| Low expression of selenoprotein S induces oxidative damage in cartilages. | Low expression of selenoprotein S induces oxidative damage in cartilages.
Cui Y, Liao Y, Chen Y, Zhao X, Zhang Y, Wang H, Li L, Zhang X, Chen K, Jia M, Tian J, Ruan X, Shi Y, Yang P, Chen J. | 09/6/2024 |
| Selenoprotein S regulates adipogenesis through IRE1alpha-XBP1 pathway. | Selenoprotein S regulates adipogenesis through IRE1α-XBP1 pathway.
Men L, Yao J, Yu S, Li Y, Cui S, Jin S, Zhang G, Ren D, Du J. | 09/5/2020 |
| Impaired exercise performance with Seps1 reduction or deletion cannot be attributed to heightened cellular stress or inflammation, but it may potentially be mediated, in part, by the effects of Seps1 on the microvasculature. | Impaired exercise performance is independent of inflammation and cellular stress following genetic reduction or deletion of selenoprotein S.
Addinsall AB, Wright CR, Kotsiakos TL, Smith ZM, Cook TR, Andrikopoulos S, van der Poel C, Stupka N. | 07/25/2020 |
| Seps1 is a novel regulator of contractile function and cellular stress responses in fast-twitch muscles. | Deficiency of selenoprotein S, an endoplasmic reticulum resident oxidoreductase, impairs the contractile function of fast-twitch hindlimb muscles.
Addinsall AB, Wright CR, Shaw CS, McRae NL, Forgan LG, Weng CH, Conlan XA, Francis PS, Smith ZM, Andrikopoulos S, Stupka N. | 07/20/2019 |
| These results suggest that VIMP may function as a novel regulator to modulate beta-cell survival, proliferation, cell cycle, unfolded protein response and insulin secretion in MIN6 cells. VIMP knockdown (KD) decreases cell proliferation and G1 cell cycle arrest. | Deficiency of VCP-Interacting Membrane Selenoprotein (VIMP) Leads to G1 Cell Cycle Arrest and Cell Death in MIN6 Insulinoma Cells.
Men L, Sun J, Ren D. | 01/26/2019 |
| It has been proposed that SelS promoted cell survival through the IRE1a-XBP1 signaling pathway. | Selenoprotein S protects against adipocyte death through mediation of the IRE1α-sXBP1 pathway.
Men L, Yu S, Yao J, Li Y, Ren D, Du J. | 01/12/2019 |
| findings suggest that SelS protects endothelial cells against TNF-alpha-induced dysfunction by inhibiting the activation of p38 MAPK and NF-kappaB pathways and implicates it as a possible modulator of vascular inflammatory diseases. | Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells.
Cui S, Men L, Li Y, Zhong Y, Yu S, Li F, Du J., Free PMC Article | 10/6/2018 |
| the genetic reduction of Seps1 appears to specifically exacerbate the inflammatory profile of fast-twitch muscle fibres, which are typically more vulnerable to degeneration in dystrophy. | A Reduction in Selenoprotein S Amplifies the Inflammatory Profile of Fast-Twitch Skeletal Muscle in the mdx Dystrophic Mouse.
Wright CR, Allsopp GL, Addinsall AB, McRae NL, Andrikopoulos S, Stupka N., Free PMC Article | 03/31/2018 |
| Pro(178) and Pro(183) of SelS play important roles in the translocation of p97(VCP) to the ER membrane and protect cells from ER stress | Pro178 and Pro183 of selenoprotein S are essential residues for interaction with p97(VCP) during endoplasmic reticulum-associated degradation.
Lee JH, Kwon JH, Jeon YH, Ko KY, Lee SR, Kim IY., Free PMC Article | 12/20/2014 |
| SelS expression is prominent in neurons and hardly detectable in astrocytes from control mice | Selenoprotein S expression in reactive astrocytes following brain injury.
Fradejas N, Serrano-Pérez Mdel C, Tranque P, Calvo S. | 03/31/2012 |
| The SEPS1 protein expression in liver of septic mouse is markedly elevated. | [Altered hepatic expression of selenoprotein S1 in septic mouse induced by LPS attack].
Su MS, He L, Yao YM, Yu Y, Wu Y, Dong JH. | 02/5/2011 |
| Selenoprotein biosynthesis becomes redirected in hepatocytes during the acute-phase response at the expense of dispensable selenoproteins (e.g., SepP) and in favor of SepS expression, thereby causing declining serum selenium and improving liver function. | Selenium controls the sex-specific immune response and selenoprotein expression during the acute-phase response in mice.
Stoedter M, Renko K, Hög A, Schomburg L. | 07/5/2010 |
| We found that suppression of SEPS1 by small interfering RNA severely increases astrocyte injure caused by OGD, suggesting that selenoprotein S protects astrocytes against ischemia. | SEPS1 gene is activated during astrocyte ischemia and shows prominent antiapoptotic effects.
Fradejas N, Pastor MD, Mora-Lee S, Tranque P, Calvo S. | 01/21/2010 |
| These findings suggest that SEPS1 could be a new ER stress-dependent survival factor that protects macrophage against ER stress-induced cellular dysfunction. | SEPS1 protects RAW264.7 cells from pharmacological ER stress agent-induced apoptosis.
Kim KH, Gao Y, Walder K, Collier GR, Skelton J, Kissebah AH., Free PMC Article | 01/21/2010 |