SGK3 (Center) antibody
- Known as:
- SGK3 (Center) (anti-)
- Catalog number:
- orb38764
- Product Quantity:
- 5 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- SGK3 (Center) antibody
Related genes to: SGK3 (Center) antibody
- 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 (Center) antibody
Related articles to: SGK3 (Center) antibody
- 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 - Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by persistent deficits in social communication and repetitive behaviors. Recent studies have indicated that heterozygous mutations in the mixed lineage leukemia 5 (MLL5) gene are implicated in ASD susceptibility and associated with neurodevelopmental abnormalities. However, the detailed mechanisms remain unclear. Here, we demonstrate that Mll5 haploinsufficiency in mice impairs microglial phagocytosis, drives neuronal hyperexcitability, and recapitulates core ASD-like behaviors. We also show that Mll5 acts as an epigenetic regulator, modulating microglial phagocytosis via the TREM2-SGK3-GSK3β signaling axis, which is associated with deficient glucose metabolism. Furthermore, microglia derived from individual with ASD exhibit parallel reductions in MLL5 expression and phagocytic function. By targeting this pathway, lithium chloride, a GSK3β inhibitor, rescues both microglial phagocytosis deficits and behavioral abnormalities in Mll5 haploinsufficienct mice. Our findings highlight MLL5's critical role in ASD and its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/04/17
Gao ShuminLin QingxiuLiu XiaotongJia MeixiangZhang An-YiFeng ZhendongHan LeiQiu NianzhuangLiu Xiao-XingZhai HuajieZhang HaizhenZhang JingDing XiaodanZhang YanLu LinShi JieLiu Jia JiaWei Ya Bin - Hypophosphataemic rickets (HR) is a group of rare hereditary renal phosphate wasting disorders caused by mutations in the PHEX, FGF23, DMP1, ENPP1, CLCN5, SGK3, SLC9A3R1, SLC34A1 or SLC34A3. - Source: PubMed
Publication date: 2026/03/30
Uçar AhmetAlbader NajlaQattan AmalBinEssa Huda AÖzdemir Ebru MısırlıÖzdemir MustafaZou MinjingAlzahrani Ali SShi Yufei