Ask about this productRelated genes to: Sgk3 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 antibody
Related articles to: Sgk3 antibody
- 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 - - 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 - Hypertrophic scars (HS) frequently result from severe burns, surgical procedures and other causes of deep skin damage. The impact of serum/glucocorticoid regulated kinase family member 3 (SGK3) on the formation of HS remains unclear. HS model rats were constructed by the scalding method. In addition, tissue samples from clinical patients were collected to detect the SGK3 levels in normal skin and HS tissues by RT-qPCR and western blotting. Human-derived HS fibroblasts (HSFBs) were isolated and identified using immunofluorescence. Cell Counting Kit-8, 5-Ethynyl-2'-deoxyuridine staining and scratch assays were applied to test the ability of the HSFBs to proliferate and migrate. The influence of an SGK3 inhibitor on wound healing in rats was assessed using hematoxylin and eosin staining, Masson staining, immunofluorescence and immunohistochemistry. In addition, the levels of collagen and the proteins involved in the mitogen-activated protein kinase (MAPK)/extracellular regulated protein kinase (ERK) pathway were measured by western blotting. SGK3 was highly expressed in HS tissues. Knockdown of SGK3 resulted in reduced SGK3 levels in HSFBs. Knockdown of SGK3 reduced the proliferation and migration ability of HSFBs and suppressed cellular fibrosis. Injection with an SGK3 inhibitor reduced the burn scar area, decreased epithelial thickness and inhibited collagen deposition in rats. This inhibitor also resulted in the downregulation of collagen and MAPK/ERK pathway-related proteins. In addition, MAPK/ERK pathway agonists attenuated the effect of SGK3 inhibition, promoting HS formation while inhibiting wound healing in rats; however, MAPK inhibitors had the opposite effect. In conclusion, inhibition of SGK3 reduces the proliferation, migration and fibrosis abilities of HSFBs as well as promotes wound healing and inhibits HS formation in rats by downregulating the MAPK/ERK pathway. - Source: PubMed
Publication date: 2026/02/12
Wang FuyongWang DuanxiangWang WeidongLi Huaqiang - Semaphorin 7A (SEMA7A), a membrane-anchored glycoprotein involved in immune and vascular signalling, has been implicated in cardiovascular diseases. However, its role in the development of abdominal aortic aneurysm (AAA) has not been defined. In this study, we investigated the role of SEMA7A in AAA progression and the underlying mechanisms. - Source: PubMed
Li FengchanZhu ZhenTang FanDu YunLyu JiaxinWu LiliNi HaofuWang YingRen LijieLu QiongyuLiu HuihuiHong LeiWang HongjieTang ChaojunZhu Li