SGK3 Antibody (Center)
- Known as:
- SGK3 Antibody (Center)
- Catalog number:
- AP7949b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SGK3 Antibody (Center)
Related genes to: SGK3 Antibody (Center)
- Gene:
- SGK3 NIH gene
- Name:
- serum/glucocorticoid regulated kinase family member 3
- Previous symbol:
- SGK2, SGKL
- Synonyms:
- -
- Chromosome:
- 8q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-12
- Date modifiied:
- 2016-11-15
Related products to: SGK3 Antibody (Center)
Related articles to: SGK3 Antibody (Center)
- Myocardial infarction (MI) leads to substantial cardiomyocyte loss and heart failure, whereas current therapies fail to promote cardiac regeneration. Our prior work demonstrated that serum and glucocorticoid-regulated kinase 3 (SGK3) promote cardiac repair. To overcome the limitations of viral gene therapy, we develop a recombinant human SGK3 (rhSGK3) protein fused with a cell-penetrating peptide and encapsulate it in a thermosensitive PLGAPEG-PLGA hydrogel for sustained local delivery. In vitro, rhSGK3 efficiently enters neonatal mouse cardiomyocytes and significantly promotes proliferation, reduces OGD/R-induced apoptosis, stabilizes OGD/R-induced mitochondrial membrane potential, and upregulates the expressions of glycolytic enzymes including PKM2, LDHA, PFKP, and HK2, while shifting energy metabolism from oxidative phosphorylation toward glycolysis. These effects are reversed by the glycolysis inhibitor 2-DG. Mechanistically, rhSGK3 activates the HIF-1α/HK2 signaling axis, and HIF-1αknockdown abolishes its pro-proliferative and anti-apoptotic effects. In an in vivo myocardial ischemia/reperfusion (I/R) mouse model, intramyocardial injection of rhSGK3-hydrogel preserves mitochondrial ultrastructure, enhances cardiomyocyte proliferation, reduces apoptosis, attenuates fibrotic scar formation, and significantly improves cardiac function at 28 days post-I/R. Importantly, HIF-1α knockdown in vivo reverses these protective effects. Together, these findings suggest that local delivery of rhSGK3 via a thermosensitive hydrogel promotes cardiac repair after I/R injury through HIF-1α/HK2-mediated glycolytic reprogramming and mitochondrial protection. This study presents a promising protein-based, gene-integration-free therapeutic strategy for myocardial repair. - Source: PubMed
Publication date: 2026/09/08
Wei TianwenSun YuxiaoLin ZhihaoWan TangjiangLiang YuchengShen ShitongYou JieyunZhang QiLi Yafei - Epidemiological evidence confirms high-fat diet (HFD) as a key risk factor for colorectal cancer (CRC) progression. Aryl hydrocarbon receptor (AhR), a ligand-dependent nuclear transcription factor enriched in intestinal tissues, regulates intestinal metabolism and tumorigenesis. However, its role and mechanism in HFD-induced CRC progression remain unclear. - Source: PubMed
Publication date: 2026/08/28
Dong QiguanWu TongYang YuchaoYang YanGao BoShi DianzhiWang HengjiaoYan Ying - Eukaryotic initiation factor 4E-binding protein 1 (EIF4EBP1/4E-BP1) is a pivotal translational regulator with context-dependent roles in breast cancer pathogenesis. Its phosphorylation status, dynamically controlled by mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), and AMP-activated protein kinase (AMPK) signaling, dictates a dualistic function: hypophosphorylated EIF4EBP1 suppresses oncogenesis by sequestering eIF4E and inhibiting cap-dependent translation of pro-tumorigenic mRNAs (e.g., cyclin D1 and c-MYC), while hyperphosphorylation promotes tumor progression and therapeutic resistance. EIF4EBP1 amplification (8p11-p12) is correlated with endocrine resistance and poor prognosis. EIF4EBP1 modulates cell cycle checkpoints, metabolic adaptation under stress, and resistance to cyclin-dependent kinase (CDK) 4 and 6 inhibitors and rapalogs via feedback loops (e.g., SGK3/Akt reactivation). Emerging therapeutic strategies, such as ATP-competitive mTOR inhibitors, bisteric compounds, and agents targeting polyamine metabolism or upstream kinases, exploit the dynamics of EIF4EBP1 phosphorylation. As a biomarker, phosphorylated EIF4EBP1 levels predict tumor aggressiveness and treatment failure, positioning it as a critical node for precision oncology. Future research must address spatial heterogeneity and leverage multi-omics/AI-driven approaches. - Source: PubMed
Liu WeijiaHou LiliTang DandanMou HaiyuWang WeijieLiu Song-BaiLi Xiaohua - Conditions resulting in elevated fibroblast growth factor 23 (FGF23) cause hypophosphatemic rickets and osteomalacia. The most common of these is X-linked hypophosphatemia. In this review we will broadly discuss the other less common and clinically distinct forms of renal hypophosphatemia, with a focus on the autosomal dominant and autosomal recessive types. - Source: PubMed
Publication date: 2026/07/07
Ferreira Carlos RImel Erik A - To investigate the expression characteristics of type II inositol polyphosphate 4-phosphatase (INPP4B), phosphatase and tensin homolog (PTEN) and serum/glucocorticoid-regulated kinase 3 (SGK3) in papillary thyroid carcinoma (PTC) and to assess the correlations among their expressions. - Source: PubMed
Publication date: 2026/06/10
Bai QingshuangWu CailanShen LinnaLi NingTan JianLi Qiang