SGK1 (Phospho-Ser78) Polyclonal Antibody
- Known as:
- SGK1 (Phospho-Ser78) Polyclonal Antibody
- Catalog number:
- 12234
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- SGK1 (Phospho-Ser78) Polyclonal Antibody
Related genes to: SGK1 (Phospho-Ser78) Polyclonal Antibody
- Gene:
- SGK1 NIH gene
- Name:
- serum/glucocorticoid regulated kinase 1
- Previous symbol:
- SGK
- Synonyms:
- -
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2016-10-05
Related products to: SGK1 (Phospho-Ser78) Polyclonal Antibody
Related articles to: SGK1 (Phospho-Ser78) Polyclonal Antibody
- Advanced maternal age is associated with increased oocyte aneuploidy and early miscarriage. Serum- and glucocorticoid-regulated kinase 1 (SGK1), a member of the serine/threonine kinase family, is downregulated in oocytes from aged mice. However, the mechanisms by which SGK1 controls oocyte maturation remain unclear. Here, we show that SGK1 localizes predominantly to spindle poles during oocyte maturation. Knockdown of SGK1 via siRNA or pharmacological inhibition disrupts spindle assembly and impairs kinetochore-microtubule attachments in mouse oocytes. This disruption leads to sustained activation of the spindle assembly checkpoint, failure of Cyclin B1 and Securin degradation, impaired metaphase I-anaphase transition, and defective first polar body extrusion. Mechanistically, we identify RanBP1 as a potential mediator of SGK1 function during meiotic progression. In porcine oocytes, SGK1 inhibition similarly compromises maturation and Cyclin B1 degradation, suggesting a conserved role across mammalian species. Together, our findings establish SGK1 as a critical regulator of spindle assembly and meiotic progression in mammalian oocytes. - Source: PubMed
Li Li-ShuYang Shu-JieLi Xiao-QingDuan Xing - Chronic psychosocial stress is a key risk factor for psychiatric disorders, often causing motivational and social impairments poorly responsive to conventional pharmacotherapies. The present study investigated the effects of chronic lurasidone treatment on behavioral and molecular alterations induced by prolonged social defeat (SD) stress in adult male rats. Rats underwent resident-intruder SD paradigm for approximately seven weeks and treated orally with lurasidone (1 or 3 mg/kg/day) during the final three weeks. Motivational drive was assessed using sucrose self-administration under fixed and progressive ratio schedules, while sociability was evaluated through social interaction tests. Molecular analysis quantified DARPP-32 dopaminergic response to social stimuli and gene expression [immediate early genes (Arc, c-Fos, Npas4, Zif268) and glucocorticoid-responsive genes (Sgk1, Fkbp5, Dusp1, Nr4a1)] across corticolimbic regions, including the nucleus accumbens and prefrontal cortex. SD stress caused anhedonia and social withdrawal. Treatment with lurasidone at 3 mg/kg, but not 1 mg/kg, effectively restored motivational performance, as indicated by normalized breaking points in the progressive ratio task. Both doses ameliorated the stress-induced social deficits, and DARPP-32 responses, although with different magnitudes. At the molecular level, SD disrupted activity-dependent and glucocorticoid-responsive transcription and functional coupling between brain regions. Lurasidone reinstated coordinated network activation, particularly during social stimulation, suggesting a dose- and context-dependent facilitation of neuronal plasticity. Overall, chronic lurasidone treatment counteracts stress-induced impairments in motivation and sociability through the restoration of corticolimbic network activity. Such effects may underlie its clinical efficacy in addressing negative and motivational symptoms across affective and psychotic disorders. - Source: PubMed
Publication date: 2026/05/26
Corridori EleonoraMarchesin AlessiaAmato CamillaBegni VeronicaSalviati SaraGambarana CarlaRiva Marco AndreaScheggi Simona - Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with non-motor symptoms including autonomic dysfunction, cognitive decline, depression, and gastrointestinal dysfunction. PD is characterized by reductions in the number of dopaminergic neurons and the tyrosine hydroxylase (TH) enzyme level; however, the reasons for these reductions have not been elucidated. The accumulation of α-syneclein (α-syn) is the neuropathological characteristic of PD. In this study, we investigated whether serum- and glucocorticoid-regulated kinase 1 (SGK1) treatment may have a positive effect on neurodegenerative changes in PD. SGK1, a serine/threonine-protein kinase involved in Na/K pump activity, is encoded by sgk1. SGK1-myc, transiently expressed in tobacco leaves, was extracted and used to treat SW480 and SH-SY5Y cells. The changes in the expression levels of the factors related to PD, i.e., TH and α-syn, were investigated in the cells and in the colons of the 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine-induced PD model. The SGK1 expression level was associated with TH and α-syn expression levels, and SGK1 treatment positively affected PD-related pathological symptoms. In addition, SGK1 treatment led to improved TH expression in the substantia nigra and striatum regions. The increase in SGK1 expression following treatment with the recombinant SGK1-myc protein resulted in beneficial alterations in the pathological factors associated with PD. These findings position SGK1 as a potential therapeutic target for early-stage PD therapy, as it is associated with the Na/K pump and gastrointestinal dysfunction, features often disrupted in early PD. - Source: PubMed
Publication date: 2026/05/22
Seo Min HyungKim Sun-HoKim Soo-HwanYeo Sujung - Glucocorticoid receptor (GR) signaling is critical to our physiology but is dysregulated in cancer by the pain, psychological distress, iatrogenic morbidity, and pathology associated with an advanced, invasive disease. Many tumors exploit glucocorticoid signaling to provide anti-apoptotic survival signals, stimulate growth and metastasis, suppress immune surveillance, and drive treatment resistance. Endogenous cortisol and exogenous glucocorticoids are typically associated with poor responses to cytotoxic chemotherapy, targeted therapy, and immunotherapy in patients with solid tumors. Translational and non-clinical data show that selective GR antagonists (SGRAs) synergize with anti-cancer agents, including taxanes, androgen receptor inhibitors, PARP inhibitors, and anti-PD(L)-1 immune checkpoint inhibitors, driving improved anti-cancer activity. In a tumor-intrinsic manner, SGRAs downregulate the anti-apoptotic proteins SGK1 and DUSP1, which induce resistance to cytotoxic chemotherapy. This synergy has been confirmed in several randomized controlled trials, which showed improved efficacy when SGRAs were added to standard-of-care taxane therapy in platinum-resistant ovarian cancer. In a distinct cellular context, SGRAs inhibit resistance to anti-androgen therapy mediated through the GR and have the potential for additive anti-cancer activity in prostate cancer. Herein, we summarize the role of glucocorticoid signaling in solid tumor biology, providing mechanistic insights into recent clinical advances and emphasizing key outstanding translational and clinical questions. - Source: PubMed
Publication date: 2026/05/22
Flint Melanie SO'Malley David MLorusso DomenicaLutgendorf Susan KOlawaiye Alexander BJubb Adrian MThaker Premal H - Mineralocorticoid receptor antagonists (MRA) exert anti-atherosclerotic properties through their combined effects on various cells and tissues. We previously found a significant interaction between TNFα-induced inflammatory pathways and mineralocorticoid receptor signaling, particularly involving serum/glucocorticoid-regulated kinase 1 (SGK1), in vascular endothelial cells. This study further elucidated the specific roles of SGK1 in vascular endothelial function. In SGK1-knockdown human aortic endothelial cells (HAECs), TNFα-induced inflammation-related molecules (e.g., E-selectin, VCAM-1, PAI-1, and MCP-1) were significantly downregulated compared to controls. Monocyte adhesion was also significantly reduced in SGK1-knockdown human umbilical vein endothelial cells, regardless of TNFα stimulation. Additionally, in these SGK1-knockdown HAECs, there was a significant attenuation of the TNFα-induced reduction of both total and phosphorylated protein levels of endothelial nitric oxide synthase (eNOS), accompanied by increased phosphorylation of protein kinase B (AKT) and adenosine monophosphate-activated protein kinase (AMPK). The upregulation of eNOS caused by SGK1 knockdown occurred at the transcriptional level alongside an increase in Krüppel-like factor 2 (KLF2) mRNA. Importantly, KLF2 knockdown negated this effect. The increase in eNOS protein levels observed with SGK1 knockdown was not seen in HAECs with combined SGK1 and KLF2 knockdown. These findings suggest a notable role of SGK1 in promoting inflammation and inhibiting vasodilation through multiple mechanisms, propositioning SGK1 as a potential therapeutic target for protecting vascular endothelial function. - Source: PubMed
Publication date: 2026/05/08
Yamamoto HiroyasuHirose AyuTakada NanakoKihara Shinji