Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis

Cox, Andrew G.; Tsomides, Allison; Kim, Andrew J.; Saunders, Diane; Hwang, Katie L.; Evason, Kimberley; Heidel, Jerry R.; Brown, Kristin K.; Yuan, Min; Lien, Evan C.; Lee, Byeong Cheol; Nissim, Sahar; Dickinson, Bryan C.; Chhangawala, Sagar; Chang, Christopher J.; Asara, John M.; Houvras, Yariv; Gladyshev, Vadim N.; Goessling, Wolfram

doi:10.1073/pnas.1600204113

Cited by 60 publications

(32 citation statements)

References 138 publications

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“…RNA quality was checked by Agilent Bioanalyzer Sequencing was performed after library construction on an Illumina HiSeq. polyA sequence data were annotated on the ZV9 genomic assembly to identify differentially affected genes (Collins et al , ), as previously described (Cox et al , ). Gene ontology (GO) and Gene set enrichment analysis (GSEA) of biological processes were determined by GO Slim (Gene Ontology Consortium) and GAGE (Luo et al , ).…”

Section: Methodsmentioning

confidence: 99%

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

et al. 2018

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The Hippo pathway and its nuclear effector Yap regulate organ size and cancer formation. While many modulators of Hippo activity have been identified, little is known about the Yap target genes that mediate these growth effects. Here, we show that yap−/− mutant zebrafish exhibit defects in hepatic progenitor potential and liver growth due to impaired glucose transport and nucleotide biosynthesis. Transcriptomic and metabolomic analyses reveal that Yap regulates expression of glucose transporter glut1, causing decreased glucose uptake and use for nucleotide biosynthesis in yap−/− mutants, and impaired glucose tolerance in adults. Nucleotide supplementation improves Yap deficiency phenotypes, indicating functional importance of glucose‐fueled nucleotide biosynthesis. Yap‐regulated glut1 expression and glucose uptake are conserved in mammals, suggesting that stimulation of anabolic glucose metabolism is an evolutionarily conserved mechanism by which the Hippo pathway controls organ growth. Together, our results reveal a central role for Hippo signaling in glucose metabolic homeostasis.

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Section: Methodsmentioning

confidence: 99%

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

et al. 2018

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“…RNA quality was checked by Agilent Bioanalyzer Sequencing was performed after library construction on an Illumina HiSeq. polyA sequence data were annotated on the ZV9 genomic assembly to identify differentially affected genes (Collins et al 2012), as previously described (Cox et al 2016b). Gene ontology (GO) and Gene Set Enrichment analysis (GSEA) of biological processes was determined by GO Slim (Gene Ontology Consortium) and GAGE (Luo et al 2009).…”

Section: Rna Transcriptomic Analysismentioning

confidence: 99%

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

Cox

Tsomides

Yimlamai

et al. 2018

Preprint

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The Hippo pathway and its nuclear effector Yap regulate organ size and cancer formation. While many modulators of Hippo activity have been identified, little is known about the Yap target genes that mediate these growth effects. Here, we show that yap-/-mutant zebrafish exhibit defects in hepatic progenitor potential and liver growth due to impaired glucose transport and nucleotide biosynthesis: transcriptomic and metabolomic analyses reveal that Yap regulates expression of glucose transporter glut1, causing decreased glucose uptake and use for nucleotide biosynthesis in yap-/-mutants, and impaired glucose tolerance in adults. Nucleotide supplementation improved Yap-deficiency phenotypes, indicating functional importance of glucose-fuelled nucleotide biosynthesis. Yapregulated Glut1 expression and glucose uptake are conserved in mammals, suggesting that stimulation of anabolic glucose metabolism is an evolutionarily conserved mechanism by which the Hippo pathway controls organ growth.Together, our results reveal a central role for Hippo signalling in metabolic homeostasis.

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“…Selenoprotein H is a newly identified selenoprotein, which is a nucleolar oxidoreductase. According to some authors, SelH regulates redox homeostasis and suppresses DNA damage (Cox et al, 2016). Selenoprotein H defends cells from aging through the effect on oxidative stress by supporting the genome (Wu et al, 2014).…”

Section: Nuclear Selenoproteinsmentioning

confidence: 99%

Modern concept of biological identification of selenoproteins

Stanishevska

2018

Regul. Mech. Biosyst.

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Humans possess 25 selenoproteins, approximately half of which are enzymes (selenoenzymes) required for preventing, regulating, or reversing oxidative damage, while others participate in providing calcium metabolism, thyroid hormone maintenance, protein synthesis, cytoskeletal structure etc. This review examines the latest evidences of the biological effects of selenoproteins according to the method of complex analysis of the material. Selenoprotein P promotes insulin resistance in type 2 diabetes, mediates myocardial ischemic-reperfusion injuries and provides protection against disease by reducing chronic oxidative stress. Selenoprotein T is expressed at the endoplasmic reticulum membrane in all cells during development, but is confined to endocrine tissues in adulthood, controls homeostasis of glucose and prevents neurodegeneration by reducing oxidative stress factors. Expression of selenoprotein K is required for efficient Ca2+ flux into melanoma cancer cells, tumour growth and metastasic potential depend on SelK but it suppresses human choriocarcinoma cells. SelK also serves to maintain the normal physiological functions of skeletal muscle. Selenoprotein N deficiency, caused by mutations in the human gene, promotes myopathy characterized by muscle weakness, spinal rigidity, respiratory insufficiency. Sel N participates in normal physiology of skeletal and smooth muscle tissues. Selenoprotein M is located in the endoplasmic reticulum, characterized by high expression in the brain, antioxidative, neuroprotective activity and regulates intracellular Ca2+ levels. Also, the overexpression of SelM was detected in human hepatocellular carcinoma. Selenoprotein S is mentioned as a regulator of ER stress and inflammatory processes. Selenoprotein F controls cell proliferation by the impact on G1period of the cell cycle. Moreover, it is implicated in the pathogenesis of some types of cancer. The Sel F deficiency reduces the migration and invasive ability of the cells. Knockdown of selenoprotein W in rodents leads to increased release of Ca2+, causes oxidative ultramicroscopic injuries of the endoplasmic reticulum and mitochondria ultrastructure, which in turn increases the levels of inflammatory factors. Selenoprotein H is involved in redox regulation, in tumourogenesis. Knockdown of selenoprotein H decreases cellular differentiation and increases proliferation and migration of cells. Selenoproteins U, V, I, O, R are recently identified and their functions are not clearly known. The data analyzed in the review help determine promising directions in the study of the selenoproteins.

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Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis

Cited by 60 publications

References 138 publications

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth

Modern concept of biological identification of selenoproteins

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