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1  but not midline, cell remodeling results in exencephaly.
2 rom dams maintained on the FD diet exhibited exencephaly.
3 vere cranial neural tube closure defects and exencephaly.
4 ng on genetic background, they may also have exencephaly.
5 type that included intracranial bleeding and exencephaly.
6  also develop head defects characteristic of exencephaly.
7 enoid bone, with 50% of mice also exhibiting exencephaly.
8 renal agenesis, abnormal cranial ganglia and exencephaly.
9 iation carcinogenesis and a low frequency of exencephaly.
10 t embryos develop spina bifida and sometimes exencephaly.
11 ia; some homozygotes develop hydrocephaly or exencephaly.
12 in the mouse neural tube and fully penetrant exencephaly.
13 lasia, cleft palate, mid-facial clefting and exencephaly.
14  incidence of NTDs, such as spina bifida and exencephaly.
15 mice show perinatal lethality resulting from exencephaly, a defect caused by failed closure of the cr
16 o close the anterior neural tube and develop exencephaly, a perinatal lethal condition.
17               Over-expression of Irf6 caused exencephaly, a rostral neural tube defect, through suppr
18 ver half of homozygous KO embryos exhibiting exencephaly, a severe defect in neural tube closure.
19  are a major cause of infant mortality, with exencephaly accounting for nearly one-third of cases.
20 ve identified a mutation in mice that causes exencephaly, acrania, facial clefting, and spina bifida,
21 a cranial neural tube defect that results in exencephaly and a marked reduction in skeletal muscle ma
22 ndbrain and spinal cord at E10.5, as well as exencephaly and abnormal spinal cord morphology.
23 ssages, abnormal development of the maxilla, exencephaly and anophthalmia.
24  a complex phenotype including spina bifida, exencephaly and cardiac outflow tract abnormalities.
25      Only 6% of Hspg2-/- mice developed both exencephaly and chondrodysplasia.
26                               Interestingly, exencephaly and cleft palate were never observed in the
27 tants die perinatally and frequently exhibit exencephaly and cranioschesis.
28 caused specific embryonic lethal phenotypes (exencephaly and edema) in most fetuses.
29 h no overt phenotype; the Rala null leads to exencephaly and embryonic lethality.
30 tor degeneration and its ablation results in exencephaly and neonatal death.
31 e the neural tube and optic fissure, causing exencephaly and retinal coloboma, common birth defects.
32 m had neural tube defects consisting of both exencephaly and spina bifida occulta, an unusual combina
33 he neural tube defects observed include both exencephaly and spina bifida, and the phenotype exhibits
34 nd posterior neuropore closure and developed exencephaly and spina bifida, important human congenital
35 nt embryos display genetically co-segregated exencephaly and spina bifida, recapitulating the phenoty
36 r and posterior neuropore closure leading to exencephaly and spina bifida.
37 requency of Trp53(YC/YC) female embryos with exencephaly and the death of most Trp53(YC/YC) female ne
38 ition, Brg1 heterozygotes are predisposed to exencephaly and tumors.
39 emale Cd embryos were most likely to display exencephaly and were more responsive than males to the F
40 ube closure including craniorachischisis and exencephaly and/or a wavy neural tube.
41  structures and included open defects (i.e., exencephaly) and gross maldevelopment.
42 (2H) homozygotes develop NTDs, both cranial (exencephaly) and spinal (spina bifida).
43 ns, including brain anomalies such as HPE or exencephaly, and digital anomalies such as absent thumbs
44 ry variable neurological features (including exencephaly, and frontal/occipital encephalocele) that w
45 ndibular hypoplasia, cleft secondary palate, exencephaly, and median facial cleft, which are among th
46  of the facial midline, cleft lip, extensive exencephaly, and microphthalmia or anophthalmia.
47 se to partially rescued embryos with massive exencephaly, and polydactyly and branched digits in the
48 diabetes-induced spina bifida aperta but not exencephaly, and this increase was shown to be associate
49 e to close the cranial neural tube, known as exencephaly/anencephaly, is a lethal congenital defect.
50 te gestation and exhibited heart defects and exencephaly, arising from defective closure of the midbr
51 mouse embryos exhibit the neural tube defect exencephaly associated with abnormal cranial mesenchyme.
52 ENU-induced open mind (opm) mutation exhibit exencephaly associated with defects in head mesenchyme d
53 ncluding macrostomia (craniofacial defects), exencephaly, body wall defects, tracheoesophageal fistul
54 ementation reduced the recurrence risk of Cd exencephaly by as much as 55%.
55 ns involving CCD2 (Specc1l CCD2) resulted in exencephaly, cleft palate and ventral body wall closure
56 cond half of development, including acrania, exencephaly, cleft palate, limb abnormalities and omphal
57 el mouse mutant (cleft lip/palate, edema and exencephaly; Clpex) with a hypo-morphic mutation in Post
58                                              Exencephaly, coloboma, and abnormal proliferation in hum
59 Crooked tail ( Cd ), a mouse strain prone to exencephaly, could provide a genetic animal model for fo
60  homozygous embryos die in utero and exhibit exencephaly, defects in neural tube closure, enlarged cr
61 ing failure of anterior neural tube closure (exencephaly), failure of digit septation (syndactyly), a
62  brain also were supported by the finding of exencephaly in about 15% of rybp heterozygous mutant emb
63 Gli3R expression, but not Gli2 loss, rescued exencephaly in Gpr161 knockout mice.
64 dependent Shh signalling appears to underlie exencephaly in mutant embryos.
65                    We also report occasional exencephaly in Nf1(-/-) mice and identify more subtle CN
66  Shmt1(+/-) and Shmt1(-/-) embryos exhibited exencephaly in response to maternal folate and choline d
67              Diabetes predominantly leads to exencephaly, induces neuroepithelial cell apoptosis and
68                                          The exencephaly is due to a primary failure of neurulation,
69                                              Exencephaly is the prominent type of defect and leads to
70 orsal neural tube is not sufficient to cause exencephaly; it appears to also depend on the action of
71 bit expansion of neural progenitor cells and exencephaly-like protrusions.
72 null mice including complete renal agenesis, exencephaly, limb and anal deformities.
73 rum of brain developmental defects including exencephaly, microcephaly, HPE, and abnormalities in emb
74 multaneous deletion of Dlx5 and 6 results in exencephaly of the anterior brain; despite this defect,
75 mbryonic lethality with e12.5 embryos having exencephaly, pericardial edema, cleft palate and abnorma
76                                          The exencephaly phenotype is exacerbated in Rala(-/-);Ralb(+
77 ages, compromised spermatogenesis, and fetal exencephaly, rendering them less amenable to studying th
78              About 9% of the mutants exhibit exencephaly secondary to a defect in neural tube closure
79 embryos show multiple developmental defects (exencephaly, situs viscerum inversus, delay in turning,
80 (ffe/ffe) mutants exhibit NTDs consisting of exencephaly, spina bifida and forebrain truncations, whi
81 bryonic lethality at E14-E17 associated with exencephaly, syndactyly, placentopathy, and kidney defec
82                               These included exencephaly, transformation of cervical segments, and ri
83                                              Exencephaly was observed only in Shmt1(-/-) embryos isol
84 id-gestation embryos had spina bifida and/or exencephaly, whereas wild-type animals of the same genet