GlutaredoxinV1, Main, Exploration, bibRecord, 000416

Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.

Identifieur interne : 000416 ( Main/Exploration ); précédent : 000415; suivant : 000417

Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.

Auteurs : Ryuta Tobe [États-Unis] ; Bradley A. Carlson [États-Unis] ; Jang Hoe Huh [Corée du Sud] ; Nadia P. Castro [États-Unis] ; Xue-Ming Xu [États-Unis] ; Petra A. Tsuji [États-Unis] ; Sang-Goo Lee [États-Unis] ; Jeyoung Bang [Corée du Sud] ; Ji-Woon Na [Corée du Sud] ; Young-Yun Kong [Corée du Sud] ; Daniel Beaglehole [États-Unis] ; Eileen Southon [États-Unis] ; Harold Seifried [États-Unis] ; Lino Tessarollo [États-Unis] ; David S. Salomon [États-Unis] ; Ulrich Schweizer [Allemagne] ; Vadim N. Gladyshev [États-Unis] ; Dolph L. Hatfield [États-Unis] ; Byeong Jae Lee [Corée du Sud]

Source :

The Biochemical journal [ 1470-8728 ] ; 2016.

RBID : pubmed:27208177

Descripteurs français

KwdFr :
- Animaux (MeSH), Disulfure de glutathion (métabolisme), Foie (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Glutathion (métabolisme), Homéostasie (génétique), Homéostasie (physiologie), Humains (MeSH), Lignée cellulaire (MeSH), Oxydoréduction (MeSH), Phosphate de pyridoxal (métabolisme), Phosphotransferases (génétique), Phosphotransferases (métabolisme), Souris (MeSH), Souris knockout (MeSH).
MESH :
- génétique : Glutarédoxines, Homéostasie, Phosphotransferases.
- métabolisme : Disulfure de glutathion, Foie, Glutarédoxines, Glutathion, Phosphate de pyridoxal, Phosphotransferases.
- physiologie : Homéostasie.
- Animaux, Humains, Lignée cellulaire, Oxydoréduction, Souris, Souris knockout.

English descriptors

KwdEn :
- Animals (MeSH), Cell Line (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Glutathione (metabolism), Glutathione Disulfide (metabolism), Homeostasis (genetics), Homeostasis (physiology), Humans (MeSH), Liver (metabolism), Mice (MeSH), Mice, Knockout (MeSH), Oxidation-Reduction (MeSH), Phosphotransferases (genetics), Phosphotransferases (metabolism), Pyridoxal Phosphate (metabolism).
MESH :
- chemical , genetics : Glutaredoxins, Phosphotransferases.
- chemical , metabolism : Glutaredoxins, Glutathione, Glutathione Disulfide, Phosphotransferases, Pyridoxal Phosphate.
- genetics : Homeostasis.
- metabolism : Liver.
- physiology : Homeostasis.
- Animals, Cell Line, Humans, Mice, Mice, Knockout, Oxidation-Reduction.

Abstract

Selenophosphate synthetase (SPS) was initially detected in bacteria and was shown to synthesize selenophosphate, the active selenium donor. However, mammals have two SPS paralogues, which are designated SPS1 and SPS2. Although it is known that SPS2 catalyses the synthesis of selenophosphate, the function of SPS1 remains largely unclear. To examine the role of SPS1 in mammals, we generated a Sps1-knockout mouse and found that systemic SPS1 deficiency led to embryos that were clearly underdeveloped by embryonic day (E)8.5 and virtually resorbed by E14.5. The knockout of Sps1 in the liver preserved viability, but significantly affected the expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione transferase Omega 1 (GSTO1). To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma (EC) cell line, which affected the glutathione system proteins and accordingly led to the accumulation of hydrogen peroxide in the cell. Furthermore, we found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 played a role in supporting and/or sustaining cancer. In addition, the overexpression of mouse or human GLRX1 led to a reversal of observed increases in reactive oxygen species (ROS) in the F9 SPS1/GLRX1-deficient cells and resulted in levels that were similar to those in F9 SPS1-sufficient cells. The results suggested that SPS1 is an essential mammalian enzyme with roles in regulating redox homoeostasis and controlling cell growth.

DOI: 10.1042/BCJ20160393
PubMed: 27208177
PubMed Central: PMC5094348

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Bang, Jeyoung" sort="Bang, Jeyoung" uniqKey="Bang J" first="Jeyoung" last="Bang">Jeyoung Bang</name>
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<author><name sortKey="Beaglehole, Daniel" sort="Beaglehole, Daniel" uniqKey="Beaglehole D" first="Daniel" last="Beaglehole">Daniel Beaglehole</name>
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<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
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<author><name sortKey="Southon, Eileen" sort="Southon, Eileen" uniqKey="Southon E" first="Eileen" last="Southon">Eileen Southon</name>
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<author><name sortKey="Seifried, Harold" sort="Seifried, Harold" uniqKey="Seifried H" first="Harold" last="Seifried">Harold Seifried</name>
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<author><name sortKey="Tessarollo, Lino" sort="Tessarollo, Lino" uniqKey="Tessarollo L" first="Lino" last="Tessarollo">Lino Tessarollo</name>
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<author><name sortKey="Salomon, David S" sort="Salomon, David S" uniqKey="Salomon D" first="David S" last="Salomon">David S. Salomon</name>
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<author><name sortKey="Schweizer, Ulrich" sort="Schweizer, Ulrich" uniqKey="Schweizer U" first="Ulrich" last="Schweizer">Ulrich Schweizer</name>
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<author><name sortKey="Hatfield, Dolph L" sort="Hatfield, Dolph L" uniqKey="Hatfield D" first="Dolph L" last="Hatfield">Dolph L. Hatfield</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Lee, Byeong Jae" sort="Lee, Byeong Jae" uniqKey="Lee B" first="Byeong Jae" last="Lee">Byeong Jae Lee</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.</title>
<author><name sortKey="Tobe, Ryuta" sort="Tobe, Ryuta" uniqKey="Tobe R" first="Ryuta" last="Tobe">Ryuta Tobe</name>
<affiliation wicri:level="2"><nlm:affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Carlson, Bradley A" sort="Carlson, Bradley A" uniqKey="Carlson B" first="Bradley A" last="Carlson">Bradley A. Carlson</name>
<affiliation wicri:level="2"><nlm:affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Huh, Jang Hoe" sort="Huh, Jang Hoe" uniqKey="Huh J" first="Jang Hoe" last="Huh">Jang Hoe Huh</name>
<affiliation wicri:level="4"><nlm:affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</nlm:affiliation>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea>School of Biological Sciences, Seoul National University, Seoul 151-742</wicri:regionArea>
<placeName><settlement type="city">Séoul</settlement>
<region type="capital">Région capitale de Séoul</region>
</placeName>
<orgName type="university">Université nationale de Séoul</orgName>
<placeName><settlement type="city">Séoul</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Castro, Nadia P" sort="Castro, Nadia P" uniqKey="Castro N" first="Nadia P" last="Castro">Nadia P. Castro</name>
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<author><name sortKey="Xu, Xue Ming" sort="Xu, Xue Ming" uniqKey="Xu X" first="Xue-Ming" last="Xu">Xue-Ming Xu</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tsuji, Petra A" sort="Tsuji, Petra A" uniqKey="Tsuji P" first="Petra A" last="Tsuji">Petra A. Tsuji</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Biological Sciences, Towson University, Towson, MD 21252, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biological Sciences, Towson University, Towson, MD 21252</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
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<author><name sortKey="Lee, Sang Goo" sort="Lee, Sang Goo" uniqKey="Lee S" first="Sang-Goo" last="Lee">Sang-Goo Lee</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
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</author>
<author><name sortKey="Bang, Jeyoung" sort="Bang, Jeyoung" uniqKey="Bang J" first="Jeyoung" last="Bang">Jeyoung Bang</name>
<affiliation wicri:level="4"><nlm:affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</nlm:affiliation>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea>School of Biological Sciences, Seoul National University, Seoul 151-742</wicri:regionArea>
<placeName><settlement type="city">Séoul</settlement>
<region type="capital">Région capitale de Séoul</region>
</placeName>
<orgName type="university">Université nationale de Séoul</orgName>
<placeName><settlement type="city">Séoul</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Na, Ji Woon" sort="Na, Ji Woon" uniqKey="Na J" first="Ji-Woon" last="Na">Ji-Woon Na</name>
<affiliation wicri:level="4"><nlm:affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</nlm:affiliation>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea>School of Biological Sciences, Seoul National University, Seoul 151-742</wicri:regionArea>
<placeName><settlement type="city">Séoul</settlement>
<region type="capital">Région capitale de Séoul</region>
</placeName>
<orgName type="university">Université nationale de Séoul</orgName>
<placeName><settlement type="city">Séoul</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Kong, Young Yun" sort="Kong, Young Yun" uniqKey="Kong Y" first="Young-Yun" last="Kong">Young-Yun Kong</name>
<affiliation wicri:level="4"><nlm:affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</nlm:affiliation>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea>School of Biological Sciences, Seoul National University, Seoul 151-742</wicri:regionArea>
<placeName><settlement type="city">Séoul</settlement>
<region type="capital">Région capitale de Séoul</region>
</placeName>
<orgName type="university">Université nationale de Séoul</orgName>
<placeName><settlement type="city">Séoul</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Beaglehole, Daniel" sort="Beaglehole, Daniel" uniqKey="Beaglehole D" first="Daniel" last="Beaglehole">Daniel Beaglehole</name>
<affiliation wicri:level="2"><nlm:affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Southon, Eileen" sort="Southon, Eileen" uniqKey="Southon E" first="Eileen" last="Southon">Eileen Southon</name>
<affiliation wicri:level="2"><nlm:affiliation>Basic Science Program, SAIC-Frederick, NCI-Frederick, Frederick, MD 21702, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Basic Science Program, SAIC-Frederick, NCI-Frederick, Frederick, MD 21702</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Seifried, Harold" sort="Seifried, Harold" uniqKey="Seifried H" first="Harold" last="Seifried">Harold Seifried</name>
<affiliation wicri:level="2"><nlm:affiliation>Nutritional Science Research Group, National Cancer Institute, Rockville, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Nutritional Science Research Group, National Cancer Institute, Rockville, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tessarollo, Lino" sort="Tessarollo, Lino" uniqKey="Tessarollo L" first="Lino" last="Tessarollo">Lino Tessarollo</name>
<affiliation wicri:level="2"><nlm:affiliation>Neural Development Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Neural Development Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Salomon, David S" sort="Salomon, David S" uniqKey="Salomon D" first="David S" last="Salomon">David S. Salomon</name>
<affiliation wicri:level="2"><nlm:affiliation>Tumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Tumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Schweizer, Ulrich" sort="Schweizer, Ulrich" uniqKey="Schweizer U" first="Ulrich" last="Schweizer">Ulrich Schweizer</name>
<affiliation wicri:level="3"><nlm:affiliation>Institut für Biochemie und Molekularbiologie, Rheinische Friedrich-Wilhelms-Universität Bonn, 53115 Bonn, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Institut für Biochemie und Molekularbiologie, Rheinische Friedrich-Wilhelms-Universität Bonn, 53115 Bonn</wicri:regionArea>
<placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region>
<region type="district" nuts="2">District de Cologne</region>
<settlement type="city">Bonn</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gladyshev, Vadim N" sort="Gladyshev, Vadim N" uniqKey="Gladyshev V" first="Vadim N" last="Gladyshev">Vadim N. Gladyshev</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Hatfield, Dolph L" sort="Hatfield, Dolph L" uniqKey="Hatfield D" first="Dolph L" last="Hatfield">Dolph L. Hatfield</name>
<affiliation wicri:level="2"><nlm:affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A. hatfield@mail.nih.gov imbglmg@snu.ac.kr.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892</wicri:regionArea>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lee, Byeong Jae" sort="Lee, Byeong Jae" uniqKey="Lee B" first="Byeong Jae" last="Lee">Byeong Jae Lee</name>
<affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea hatfield@mail.nih.gov imbglmg@snu.ac.kr.</nlm:affiliation>
<country wicri:rule="url">Corée du Sud</country>
</affiliation>
</author>
</analytic>
<series><title level="j">The Biochemical journal</title>
<idno type="eISSN">1470-8728</idno>
<imprint><date when="2016" type="published">2016</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Cell Line (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Glutathione Disulfide (metabolism)</term>
<term>Homeostasis (genetics)</term>
<term>Homeostasis (physiology)</term>
<term>Humans (MeSH)</term>
<term>Liver (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Phosphotransferases (genetics)</term>
<term>Phosphotransferases (metabolism)</term>
<term>Pyridoxal Phosphate (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Disulfure de glutathion (métabolisme)</term>
<term>Foie (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Homéostasie (génétique)</term>
<term>Homéostasie (physiologie)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Phosphate de pyridoxal (métabolisme)</term>
<term>Phosphotransferases (génétique)</term>
<term>Phosphotransferases (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>Phosphotransferases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term>
<term>Glutathione</term>
<term>Glutathione Disulfide</term>
<term>Phosphotransferases</term>
<term>Pyridoxal Phosphate</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Homeostasis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term>
<term>Homéostasie</term>
<term>Phosphotransferases</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Liver</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Disulfure de glutathion</term>
<term>Foie</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Phosphate de pyridoxal</term>
<term>Phosphotransferases</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Homéostasie</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Homeostasis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Oxidation-Reduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Oxydoréduction</term>
<term>Souris</term>
<term>Souris knockout</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Selenophosphate synthetase (SPS) was initially detected in bacteria and was shown to synthesize selenophosphate, the active selenium donor. However, mammals have two SPS paralogues, which are designated SPS1 and SPS2. Although it is known that SPS2 catalyses the synthesis of selenophosphate, the function of SPS1 remains largely unclear. To examine the role of SPS1 in mammals, we generated a Sps1-knockout mouse and found that systemic SPS1 deficiency led to embryos that were clearly underdeveloped by embryonic day (E)8.5 and virtually resorbed by E14.5. The knockout of Sps1 in the liver preserved viability, but significantly affected the expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione transferase Omega 1 (GSTO1). To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma (EC) cell line, which affected the glutathione system proteins and accordingly led to the accumulation of hydrogen peroxide in the cell. Furthermore, we found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 played a role in supporting and/or sustaining cancer. In addition, the overexpression of mouse or human GLRX1 led to a reversal of observed increases in reactive oxygen species (ROS) in the F9 SPS1/GLRX1-deficient cells and resulted in levels that were similar to those in F9 SPS1-sufficient cells. The results suggested that SPS1 is an essential mammalian enzyme with roles in regulating redox homoeostasis and controlling cell growth.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27208177</PMID>
<DateCompleted><Year>2017</Year>
<Month>05</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1470-8728</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>473</Volume>
<Issue>14</Issue>
<PubDate><Year>2016</Year>
<Month>07</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>The Biochemical journal</Title>
<ISOAbbreviation>Biochem J</ISOAbbreviation>
</Journal>
<ArticleTitle>Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.</ArticleTitle>
<Pagination><MedlinePgn>2141-54</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1042/BCJ20160393</ELocationID>
<Abstract><AbstractText>Selenophosphate synthetase (SPS) was initially detected in bacteria and was shown to synthesize selenophosphate, the active selenium donor. However, mammals have two SPS paralogues, which are designated SPS1 and SPS2. Although it is known that SPS2 catalyses the synthesis of selenophosphate, the function of SPS1 remains largely unclear. To examine the role of SPS1 in mammals, we generated a Sps1-knockout mouse and found that systemic SPS1 deficiency led to embryos that were clearly underdeveloped by embryonic day (E)8.5 and virtually resorbed by E14.5. The knockout of Sps1 in the liver preserved viability, but significantly affected the expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione transferase Omega 1 (GSTO1). To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma (EC) cell line, which affected the glutathione system proteins and accordingly led to the accumulation of hydrogen peroxide in the cell. Furthermore, we found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 played a role in supporting and/or sustaining cancer. In addition, the overexpression of mouse or human GLRX1 led to a reversal of observed increases in reactive oxygen species (ROS) in the F9 SPS1/GLRX1-deficient cells and resulted in levels that were similar to those in F9 SPS1-sufficient cells. The results suggested that SPS1 is an essential mammalian enzyme with roles in regulating redox homoeostasis and controlling cell growth.</AbstractText>
<CopyrightInformation>© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tobe</LastName>
<ForeName>Ryuta</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Carlson</LastName>
<ForeName>Bradley A</ForeName>
<Initials>BA</Initials>
<AffiliationInfo><Affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huh</LastName>
<ForeName>Jang Hoe</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Castro</LastName>
<ForeName>Nadia P</ForeName>
<Initials>NP</Initials>
<AffiliationInfo><Affiliation>Tumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Xue-Ming</ForeName>
<Initials>XM</Initials>
<AffiliationInfo><Affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tsuji</LastName>
<ForeName>Petra A</ForeName>
<Initials>PA</Initials>
<AffiliationInfo><Affiliation>Department of Biological Sciences, Towson University, Towson, MD 21252, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Sang-Goo</ForeName>
<Initials>SG</Initials>
<AffiliationInfo><Affiliation>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bang</LastName>
<ForeName>Jeyoung</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Na</LastName>
<ForeName>Ji-Woon</ForeName>
<Initials>JW</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kong</LastName>
<ForeName>Young-Yun</ForeName>
<Initials>YY</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Beaglehole</LastName>
<ForeName>Daniel</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Southon</LastName>
<ForeName>Eileen</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Basic Science Program, SAIC-Frederick, NCI-Frederick, Frederick, MD 21702, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Seifried</LastName>
<ForeName>Harold</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Nutritional Science Research Group, National Cancer Institute, Rockville, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tessarollo</LastName>
<ForeName>Lino</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Neural Development Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Salomon</LastName>
<ForeName>David S</ForeName>
<Initials>DS</Initials>
<AffiliationInfo><Affiliation>Tumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schweizer</LastName>
<ForeName>Ulrich</ForeName>
<Initials>U</Initials>
<AffiliationInfo><Affiliation>Institut für Biochemie und Molekularbiologie, Rheinische Friedrich-Wilhelms-Universität Bonn, 53115 Bonn, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gladyshev</LastName>
<ForeName>Vadim N</ForeName>
<Initials>VN</Initials>
<AffiliationInfo><Affiliation>Division of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hatfield</LastName>
<ForeName>Dolph L</ForeName>
<Initials>DL</Initials>
<AffiliationInfo><Affiliation>Molecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A. hatfield@mail.nih.gov imbglmg@snu.ac.kr.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Byeong Jae</ForeName>
<Initials>BJ</Initials>
<AffiliationInfo><Affiliation>School of Biological Sciences, Seoul National University, Seoul 151-742, Korea hatfield@mail.nih.gov imbglmg@snu.ac.kr.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 AG038004</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R37 GM065204</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA080946</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM065204</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM061603</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>05</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Biochem J</MedlineTA>
<NlmUniqueID>2984726R</NlmUniqueID>
<ISSNLinking>0264-6021</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>5V5IOJ8338</RegistryNumber>
<NameOfSubstance UI="D011732">Pyridoxal Phosphate</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.-</RegistryNumber>
<NameOfSubstance UI="D010770">Phosphotransferases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.9.3</RegistryNumber>
<NameOfSubstance UI="C062762">selenophosphate synthetase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber>
<NameOfSubstance UI="D005978">Glutathione</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>ULW86O013H</RegistryNumber>
<NameOfSubstance UI="D019803">Glutathione Disulfide</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019803" MajorTopicYN="N">Glutathione Disulfide</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010770" MajorTopicYN="N">Phosphotransferases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011732" MajorTopicYN="N">Pyridoxal Phosphate</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">cancer</Keyword>
<Keyword MajorTopicYN="Y">reactive oxygen species (ROS)</Keyword>
<Keyword MajorTopicYN="Y">redox regulation</Keyword>
<Keyword MajorTopicYN="Y">selenium</Keyword>
<Keyword MajorTopicYN="Y">selenocysteine</Keyword>
<Keyword MajorTopicYN="Y">selenophosphate synthetase 1</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>11</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>05</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>5</Month>
<Day>22</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>5</Month>
<Day>22</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2017</Year>
<Month>5</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">27208177</ArticleId>
<ArticleId IdType="pii">BCJ20160393</ArticleId>
<ArticleId IdType="doi">10.1042/BCJ20160393</ArticleId>
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Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.

Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.

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