期刊
NUCLEIC ACIDS RESEARCH
卷 35, 期 12, 页码 3963-3973出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkm355
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资金
- NIDDK NIH HHS [R01 DK047320, DK47320, DK52963, R56 DK047320, R01 DK052963] Funding Source: Medline
- NINDS NIH HHS [R01 NS40302, R01 NS040302] Funding Source: Medline
Selenoprotein P (Sel P) is a selenium-rich glycoprotein believed to play a key role in selenium ( Se) transport throughout the body. Development of a Sel P knockout mouse model has supported this notion and initial studies have indicated that selenium supply to various tissues is differentially affected by genetic deletion of Sel P. Se in the form of the amino acid, selenocysteine, is incorporated into selenoproteins at UGA codons. Thus, Se availability affects not only selenoprotein levels, but also the turnover of selenoprotein mRNAs via the nonsense-mediated decay pathway. We investigated how genetic deletion of Sel P in mice affected levels of the mRNAs encoding all known members of the murine selenoprotein family, as well as three non-selenoprotein factors involved in their synthesis, selenophosphate synthetase 1 (SPS1), SECIS-binding protein 2 (SBP2) and SECp43. Our findings present a comprehensive description of selenoprotein mRNA expression in the following murine tissues: brain, heart, intestine, kidney, liver, lung, spleen and testes. We also describe how abundance of selenoproteins and selenoprotein-synthesis factors are affected by genetic deletion of Sel P in some of these tissues, providing insight into how the presence of this selenoprotein influences selenoprotein mRNA levels, and thus, the selenoproteome.
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