D
Diana M. Juriloff
Researcher at University of British Columbia
Publications - 68
Citations - 3237
Diana M. Juriloff is an academic researcher from University of British Columbia. The author has contributed to research in topics: Exencephaly & Neural tube. The author has an hindex of 29, co-authored 68 publications receiving 3105 citations. Previous affiliations of Diana M. Juriloff include McGill University.
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Journal ArticleDOI
Evidence for multi‐site closure of the neural tube in humans
Margot I. Van Allen,Dagmar K. Kalousek,Gerold F. Chernoff,Diana M. Juriloff,Muriel J. Harris,Barbara McGillivray,Siu-Li Yong,Sylvie Langlois,Patrick MacLeod,David Chitayat,Jan M. Friedman,R. Doug Wilson,Deborah E. McFadden,J T Pantzar,Susan Ritchie,Judith G. Hall +15 more
TL;DR: With the multi-site NT closure model, it is found that the majority of NTDs can be explained by failure of fusion of one of the closures or their contiguous neuropores.
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An update to the list of mouse mutants with neural tube closure defects and advances toward a complete genetic perspective of neural tube closure
TL;DR: The many NTD mutants are the foundation for a future complete genetic understanding of the processes of neural fold elevation and fusion along mechanistically distinct cranial-caudal segments of the neural tube, and they point to several candidate processes for study in human NTD etiology.
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Mouse mutants with neural tube closure defects and their role in understanding human neural tube defects.
TL;DR: If the human homologs of the mouse NTD mutants contribute to risk of common human NTDs, it seems likely to be in multifactorial combinations of hypomorphs and low-penetrance heterozygotes, as exemplified by mouse digenic mutants and the oligogenic SELH/Bc strain.
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Mouse models for neural tube closure defects
TL;DR: The genes mutated in several mouse NTD models involve actin regulation, support the postulated key role of actin in neural fold elevation, and may be a good candidate pathway to search for human NTD genes.
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A consideration of the evidence that genetic defects in planar cell polarity contribute to the etiology of human neural tube defects.
TL;DR: Results demonstrate that PCP gene alterations contribute to the etiology of human NTDs, and it is recommended that future research should explore other types ofPCP gene variant such as regulatory mutations and low frequency deleterious polymorphisms.