We are analyzing https://link.springer.com/article/10.1007/s12011-018-1521-9.

Title:
The Thioredoxin-Like Family of Selenoproteins: Implications in Aging and Age-Related Degeneration | Biological Trace Element Research
Description:
The thioredoxin-like (Rdx) family proteins contain four selenoproteins (selenoprotein H, SELENOH; selenoprotein T, SELENOT; selenoprotein V, SELENOV; selenoprotein W, SELENOW) and a nonselenoprotein Rdx12. They share a CxxU or a CxxC (C, cysteine; x, any amino acid; U, selenocysteine) motif and a stretch of eGxFEI(V) sequence. From the evolutionary perspective, SELENOW and SELENOV are clustered together and SELENOH and SELENOT are in another branch. Selenoproteins in the Rdx family exhibit tissue- and organelle-specific distribution and are differentially influenced in response to selenium deficiency. While SELENOH is nucleus-exclusive, SELENOT resides mainly in endoplasmic reticulum and SELENOW in cytosol. SELENOV is expressed essentially only in the testes with unknown cellular localization. SELENOH and SELENOW are more sensitive than SELENOT and SELENOV to selenium deficiency. While physiological functions of the Rdx family of selenoproteins are not fully understand, results from animal models demonstrated that (1) brain-specific SELENOT knockout mice are susceptible to 1-methyl-4-phenylpyridinium-induced Parkinson’s disease in association with redox imbalance and (2) adult zebrafishes with heterozygous SELENOH knockout are prone to dimethylbenzanthracene-induced tumorigenesis together with increased DNA damage and oxidative stress. Further animal and human studies are needed to fully understand physiological roles of the Rdx family of selenoproteins in redox regulation, genome maintenance, aging, and age-related degeneration.
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pubmed, article, selenoprotein, cas, google, scholar, zhang, central, biol, selenium, selenoproteins, gladyshev, family, zhu, cheng, redox, hatfield, thioredoxinlike, rdx, regulation, anouar, privacy, cookies, content, research, selenoh, selenot, deficiency, expression, chem, lee, wenzhou, author, state, publish, search, aging, jianhong, selenov, selenow, selenocysteine, mice, human, genome, access, chapter, protein, evolution, cells, nutr,

Topics {✒️}

month download article/chapter jian-hong zhu wen-hsing cheng talen-mediated gene targeting pacap-regulated gene involved age-related degeneration published pacap-regulated gene selenoprotein 1-methyl-4-phenylpyridinium-induced parkinson full article pdf lobanov av high-fat diet murine fibroblast cells article zhang privacy choices/manage cookies author information authors increased dna damage age-related degeneration organelle-specific distribution age reveal common knockout mice created human beta-cells redox-modulatory interaction selenium-compromised conditions mitochondrial dna regulates genes involved metal-responsive genes european economic area unknown cellular localization novoselov sv telomere-dysfunctional mice regulates upr signaling protects dopaminergic neurons intracellular ca2+ mobilization suppresses cellular senescence preventing superoxide formation stoytcheva zr phase ii detoxification von berswordt-wallrabe author correspondence essential oxidoreductase activity dietary selenium deficiency article log mississippi state university conditions privacy policy labunskyy vm related subjects article cite wenzhou medical university accepting optional cookies heterozygous selenoh knockout

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         headline:The Thioredoxin-Like Family of Selenoproteins: Implications in Aging and Age-Related Degeneration
         description:The thioredoxin-like (Rdx) family proteins contain four selenoproteins (selenoprotein H, SELENOH; selenoprotein T, SELENOT; selenoprotein V, SELENOV; selenoprotein W, SELENOW) and a nonselenoprotein Rdx12. They share a CxxU or a CxxC (C, cysteine; x, any amino acid; U, selenocysteine) motif and a stretch of eGxFEI(V) sequence. From the evolutionary perspective, SELENOW and SELENOV are clustered together and SELENOH and SELENOT are in another branch. Selenoproteins in the Rdx family exhibit tissue- and organelle-specific distribution and are differentially influenced in response to selenium deficiency. While SELENOH is nucleus-exclusive, SELENOT resides mainly in endoplasmic reticulum and SELENOW in cytosol. SELENOV is expressed essentially only in the testes with unknown cellular localization. SELENOH and SELENOW are more sensitive than SELENOT and SELENOV to selenium deficiency. While physiological functions of the Rdx family of selenoproteins are not fully understand, results from animal models demonstrated that (1) brain-specific SELENOT knockout mice are susceptible to 1-methyl-4-phenylpyridinium-induced Parkinson’s disease in association with redox imbalance and (2) adult zebrafishes with heterozygous SELENOH knockout are prone to dimethylbenzanthracene-induced tumorigenesis together with increased DNA damage and oxidative stress. Further animal and human studies are needed to fully understand physiological roles of the Rdx family of selenoproteins in redox regulation, genome maintenance, aging, and age-related degeneration.
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      description:The thioredoxin-like (Rdx) family proteins contain four selenoproteins (selenoprotein H, SELENOH; selenoprotein T, SELENOT; selenoprotein V, SELENOV; selenoprotein W, SELENOW) and a nonselenoprotein Rdx12. They share a CxxU or a CxxC (C, cysteine; x, any amino acid; U, selenocysteine) motif and a stretch of eGxFEI(V) sequence. From the evolutionary perspective, SELENOW and SELENOV are clustered together and SELENOH and SELENOT are in another branch. Selenoproteins in the Rdx family exhibit tissue- and organelle-specific distribution and are differentially influenced in response to selenium deficiency. While SELENOH is nucleus-exclusive, SELENOT resides mainly in endoplasmic reticulum and SELENOW in cytosol. SELENOV is expressed essentially only in the testes with unknown cellular localization. SELENOH and SELENOW are more sensitive than SELENOT and SELENOV to selenium deficiency. While physiological functions of the Rdx family of selenoproteins are not fully understand, results from animal models demonstrated that (1) brain-specific SELENOT knockout mice are susceptible to 1-methyl-4-phenylpyridinium-induced Parkinson’s disease in association with redox imbalance and (2) adult zebrafishes with heterozygous SELENOH knockout are prone to dimethylbenzanthracene-induced tumorigenesis together with increased DNA damage and oxidative stress. Further animal and human studies are needed to fully understand physiological roles of the Rdx family of selenoproteins in redox regulation, genome maintenance, aging, and age-related degeneration.
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      dateModified:2018-09-18T00:00:00Z
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         Selenium
         Selenoprotein H
         Selenoprotein T
         Selenoprotein W
         Selenoprotein V
         Biochemistry
         general
         Biotechnology
         Nutrition
         Oncology
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