## Abstract ## BACKGROUND Neural tube defects (NTDs) are congenital malformations arising mostly from incomplete neural tube closure during early embryogenesis. Most NTDs in humans have a complex etiology, with involvement of both genetic and environmental factors. More than 100 mouse models for h
Failure of homocysteine to induce neural tube defects in a mouse model
β Scribed by Gregory D. Bennett; Janee VanWaes; Kristine Moser; Tammy Chaudoin; Lois Starr; Thomas H. Rosenquist
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 127 KB
- Volume
- 77
- Category
- Article
- ISSN
- 1542-9733
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
## BACKGROUND: Valproic acid (VPA) causes the failure of neural tube closure in newborn mice. However, the molecular mechanism of its teratogenesis is unknown. This study was conducted to investigate the genomewide effects of VPA disruption of normal neural tube development in mice. METHODS: Micro
## Abstract The number of mouse mutants and strains with neural tube defects (NTDs) now exceeds 240, including 205 representing specific genes, 30 for unidentified genes, and 9 multifactorial strains. These mutants identify genes needed for embryonic neural tube closure. Reports of 50 new NTD mutan
## Abstract In this paper, we trace the history of current research into the genetic and biochemical mechanisms that underlie folateβpreventable neural tube defects (NTDs). The inspired suggestion by Smithells that common vitamins might prevent NTDs ignited a decade of biochemical investigationsβfi
Neural tube defects (NTDs), although prevalent and easily diagnosed, are etiologically heterogeneous, rendering mechanistic interpretation problematic. To date, there is evidence that mammalian neural tube closure (NTC) initiates and fuses intermittently at four discrete locations. Disruption of thi