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1 weeks of age, the time of seizure onset for 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 loss of cerebellar Purkinje neurons in aged homozygous mice.
8 gous mice but the increase was attenuated 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 -BP1 and S6 in muscle and adipose tissues of homozygous mice.
12 otoacoustic emissions (SOAEs) in 70% of the homozygous mice.
13 increased in vivo thrombosis, in Pro32Pro33 homozygous mice.
14 d aberrant collagen fibers in tibiae of seal homozygous mice.
15 can be used to distinguish heterozygous from homozygous mice.
16 us with more severe deficits detected in the homozygous mice.
17 e of NDUFS4 protein in all tissues tested of homozygous mice.
18 d forkhead box A2 (Foxa2), were decreased in homozygous mice.
19 d by the early embryonic lethality of HMG-17 homozygous mice.
20 increased in Cx50D47A lenses, especially in homozygous mice.
21 s was not affected by the lack of Arc in GFP homozygous mice.
22 nked with phenotypes of Er-heterozygous and -homozygous mice.
23 activities were significantly reduced in the homozygous mice.
24 ance in most WT and CF heterozygous, but not homozygous mice.
25 o be essential as has been observed in ERCC1 homozygous -/- mice.
26 d (3H-U69,593) binding were abolished in the homozygous (-/-) mice.
30 cultures from adult ears and kidneys of Atm homozygous mice and found that these cultures immortaliz
31 recessive trait causing a dwarf phenotype in homozygous mice and has been mapped to the distal region
32 alters inner and outer retinal layers in cbs homozygous mice and older cbs heterozygous mice, and it
33 MYCN) extended tumor latency and survival in homozygous mice and prevented oncogenesis in hemizygous
34 l of PR mRNA in ovariectomized wild-type and homozygous mice, and a marked increase in expression aft
40 e known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and d
41 served in older homozygous animals, although homozygous mice are smaller than wild type littermates t
45 20(DeltaRRM)mice with a further reduction in homozygous (-/-) mice at only the intact myocyte level.
47 -V2475F mutation appears embryonic-lethal in homozygous mice, but heterozygous mice have no alteratio
49 in wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice carrying a null mutation of c-fos.
52 t dendrite complexity is severely reduced in homozygous mice deficient in Reelin signaling both in vi
56 d onto the PL/J inbred strain, virtually all homozygous mice developed a chronic inflammatory skin di
63 re phenotypically normal, but 50- 85% of the homozygous (-/-) mice died in utero at embryonic day 11.
71 n CD18 was generated by gene targeting, with homozygous mice displaying increased circulating neutrop
76 nsive defects were found in the brain of the homozygous mice, especially in the ventral region of the
83 transmission were bred to homozygosity, the homozygous mice expressed no GUS enzyme activity but exp
84 e of congenital hypothyroid goiter; further, homozygous mice expressing two cog/cog alleles (linked t
85 formation and bone mass in both F508del-Cftr homozygous mice (F508del Cftr(tm1Eur)) and Cftr(+/+) lit
91 and cell size is also found in hypomorphic, homozygous mice harboring a single amino acid mutation (
103 t the defect in development in CD8 transgene homozygous mice is the result of a reduction in secondar
106 a3 gene by deletion of exon 5 and found that homozygous (-/-) mice lacked detectable mRNA on Northern
109 e observed alterations of eye development in homozygous mice leading to severe anatomical and morphol
113 IL-4Ralpha-/-, beta2-microglobulin-/- double homozygous mice produced less IL-4 than did either IL-4R
116 on of cartilage link protein gene (Crtl1) in homozygous mice resulted in a severe chondrodysplasia an
122 ss IA Pi3k catalytic subunits; nevertheless, homozygous mice still displayed hypoglycaemia, lower ins
123 ular damage beginning at 3 weeks of age, and homozygous mice supported up to 97% parenchymal repopula
126 sis of ALS and FTLD-TDP, we generated TDP-25 homozygous mice (TgTDP-25(+/+)), thereby further increas
127 roexcitatory changes were more pronounced in homozygous mice than in heterozygotes, consistent with t
128 spontaneous null allele of Ednrb results in homozygous mice that are predominantly white and die as
130 uman osteocalcin promoter, were crossed with homozygous mice that express loxP-flanked Cnb1 (Cnb1(f/f
131 Med30 causing progressive cardiomyopathy in homozygous mice that, although viable during lactation,
133 the most severe phenotype is observed in the homozygous mice, this model will still provide a test-be
134 therefore used the skin of heterozygous and homozygous mice to create a cDNA library, and we report
137 for wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were 92%, 53%, and <5%, respective
138 n or obese (gold-thioglucose [GTG]-injected) homozygous (-/-) mice were compared with lean or obese a
139 Tes wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were divided into four groups: mic
141 mEC layer II neurons of heterozygous and homozygous mice were hyperexcitable and generated long-l
147 c microvesicular steatosis in pubescent male homozygous mice, which is absent in transgenic females.
149 Most importantly, chronic treatment of the homozygous mice with naltrexone did not produce the expe
151 2 months of age in the Alb-Cre+/-/Cprlox+/+ (homozygous) mice, with corresponding decreases in liver
152 Interestingly, while such a mutation in homozygous mice would lead to limited survival of approx
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