Редактирование: GPX2

Glutathione peroxidase 2 (EC 1.11.1.9) (GPx-2) (GSHPx-2) (Gastrointestinal glutathione peroxidase) (Glutathione peroxidase-gastrointestinal) (GPx-GI) (GSHPx-GI) (Glutathione peroxidase-related protein 2) (GPRP-2)

==Publications==

{{medline-entry
|title=RNA Exosome Complex-Mediated Control of Redox Status in Pluripotent Stem Cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29020613
|abstract=The RNA exosome complex targets AU-rich element (ARE)-containing mRNAs in eukaryotic cells. We identified a transcription factor, [[ZSCAN10]], which binds to the promoters of multiple RNA exosome complex subunits in pluripotent stem cells to maintain subunit gene expression. We discovered that induced pluripotent stem cell clones generated from aged tissue donors (A-iPSC) show poor expression of [[ZSCAN10]], leading to poor RNA exosome complex expression, and a subsequent elevation in ARE-containing RNAs, including glutathione peroxidase 2 (Gpx2). Excess [[GPX2]] leads to excess glutathione-mediated reactive oxygen species scavenging activity that blunts the DNA damage response and apoptosis. Expression of [[ZSCAN10]] in A-iPSC recovers RNA exosome gene expression, the DNA damage response, and apoptosis. These findings reveal the central role of [[ZSCAN10]] and the RNA exosome complex in maintaining pluripotent stem cell redox status to support a normal DNA damage response.
|mesh-terms=* Age Factors
* Apoptosis
* DNA Damage
* Exosome Multienzyme Ribonuclease Complex
* Gene Expression
* Gene Expression Regulation
* Genomic Instability
* Glutathione
* Glutathione Peroxidase
* Homeostasis
* Induced Pluripotent Stem Cells
* Oxidation-Reduction
* Pluripotent Stem Cells
* Reactive Oxygen Species
* Tissue Donors
* Transcription Factors
|keywords=* DNA damage response
* GPX2
* RNA exosome complex
* ROS
* aging
* glutathione
* homeostatic balance
* induced pluripotent stem cells
* pluripotent stem cells
* reactive oxygen species
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5639470
}}
{{medline-entry
|title=Maternal obesity in the rat impairs male offspring aging of the testicular antioxidant defence system.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28063465
|abstract=A high-fat diet during intrauterine development predisposes offspring (F ) to phenotypic alterations, such as lipid synthesis imbalance and increased oxidative stress, causing changes in male fertility. The objective of this study was to evaluate the effects of maternal obesity during pregnancy and lactation on antioxidant enzymes in the F  testes. Female Wistar rats (F ) were fed either a control (C, 5% fat) or an obesogenic (MO, maternal obesity, 25% fat) diet from weaning and throughout subsequent pregnancy and lactation. F  offspring were weaned to the control diet. Testes were retrieved at 110, 450 and 650 postnatal days (PND) for real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and immunohistochemical (IHC) antioxidant enzyme analyses. Catalase was similar between groups by RT-qPCR, whereas by IHC it was higher in the MO group at all ages than in the C group. Superoxide dismutase 1 ([[SOD1]]) had lower expression at PND 110 in MO than in C by both techniques; at PND 450 and 650 by immunoanalysis [[SOD1]] was higher in MO than in C. Glutathione peroxidase 1 (GPX1), [[GPX2]] and [[GPX4]] by RT-qPCR were similar between groups and ages; by IHC GPX1/2 was higher in MO than in C, whereas [[GPX4]] showed the opposite result at PND 110 and 450. In conclusion, antioxidant enzymes in the rat testes are modified with age. Maternal obesity negatively affects the F  testicular antioxidant defence system, which, in turn, can explain the decrease in reproductive capacity.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Catalase
* Diet, High-Fat
* Female
* Glutathione Peroxidase
* Male
* Maternal Nutritional Physiological Phenomena
* Obesity
* Oxidative Stress
* Pregnancy
* Prenatal Exposure Delayed Effects
* Rats
* Rats, Wistar
* Superoxide Dismutase
* Testis

|full-text-url=https://sci-hub.do/10.1071/RD16277
}}
{{medline-entry
|title=[[FOXM1]] regulates proliferation, senescence and oxidative stress in keratinocytes and cancer cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27385468
|abstract=Several transcription factors, including the master regulator of the epidermis, p63, are involved in controlling human keratinocyte proliferation and differentiation. Here, we report that in normal keratinocytes, the expression of [[FOXM1]], a member of the Forkhead superfamily of transcription factors, is controlled by p63. We observe that, together with p63, [[FOXM1]] strongly contributes to the maintenance of high proliferative potential in keratinocytes, whereas its expression decreases during differentiation, as well as during replicative-induced senescence. Depletion of [[FOXM1]] is sufficient to induce keratinocyte senescence, paralleled by an increased ROS production and an inhibition of ROS-scavenger genes (SOD2, [[CAT]], [[GPX2]], PRDX). Interestingly, [[FOXM1]] expression is strongly reduced in keratinocytes isolated from old human subjects compared with young subjects. [[FOXM1]] depletion sensitizes both normal keratinocytes and squamous carcinoma cells to apoptosis and ROS-induced apoptosis. Together, these data identify [[FOXM1]] as a key regulator of ROS in normal dividing epithelial cells and suggest that squamous carcinoma cells may also use [[FOXM1]] to control oxidative stress to escape premature senescence and apoptosis.
|mesh-terms=* Carcinoma, Squamous Cell
* Cell Death
* Cell Differentiation
* Cell Line, Tumor
* Cell Proliferation
* Cellular Senescence
* Forkhead Box Protein M1
* Humans
* Keratinocytes
* Oxidative Stress
* Reactive Oxygen Species
* Skin Aging
|keywords=* FOXM1
* head and neck cancer
* oxidative stress
* p63
* senescence
* skin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993337
}}