mProX™ Human SGK3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Silencing of SGK3 in MM cell lines.
At day 3 post-electroporation, cells were harvested, and phosphorylation levels of Akt and potential SGK3 downstream substrates were measured in stEGFP vs. stSGK3 transfected MM cell lines. Two gels were employed for each cell line, and the representative β-actin control was obtained from the gel also stained for P-Akt (Thr308) (in all cell lines) and pan-Akt (L-363, MM.1s) or P-FOXO1/3A and P-GSK-3β (JJN-3).
Ref: Hausmann, Stefan, et al. "Loss of serum and glucocorticoid-regulated kinase 3 (SGK3) does not affect proliferation and survival of multiple myeloma cell lines." Plos one 10.4 (2015): e0122689.
Pubmed: 25837824
DOI: 10.1371/journal.pone.0122689
Research Highlights
Wang, Min. et al. "The SGK3-Catalase antioxidant signaling axis drives cervical cancer growth and therapy resistance." Redox biology, 2023.
In cervical cancers with PIK3CA helical domain mutations, SGK3 functions as a key factor in promoting cell growth and resistance to drugs by mitigating oxidative stress. When faced with oxidative stress, SGK3 becomes activated and acts as an anti-ROS agent by both enhancing the stability and activation of the antioxidant enzyme catalase. SGK3 accomplishes this by interacting with catalase, phosphorylating it to boost its tetrameric configuration and functionality. Furthermore, SGK3 phosphorylates GSK3β, safeguarding catalase from GSK3β-β-TrCP-mediated ubiquitination and subsequent proteasomal degradation. Inhibiting SGK3 not only enhances the cytotoxic effects of the CDK4/6 inhibitor Palbociclib but also conquers cisplatin resistance through ROS-mediated mechanisms. These findings reveal SGK3's role in preserving redox balance and propose the therapeutic targeting of the SGK3-catalase antioxidant signaling pathway to enhance the treatment outcomes for cervical cancers with PIK3CA helical domain mutations.
Wang, Min. et al. "The SGK3-Catalase antioxidant signaling axis drives cervical cancer growth and therapy resistance." Redox biology, 2023.
Pubmed:
37866161
DOI:
10.1016/j.redox.2023.102931
S, Mahmood. "Serum Glucocorticoid-Regulated Kinase-1 in Ischemia-Reperfusion Injury; Blessing or Curse." Journal of Pharmacology and Experimental Therapeutics, 2023.
The serum-glucocorticoid-regulated kinase (SGK) family, consisting of three paralogs (SGK-1, SGK-2, SGK-3), with SGK-1 being the most extensively studied, plays a crucial role in regulating cellular processes, such as survival and proliferation. It has also been implicated in the development of certain cancers, leading to the development of small-molecule inhibitors. Additionally, SGK-1 has been found to regulate important physiological functions, including renal solute transport, and is involved in the pathogenesis of non-neoplastic conditions affecting major organs like the heart and kidney. Therefore, targeting SGK-1 could provide therapeutic benefits in diseases like myocardial infarction and acute kidney injury. This review primarily focuses on the role of SGK-1 in pathologies related to ischemia-reperfusion injury in various organs. With SGK-1's involvement in cell death and its potential to promote cell survival, therapeutic modulation of this protein could have a positive impact on conditions associated with ischemia-reperfusion injury.
S, Mahmood. "Serum Glucocorticoid-Regulated Kinase-1 in Ischemia-Reperfusion Injury; Blessing or Curse." Journal of Pharmacology and Experimental Therapeutics, 2023.
Pubmed:
37770199
DOI:
10.1124/jpet.123.001846