Critically elucidating the role of selenium is arie dating anyone now

A combined Dio1/Dio2 knockout mouse has a similar mild phenotype but exhibits a greater alteration of brain gene expression [21], while deiodinase 3 (Dio3) knockout mice have been shown to have reduced viability, fertility and growth retardation [22]. The resulting mutant mice suffered growth retardation, delayed skeletal ossification and a pronounced chondronecrosis of cartilages in various tissues. Selenoprotein P (Sel P) knockout mice manifest neurological defects with ataxia and seizures [23,24], and recently a selenoprotein R (Sel R) knockout mouse has been shown to be viable and appeared normal despite a tissue-dependent increase in oxidative stress [25]. Mice lacking the ability to synthesize selenoproteins in neuronal tissue lost postural control and developed seizure-like behavior. The mice appeared to phenotypically mimic numerous pathological features of Kashin-Beck disease providing further evidence that Se deficiency may be important in the development of this disease. uses cookies to improve performance by remembering your session ID when you navigate from page to page. Please set your browser to accept cookies to continue. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( H.)licensee Molecular Diversity Preservation International, Basel, Switzerland. This cookie stores just a session ID; no other information is captured.

critically elucidating the role of selenium-11

Knockout of thioredoxin reductase 1 (TR1) [17] and thioredoxin reductase 3 (TR3) [18] have also been shown to be embryonic lethal. For example, Kashin-Beck disease, which is found in various regions of China and has been described in North Korea and Siberia, is an osteoarticular disease involving cartilage and is characterized by stunted growth, skeletal deformities and arthropathy of multiple joints [47]. E., Sengupta A., Schweizer U., Shrimali R., Rao M., Zhong N., Wang S., Feigenbaum L., Lee B. Se is incorporated into protein by way of the Se-containing amino acid, selenocysteine (Sec). H.)Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; E-mails: [email protected] (M-H. There are 24 Se-containing protein (selenoprotein) genes in rodents and 25 in humans [8]. The synthesis of selenoproteins is dependent on Sec t RNA for insertion of Sec, the 21st amino acid in the genetic code, into protein. One of the unique properties of selenoproteins is that their synthesis is dependent on Sec t RNA and, if the expression of this t RNA is altered, then the expression of the resulting class of selenoproteins is altered [9,10]. We have taken advantage of this dependency to modulate the expression of Sec t RNA that in turn modulates the expression of selenoproteins by generating transgenic, conditional knockout, transgenic/standard knockout and transgenic/conditional knockout mouse models, all of which involve the Sec t RNA gene, to elucidate the intracellular roles of this protein class. We have taken advantage of the fact that selenoprotein expression can be controlled by manipulating the expression of Sec t RNA to generate a number of mouse models for elucidating the intracellular roles of selenoproteins [9,10,11,12], which is the subject of this review. Histological analysis of hair follicles revealed a decreased number of follicles with growth retardation, while histological analysis of epidermal tissue revealed moderate epidermal hyperplasia along with acute focal coagulative necrosis of the epidermis. Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; E-mails: [email protected] (M-H. It should be noted that numerous other studies have reported the targeted removal of individual selenoproteins which have elucidated their intracellular roles. The initiation of hair follicle formation appeared normal, but hair follicles underwent premature repression in knockout mice.

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