SGK1 polyclonal antibody
- Known as:
- SGK1 pab (anti-)
- Catalog number:
- PAB9960
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SGK1 polyclonal antibody
Related genes to: SGK1 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 polyclonal antibody
Related articles to: SGK1 polyclonal antibody
- Endothelial and macrophage inflammation and sterol transport play an important role in atherogenesis. Serum/glucocorticoid-regulated kinase 1 (SGK1) is a member of the serine/threonine kinase family sharing approximately 54% identity with Akt. It has been implicated in smooth muscle cell calcification and macrophage inflammation during atherosclerosis; however, the role of SGK1 in endothelial dysfunction and endothelial or macrophage lipid metabolism is less characterized. In this study, we intraperitoneally injected high-cholesterol diet-fed male ApoE-knockout mice with the SGK1 inhibitor EMD638683 (10 mg/kg) every other day for 2 weeks, followed by histopathological and transcriptome analysis of the atherosclerotic lesion. To study the SGK1-associated mechanism in vascular inflammation in vitro, SGK1 silencing was performed in primary human umbilical vein endothelial cells (HUVECs), followed by treatment with pro-inflammatory cytokines. In THP-1-differentiated macrophages, SGK1 silencing followed by treatment with lipopolysaccharides was used. We showed that ApoE-knockout mice treated with EMD638683 show reduced atherosclerotic plaque area and attenuated endothelial and macrophage inflammation. Further transcriptome analysis of thoracic aortae showed that SGK1 inhibition downregulated inflammation and lipid metabolism-associated genes. In vitro, interleukin-1β treatment induces SGK1 phosphorylation. SGK1 inhibitor or siRNA reduced endothelial inflammation induced by pro-inflammatory cytokine treatments in HUVECs through nuclear factor κ light chain enhancer of activated B cell (NF-κB) signaling. In THP-1-differentiated macrophages, SGK1 inhibition or knockdown by siRNA is associated with reduced levels of pro-inflammatory cytokines, NF-κB, and sterol regulatory element binding protein 1 (SREBP1) pathway activation, following lipopolysaccharide treatment. SREBP1 inhibition by fatostatin or siRNA reduced p65 phosphorylation. In conclusion, the inhibition of SGK1 has been shown to reduce atherosclerotic plaque area and attenuate endothelial and macrophage inflammation in ApoE-knockout mice via NF-κB and SREBP1 signaling. These results not only contribute to our understanding of the complex interplay between vascular inflammation and lipid metabolism but also hold promise for the development of novel therapeutic strategies for atherosclerosis. - Source: PubMed
Publication date: 2026/06/11
Li Yang-XianDing Shu-XiangHong Hui-LingCao Xiao-YunHan Yu-MengTian Jin-WeiFung Sin-HangTsui Stephen Kwok-WingWu Ya-LanTian Xiao Yu - Plasma-activated medium (PAM), a redox-active anticancer modality, induces cytotoxicity in multiple tumor models, but the mechanisms underlying PAM-induced tumor cell death remain incompletely understood. Here, using A549 lung cancer cells together with additional tumor models, we identify a lysosome - mitochondria Ca circuit that drives a distinct form of PAM-induced tumor-selective cell death. PAM promotes the coupling of the lysosomal Ca channel TRPML1 to the mitochondrial outer membrane protein VDAC1 at organelle contact sites, leading to lysosomal Ca release, mitochondrial Ca overload, membrane depolarization, cytochrome c release, and cell death. Mechanistically, PAM suppresses mTORC2 - SGK1 signaling, reduces VDAC1 phosphorylation at Ser104, and stabilizes VDAC1 on mitochondria. Accumulated VDAC1 then engages TRPML1 through Lys109 and Arg163 to facilitate pathological Ca transfer. Disrupting this interface, or restoring phosphomimetic control of VDAC1, attenuated mitochondrial Ca overload, improved cell survival, and weakened the antitumor effect of PAM in vivo. Pan-cancer analyses further suggested that although high VDAC1 expression is associated with poor prognosis, it may help stratify tumors more likely to respond to PAM. Together, these findings establish the VDAC1 - TRPML1 axis as a key mechanistic link between PAM-induced redox stress and lysosome - mitochondria Ca-dependent tumor cell death, and highlight this pathway as a potential therapeutic target and response biomarker. - Source: PubMed
Publication date: 2026/06/03
Huang PengpengZheng YanZhou ChuanzanDing ChengbiaoZhang QiFeng DechaoWu Zhengwei - Based on the previously identified lead compound H1, a 4-trifluoromethyl-2-arylaminoquinoline derivative, this study designed and synthesized 13 novel derivatives to enrich structural diversity and optimize bioactivity, and further evaluated their SGK1 inhibitory activity and anti-prostate cancer effects. The results revealed that compound 7h exhibited stronger SGK1 inhibitory ability and superior in vitro antitumor activity, as well as better SGK family selectivity than H1. Mechanistic experiments verified that 7h induced cell apoptosis, caused S-phase cell cycle arrest and inhibited cell migration in a concentration or time-dependent manner. It directly bound to and stabilized SGK1, and effectively downregulated the phosphorylation of downstream MDM2 and GSK-3β. Molecular docking indicated that 7h functioned as an ATP-competitive inhibitor by targeting the ATP-binding pocket of SGK1. The methylene modification of 7h strengthened its binding interaction with SGK1, which accounted for its enhanced bioactivity. Moreover, 7h possessed favorable ADME properties with high oral absorption, qualified blood-brain barrier penetration and no CYP inhibition risk. Collectively, the structurally optimized compound 7h serves as a high-efficiency and druggable lead candidate, providing a reliable foundation for the further development of novel anti-prostate cancer drugs. - Source: PubMed
Publication date: 2026/05/28
Zhou YafangCheng ShaLi ChengLiu XinyuYu JiaYu GangYi PingZeng XiaopingTu WeiMeng XuelingLiu KunPeng XiaolinZan NingningLuo HengXu BixueXu Guangcan - The limiting step in immune-active drug development is increasingly not candidate generation but testing whether a candidate therapy is effective in a system that preserves tissue architecture, vascular exposure, multicellular interaction, and repeated pharmacodynamic sampling without patient exposure. We developed an acellular normothermic machine-perfusion platform for intact porcine spleen designed as a translational immune-organ assay. Across independent acellular perfusions, the circuit maintained physiologic parameters, preserved red- and white-pulp histology, and yielded viable effluent cells suitable for serial flow cytometry and multiomics. High-dose methylprednisolone was used as a clinically familiar perturbation to determine whether the platform could resolve steroid immunosuppression at mechanistically distinct levels. Effluent RNA-seq identified canonical glucocorticoid-responsive transcriptional programs, including DUSP1, FKBP5, PER1, DDIT4, SGK1, KLF9, ANXA1, NF-κB feedback regulators, and JAK/STAT suppressor pathways. SOCS3 was a prominent early signal in the perfusion transcriptome and was validated orthogonally at the protein level in prednisone-treated, CD3/CD28-activated primary murine splenocytes, strengthening its role as a candidate pharmacodynamic marker. In parallel, data independent acquisition (DIA) proteomics of effluent cell pellets nominated a non-transcriptional protein-level response: a Sus scrofa LGALS13-annotated, CLC/Galectin-10-like galectin detected despite absence of the corresponding effluent-cell transcript. Because this porcine LGALS13-annotated protein group is treated here as an orthologous CLC/Galectin-10-like signal rather than as canonical human placental Galectin-13/PP13, we tested recombinant human Galectin-10 in vitro. Human Galectin-10 induced marked apoptosis of CD3/CD28-stimulated Jurkat cells, prioritizing this axis for future mechanistic testing without proving causality in the perfused spleen. These data establish acellular spleen perfusion as a serial multiomic platform for translational immunopharmacology and motivate deployment with otherwise-discarded human donor spleens. - Source: PubMed
Publication date: 2026/05/19
Callais Nicholas AWelch ShawnRainwater Randall RSchaller JohnDeng ShuoqiuAzevedo-Pouly AnaBurdine Marie SchlutermanBurdine Lyle - 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