SGK3 Antibody (Center) Blocking Peptide
- Known as:
- SGK3 Antibody (Center) Blocking Peptide
- Catalog number:
- BP7949b
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SGK3 Antibody (Center) Blocking Peptide
Related genes to: SGK3 Antibody (Center) Blocking Peptide
- 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) Blocking Peptide
Related articles to: SGK3 Antibody (Center) Blocking Peptide
- 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 - BACKGROUND: 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. OBJECTIVE: To identify the genetic defects in a patient with late-onset hypophosphatemia. SUBJECTS: A 15-year old boy with hypophosphatemic rickets, his unaffected parents and 7 siblings. DESIGN: Patients and their family members were initially analyzed for PHEX and FGF23 mutations by PCR-sequencing analysis. Exome and whole-genome sequencing were subsequently performed to identify causative genetic defects. RESULTS: The patient was normal until the age of 11 years old. He presented with severe rickets, hypophosphatemia with increased renal phosphate wasting, normal serum calcium, 1,25(OH)2D and parathyroid hormone (PTH), and mild elevation of serum FGF23. No mutation was detected in the genes known to cause HR such as PHEX, FGF23, DMP1, ENPP1, CLCN5, SGK3, FAM20C, SLC9A3R1, SLC34A1 or SLC34A3 by exome sequencing. A heterozygous variant c.448 C>T (p.Arg150Cys) in the PTH1R gene was found in the patient, his unaffected father and 5 siblings. The same heterozygous variant was previously reported in human enchondromatosis and caused enchondroma-like lesions in transgenic mice. A large heterozygous deletion of more than 7 Kb in the SGK3 distal promoter was identified in the patient by whole genome sequencing. CONCLUSIONS: SGK3 distal promoter deletion is likely the candidate gene causing the disease. PTH1R Arg150Cys variant may contribute to the disease phenotype. SGK3 promoter deletion should be considered in patients with late-onset genetic hypophosphatemic rickets. - Source: PubMed
Publication date: 2026/03/30
Uçar AhmetAlbader NajlaQattan AmalBinEssa Huda AÖzdemir Ebru MısırlıÖzdemir MustafaZou MinjingAlzahrani Ali SShi Yufei - Bitter taste receptor member 46 (TAS2R46) has a high gene abundance in enteric epithelial cells; however, the biological functions of TAS2R46 are unclear. Intestinal barrier damage caused by diabetes is widely known, but the molecular mechanism remains to be elucidated. So, our study aimed to verify that TAS2R46 signaling exerts a vital role in improving intestinal barrier injury derived from diabetes, and clarified the underlying molecular mechanisms. In the present study, we found that the TAS2R46 agonist quinine ameliorated intestinal barrier dysfunction, as evidenced by increases in the protein expression of Zonula occluden 1, occludin, and E-cadherin, as well as reduction of glycogen deposition and morphological improvement of enteric cells using PAS and H&E staining, respectively, in the colon of diabetic mice. Meanwhile, quinine activated TAS2R46 signaling, as revealed by elevations in protein expression of TAS2R46 and its key downstream element phospholipase C β2 in colon. Furthermore, the TAS2R46 agonist strychnine and hydrocortisone attenuated enteric epithelial barrier injury, activated TAS2R46 signaling, and suppressed pro-inflammatory NF-κB signaling in the high glucose-cultured Caco-2 cells, a human enteric epithelium cell line, whereas the effects were abolished after TAS2R46 blockage or knockdown. Further, results from RNA sequencing showed that up-regulation of serine/threonine protein kinase SGK3 and transport protein SNX16 might mediate the effects of TAS2R46 activation. In summary, activation of TAS2R46 signaling contributed to alleviation of intestinal barrier injury in diabetes, which was accomplished by activation of SGK3/NF-κB pathway and enhancement of SNX16/E-cadherin axis in the gut. - Source: PubMed
Publication date: 2026/02/24
Wang Jiang-MengTian SaiDuan Jing-YuZhang Chun-PingLiu Yao-Wu