ライフサイエンスコーパス: cyclopia

1 of larval eye tissue in the dorsal midline (cyclopia).

2 lling, the stalks are not specified, causing cyclopia.

3 ly been described to show HPE and associated cyclopia.

4 the ventral diencephalon, which resulted in cyclopia.

5 a small, linear heart tube, an open gut and cyclopia.

6 or null alleles of both Nodal and Smad2 have cyclopia.

7 tein core into one-cell stage embryos caused cyclopia.

8 ifested in the head as holoprosencephaly and cyclopia.

9 the response of tissues to SHH, also produce cyclopia.

10 ead structures, abnormal embryo turning, and cyclopia.

11 on stage, displayed rostral head defects and cyclopia.

12 in ventral forebrain development, leading to cyclopia.

13 l neural tube, leading to neural defects and cyclopia.

14 lso absent in oep mutants, leading to severe cyclopia.

15 rosencephaly (a single cerebral hemisphere), cyclopia (a single midline eye), and loss of ventral mid

16 ans, holoprosencephaly (HPE), which includes cyclopia, a phenotype also seen in mice and other verteb

17 y associated with facial anomalies including cyclopia, a primitive nasal structure (proboscis) and/or

18 s include absence of distal limb structures, cyclopia, absence of ventral cell types within the neura

19 d loss of Shh function in the mouse produces cyclopia and alobar forebrain development.

20 brafish development and also exacerbated the cyclopia and axial mesendoderm convergence and extension

21 ibits the Dpp target race and thereby causes cyclopia and defective head involution.

22 disrupts embryonic development, resulting in cyclopia and defects in endoderm, prechordal plate, and

23 njection of wild-type pard3 mRNA resulted in cyclopia and eyeless embryos.

24 The steroidal alkaloid cyclopamine produces cyclopia and holoprosencephaly when administered to gast

25 from reduction of head structures-including cyclopia and holoprosencephaly-to expansion of ventral t

26 en viewed in full, this spectrum ranges from cyclopia and hypotelorism to hypertelorism and facial du

27 Shh null mice have cyclopia and loss of branchial arch structures.

28 nt causes a spectrum of phenotypes including cyclopia and midline bifurcations (MB).

29 ars as potent teratogens capable of inducing cyclopia and other birth defects.

30 bnormal extension of axial tissue results in cyclopia and other midline defects in the head.

31 ggy-winkle hedgehog function exhibit partial cyclopia and other specific midline abnormalities, provi

32 Facial defects in HPE range from cyclopia and proboscis in severe cases to solitary media

33 etion increases the incidence of MB, but not cyclopia, and as such Wnt5b is a "unique" risk factor fo

34 In addition, mutant embryos have partial cyclopia, and defects in jaw cartilage, circulation and

35 , complex craniofacial abnormalities such as cyclopia, and defects in left-right patterning, indicati

36 ding rostral truncations, holoprosencephaly, cyclopia, as well as alterations in the first branchial

37 a teratogenic steroidal alkaloid that causes cyclopia by blocking Sonic hedgehog (Shh) signal transdu

38 ow that two complex dysmorphologies - MB and cyclopia - can be promoted by either common or unique ri

39 The variable phenotypes include cyclopia, holoprosencephaly, and rostral truncations of

40 prechordal plate genes, and the formation of cyclopia in knym119 and trim209 mutants.

41 Here we examine MBs and their relation to cyclopia in maternal-zygotic squint (MZsqt) mutants.

42 There is a concordance of MB with cyclopia in MZsqt embryos.

43 We show that cyclopia in these mutants is not due to an incompetence

44 of the region containing these cells induced cyclopia in wild types.

45 al or complete cyclopia, kny mutants exhibit cyclopia infrequently, while knym119 trim209 double-muta

46 Cyclopia is observed in trilobite (tri) and knypek (kny)

47 show a high frequency of partial or complete cyclopia, kny mutants exhibit cyclopia infrequently, whi

48 Overexpression of pcdh18a in embryos caused cyclopia, mislocalization of hatching gland tissue, and

49 ally, depletion of Wnt11 or Hsp90b increases cyclopia only.

50 complex craniofacial malformations including cyclopia, or both.

51 Our results correlate the cyclopia phenotype with the abnormal location of hh-expr

52 esulting morphological phenotype consists of cyclopia, reduction of cell death, and failure of head i

53 it a variety of facial features ranging from cyclopia to subtle midline asymmetries.