Evidence map›Paper›PMID 27208177›Full record

ArticleThe Biochemical journal2016

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

Ryuta Tobe, Bradley A Carlson, Jang Hoe Huh, Nadia P Castro, Xue-Ming Xu, Petra A Tsuji, Sang-Goo Lee, Jeyoung Bang, Ji-Woon Na, Young-Yun Kong and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. SEPHS1: Its evolution, function and roles in development and diseases.Archives of biochemistry and biophysics · 2022
    Article
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  18. Review
  19. A Genetic Screen Using theG3 (Bethesda, Md.) · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 2 countries.

Ryuta TobeMolecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Bradley A CarlsonMolecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Jang Hoe HuhSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea.
Nadia P CastroTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Xue-Ming XuMolecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Petra A TsujiDepartment of Biological Sciences, Towson University, Towson, MD 21252, U.S.A.
Sang-Goo LeeDivision of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.
Jeyoung BangSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea.
Ji-Woon NaSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea.
Young-Yun KongSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea.
Daniel BeagleholeMolecular Biology of Selenium, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Eileen SouthonBasic Science Program, SAIC-Frederick, NCI-Frederick, Frederick, MD 21702, U.S.A.
Harold SeifriedNutritional Science Research Group, National Cancer Institute, Rockville, MD 20892, U.S.A.
Lino TessarolloNeural Development Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
David S SalomonTumor Growth Factor Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Ulrich SchweizerInstitut für Biochemie und Molekularbiologie, Rheinische Friedrich-Wilhelms-Universität Bonn, 53115 Bonn, Germany.
Vadim N GladyshevDivision of Genetics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.
Dolph L HatfieldMolecular 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.
Byeong Jae LeeSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea hatfield@mail.nih.gov imbglmg@snu.ac.kr.
Seoul National University · KRUniversity of Bonn · DE

Funding

Gene Targeting FacilityZICBC011265 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2010 to 2025
$8.9M
Selenoproteins as Targets for Cancer PreventionR01CA080946 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2001 to 2018
$4.5M
IDENTITY OF TERMINATOR AND SELENOCYSTEINE UGA CODONSR01GM061603 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2000 to 2016
$4.0M
Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
Functions of Mammalian Thioredoxin ReductasesR01GM065204 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2002 to 2009
$2.2M
Understanding the Causes of AgingR01AG038004 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2010 to 2013
$1.1M
NCI NIH HHS R01 CA080946NIA NIH HHS R01 AG038004NIGMS NIH HHS R01 GM061603NIGMS NIH HHS R01 GM065204NIGMS NIH HHS R37 GM065204
6 · The paper itself

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.

Indexed as

AnimalsCell LineGlutaredoxinsGlutathioneGlutathione DisulfideHomeostasisHumansLiverMiceMice, KnockoutOxidation-ReductionPhosphotransferasesPyridoxal PhosphateGlrx protein, mouseGlutaredoxinsGlutathioneGlutathione DisulfidePhosphotransferasesPyridoxal Phosphateselenophosphate synthetasecancerreactive oxygen species (ROS)redox regulationseleniumselenocysteineselenophosphate synthetase 1

Identifiers

PMID27208177
PMCPMC5094348
OpenAlexW2398924449

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.