Results from human embryo specimens showed that LIFR mRNA expression was significantly down-regulated in spinal cords of human fetuses with neural tube defects compared with normal controls at a gestational age of 24 to 33 weeks.
We used Moran's I and Getis-Ord Gi* to evaluate spatial clustering for neural tube defects, critical congenital heart defects (CCHDs), and oral clefts among births whose residence geocoded to the ZIP code or finer level.
We used Moran's I and Getis-Ord Gi* to evaluate spatial clustering for neural tube defects, critical congenital heart defects (CCHDs), and oral clefts among births whose residence geocoded to the ZIP code or finer level.
Using ribosomal protein 24 hypomorphic mice (<i>Rpl24<sup>Bst/+</sup></i> ) as a genetic tool to dampen global protein synthesis, we found that <i>Lin28a<sup>-/-</sup>;Rpl24<sup>Bst/+</sup></i> compound mutants exhibited NTDs resembling those seen in <i>Lin28a/b</i> dKO mice.
We also report that p53S decreased expression of UTX at mRNA and protein level via increasing Xist transcript, result in high female-specific H3K27me3 expression and repressed Mash1 transcription, which facilitating abnormal proliferation, differentiation, and apoptosis, result in the mis-regulation of neurodevelopment and neural tube defects (NTDs).
We also report that p53S decreased expression of UTX at mRNA and protein level via increasing Xist transcript, result in high female-specific H3K27me3 expression and repressed Mash1 transcription, which facilitating abnormal proliferation, differentiation, and apoptosis, result in the mis-regulation of neurodevelopment and neural tube defects (NTDs).
Furthermore, doubly heterozygous mouse embryos lacking one copy each of Shroom3 and Folr1 exhibit a low rate of neural tube defects and also have lower levels of activated myosin light chain and MLCK.
This study established the role of transcription factor Sox19b and epigenetic factor EZH2 regulatory network on NSC development, which provides new clues and theoretical guidance for the clinical treatment of neural tube defects.