Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice-Reference-Cited by-同舟云学术

Disruption of Slc52a3 gene causes neonatal lethality with riboflavin deficiency in mice

Published:2016-06 Issue:1 Volume:6 Page:
ISSN:2045-2322
Container-title:Scientific Reports
language:en
Short-container-title:Sci Rep

Author:

Yoshimatsu Hiroki,Yonezawa Atsushi,Yamanishi Kaori,Yao Yoshiaki,Sugano Kumiko,Nakagawa Shunsaku,Imai Satoshi,Omura Tomohiro,Nakagawa Takayuki,Yano Ikuko,Masuda Satohiro,Inui Ken-ichi,Matsubara Kazuo

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/srep27557.pdf

Reference41 articles.

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2. Powers, H. J. Riboflavin (vitamin B-2) and health. Am J Clin Nutr 77, 1352–1360 (2003).

3. Robitaille, J., Carmichael, S. L., Shaw, G. M. & Olney, R. S. Maternal nutrient intake and risks for transverse and longitudinal limb deficiencies: data from the National Birth Defects Prevention Study, 1997–2003. Birth Defects Res A Clin Mol Teratol 85, 773–779 (2009).

4. Smedts, H. P. et al. Maternal intake of fat, riboflavin and nicotinamide and the risk of having offspring with congenital heart defects. Eur J Nutr 47, 357–365 (2008).

5. Foraker, A. B., Khantwal, C. M. & Swaan, P. W. Current perspectives on the cellular uptake and trafficking of riboflavin. Adv Drug Deliv Rev 55, 1467–1483 (2003).

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