, EGFPf-positive DRGs from homozygous mice (TRPM8(EGFPf/EGFPf)) had drastically red
157                                     In these homozygous mice, we observed increased intrinsic efficac
158 for wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were 92%, 53%, and <5%, respective
159 n or obese (gold-thioglucose [GTG]-injected) homozygous (-/-) mice were compared with lean or obese a
160 Tes wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were divided into four groups: mic
161              The corneas of heterozygous and homozygous mice were characterized by clinical observati
162     mEC layer II neurons of heterozygous and homozygous mice were hyperexcitable and generated long-l
163                                 Mertk(nmf12) homozygous mice were mated to mice lacking the entire Tn
164                                 Accordingly, homozygous mice were more severely affected than heteroz
165 tion for the D252H mutant protein, the D252H homozygous mice were more severely affected than null ho
166 gical and developmental abnormalities, while homozygous mice were non-viable.
167                   The embryonic and neonatal homozygous mice were reduced in size by approximately 25
168               In a humanized mouse model, AA homozygous mice were similarly protected against stress-
169       Compared to wild-type mice, the GNPTAB homozygous mice were smaller, had elevated levels of ser
170                                The lenses of homozygous mice were the first to opacify at any given d
171                                              Homozygous mice were used instead of the more commonly u
172 c microvesicular steatosis in pubescent male homozygous mice, which is absent in transgenic females.
173                                              Homozygous mice with a null mutation in the MMP-9/gelati
174   Most importantly, chronic treatment of the homozygous mice with naltrexone did not produce the expe
175                                              Homozygous mice with the equivalent P465L mutation die i
176 In another mouse model using female NCr nude homozygous mice with U87 xenografts, tumor growth was si
177 2 months of age in the Alb-Cre+/-/Cprlox+/+ (homozygous) mice, with corresponding decreases in liver
178      Interestingly, while such a mutation in homozygous mice would lead to limited survival of approx

 
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