| 2004 |
SELENOS (SelS) gene expression is upregulated by glucose deprivation and ER stress inducers (tunicamycin, thapsigargin) in HepG2 cells, in parallel with GRP78, identifying it as a novel glucose-regulated protein. Overexpression of SelS increased Min6 cell resistance to oxidative stress-induced toxicity, indicating a role in regulating cellular redox balance. |
Cell treatment with ER stress inducers, Western blot for protein levels, overexpression with viability assay |
FEBS letters |
Medium |
15063746
|
| 2007 |
SEPS1 overexpression in RAW264.7 macrophages protects against ER stress-induced apoptosis and promotes cell survival; conversely, siRNA-mediated suppression of SEPS1 sensitizes macrophages to ER stress-induced cell death. The protective action is specifically dependent on ER stress-mediated cell death signaling. |
Overexpression studies, siRNA knockdown, cell viability/apoptosis assays with pharmacological ER stress agents |
Biochemical and biophysical research communications |
Medium |
17210132
|
| 2007 |
SEPS1 protein is secreted from hepatoma cells via the ER-Golgi pathway (secretion abolished by Brefeldin A and cycloheximide). Secreted SEPS1 is detectable in human serum and associates with LDL and possibly VLDL fractions. |
Brefeldin A and cycloheximide inhibitor studies, sandwich ELISA, serum fractionation |
Biochemical and biophysical research communications |
Medium |
17374524
|
| 2008 |
siRNA-mediated silencing of SelS in HepG2 cells aggravates LPS-induced increases in ROS, NO, iNOS activity, and SAA1 secretion, and further decreases GPx-1 activity. This implicates SelS as a negative regulator of inflammatory mediator production, likely through its role as a component of the ERAD retro-translocation channel and its antioxidative properties. |
siRNA knockdown, ROS measurement, NO/iNOS assay, RT-PCR, ELISA for SAA1, GPx activity assay |
Archives of biochemistry and biophysics |
Medium |
18675776
|
| 2008 |
SEPS1 gene is induced in astrocytes by oxygen and glucose deprivation (OGD/ischemia model). siRNA knockdown of SEPS1 severely increases astrocyte injury caused by OGD, demonstrating that SEPS1 protects astrocytes against ischemia by modulating ER stress. |
RNA differential display, siRNA knockdown, OGD cell injury assay |
Journal of molecular neuroscience |
Medium |
18498015
|
| 2009 |
SEPS1 overexpression in HepG2 cells reduces levels of active ATF6, inhibits GRP78 promoter activity, and suppresses NF-κB activity in the context of Z-variant alpha1-antitrypsin (ZAAT)-induced ER stress. Selenium supplementation enhances these effects, demonstrating a chaperone-like activity that decreases the unfolded protein response and ER overload response. |
Transfection/overexpression, GRP78 promoter-reporter assay, ATF6 Western blot, NF-κB activity assay, glutathione peroxidase activity assay |
The Journal of biological chemistry |
Medium |
19398551
|
| 2010 |
siRNA-mediated silencing of SelS in HepG2 cells aggravates beta-mercaptoethanol-induced ER stress and cell apoptosis. Selenite pretreatment (which increases SelS expression) alleviates beta-ME-induced apoptosis, demonstrating that SelS protects cells from ER stress-induced apoptosis. |
siRNA knockdown, sodium selenite supplementation, apoptosis assay, Western blot for GRP78 |
Biochimica et biophysica acta |
Medium |
20114070
|
| 2014 |
siRNA knockdown of SEPS1 in mice with LPS-induced sepsis increases TNF-α and IL-6 production, worsens organ damage (elevated ALT, AST, BUN, LDH, CK, CK-MB), and significantly activates p38 MAPK phosphorylation, indicating that SEPS1 suppresses inflammatory cytokine production partly by inhibiting the p38 MAPK pathway. |
In vivo siRNA knockdown in LPS-sepsis mouse model, Western blot for p38 MAPK phosphorylation, ELISA for cytokines, biochemical organ damage markers |
Molecular medicine reports |
Medium |
24573439
|
| 2019 |
In Nrf2 knockout mice, SELENOS expression is reduced in thyroid follicular cells; conversely, siRNA-mediated reduction of SELENOS in PCCL3 rat thyroid cells reduces Nrf2 signaling activity. This bidirectional positive feedback between Nrf2 and SelS pathways was supported by immunohistochemistry showing reduced SelS in thyroid follicular cells of Hashimoto's thyroiditis patients. |
Nrf2 knockout mouse model, siRNA knockdown in thyroid cell line, immunohistochemistry, Nrf2 activity assay |
Thyroid |
Medium |
31426718
|
| 2020 |
The Cul5-type ubiquitin ligase KLHDC1 targets truncated (Sec-lacking) SELENOS for proteasomal degradation. Truncated SELENOS lacks oxidoreductase activity and its accumulation (when KLHDC1 is knocked down) decreases ER stress-induced cell death; knockdown of SELENOS itself increases the proportion of cells with lower ROS levels. This establishes SELENOS as an oxidoreductase that promotes ROS production and that KLHDC1 eliminates its inactive truncated form. |
Co-IP/ubiquitin ligase identification, KLHDC1 knockdown in U2OS cells, proteasome inhibition, ROS measurement, cell death assay |
iScience |
High |
32200094
|
| 2018 |
In C2C12 myoblasts, siRNA knockdown of Seps1 (~50–75%) exacerbates palmitate-induced oxidative and ER stress, decreasing cell viability and proliferation, increasing H2O2 levels, lowering the GSH:GSSG ratio, and enhancing ER and oxidative stress marker gene expression. Even without palmitate, Seps1 knockdown increased oxidative stress in myoblasts. In contrast, in differentiated myotubes, the same knockdown did not significantly enhance ER stress markers under palmitate treatment, demonstrating cell-type-specific antioxidant function. |
siRNA knockdown (two constructs), cell viability assay, H2O2 measurement, GSH:GSSG ratio, RT-PCR for stress markers |
Physiological reports |
Medium |
30557449
|
| 2023 |
Regorafenib suppresses SELENOS expression in colorectal cancer cells, which promotes ROS production and activates ER stress, JNK, and p38 signaling pathways. SELENOS knockdown sensitizes cells to regorafenib-induced ROS-mediated anti-tumor effects, confirming SELENOS functions as an antioxidant suppressor of ROS in CRC cells. |
SELENOS knockdown, ROS measurement, Western blot for signaling pathway activation, mouse xenograft model |
European journal of pharmacology |
Medium |
37598924
|
| 2022 |
In yellow catfish liver, dietary sodium selenite (vs. selenomethionine) increases HSF1 binding to the SELENOS promoter, upregulating SELENOS expression, which in turn activates the XBP1s/PPARγ pathway to promote lipogenesis. RNA interference of SELENOS or PPARγ abolished selenite-induced lipid accumulation, establishing the HSF1-SELENOS-IRE1α-XBP1s-PPARγ axis in lipid metabolism regulation. |
RNA interference (SELENOS and PPARγ), ChIP for HSF1 binding, Western blot, lipid/triglyceride measurement, enzyme activity assays |
Biochimica et biophysica acta. Gene regulatory mechanisms |
Medium |
35248747
|
| 2026 |
SELENOS knockdown in C2C12 cells and myotubes exacerbates ER stress-induced apoptosis and impairs myotube differentiation under heat stress conditions, supporting a contributory role for SELENOS in ER stress-related responses and apoptosis-associated signaling in muscle cells. |
SELENOS siRNA knockdown in C2C12 cells/myotubes, ER stress marker measurement (GRP78, PERK, CHOP), apoptosis markers (Bax, Bcl-2, Caspase-9), differentiation assay |
The Journal of nutrition |
Medium |
42025965
|