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@ARTICLE{Zhao2006,
author = {Zhao, L. and Wang, G. and Lu, D. and Wu, J. and Song, F. and Dong,
J. and Bi, Z. and Li, Y.},
title = {Homocysteine, hRIP3 and congenital cardiovascular malformations},
journal = {Anat Embryol (Berl)},
year = {2006},
volume = {211},
pages = {203-12},
number = {3},
note = {WHAT I DON'T WANT TO BE PUBLISHED IN THE FINAL DOCUMENT},
abstract = {Elevated serum homocysteine (Hcys) levels have been suggested to contribute
to congenital cardiovascular malformations, neural tube defects,
and cardiovascular diseases. To investigate the mechanisms resulting
in cardiovascular diseases and birth defects, Kuang-Hueih Chen et
al. identified and characterized a novel gene, named rHCY2, whose
expression was markedly up-regulated when Hcys was elevated in rat.
In vivo, rHCY2 gene could induce chicken embryonic cells apoptosis
and embryonic malformations. Its N-terminal kinase domain is apparently
similar to human receptor-interacting serine-threonine kinase 3 (hRIP3).
In view of this, we hypothesize that a link between the teratogenic
effects of Hcys and hRIP3 is theoretically plausible. However, given
the lack of data on the topic, it remains to be seen whether an elevated
serum Hcys level will increase the expression of hRIP3. Using normal
and abnormal human fetal hearts and cultured normal human fetal cardiomyocytes,
we show that congenital cardiovascular malformations are associated
with the overexpression of hRIP3, and evidence is found for a certain
association between overexpression of hRIP3 and homocysteine-induced
congenital cardiovascular malformations. Folic acid and anti-hRIP3
antibodies seem to favor maintenance of the shape and ultrastructure
of cultured human fetal cardiomyocytes.},
keywords = {Amino Acid Sequence Animals Cells, Cultured Heart/embryology/physiology
Heart Defects, Congenital/*embryology/*enzymology/pathology Homocysteine/*physiology
Humans Mice Molecular Sequence Data Myocytes, Cardiac/enzymology/ultrastructure
Protein Kinases/genetics/*physiology Receptor-Interacting Protein
Serine-Threonine Kinases}
} |
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