GSK3B Protein
- Known as:
- GSK3B Protein
- Catalog number:
- 10044-H07B
- Product Quantity:
- 20
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- GSK3B Protein
Related genes to: GSK3B Protein
- Gene:
- GSK3B NIH gene
- Name:
- glycogen synthase kinase 3 beta
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-15
- Date modifiied:
- 2016-10-05
Related products to: GSK3B Protein
Related articles to: GSK3B Protein
- Esophageal cancer (EC) is a frequently diagnosed malignancy with limited available treatment options. Emerging evidence has underscored the significant role of tripartite motif (TRIM) proteins in various cancers. However, the specific role of TRIM11 in EC has not been elucidated. Here, we conducted a comprehensive bioinformatics analysis, along with cell line models and animal culture experiments, to investigate the role of and molecular mechanisms through which TRIM11 contributes to EC progression, and evaluate its potential as a candidate marker associated with adverse clinicopathological features. Transcriptomic analysis was conducted using data from TCGA, GTEx, CCLE, and other publicly available databases to assess TRIM11 expression and its correlation with clinicopathological features, immune infiltration and TRIM11's relationship with treatment response in EC. In vitro experiments showed that TRIM11 overexpression significantly promoted EC cell proliferation, migration, and invasion. Flow cytometry analysis revealed that TRIM11 increased the proportion of cells entering the S phase. Mechanistically, co-immunoprecipitation assays demonstrated that endogenous TRIM11 directly interacted with Axin2 and GSK3β, two core components of the β-catenin destruction complex. Additionally, TRIM11 knockdown altered the expression of key proteins in the β-catenin signaling pathway, including CyclinD1, GSK3β, Axin2, and β-catenin. Collectively, these findings highlight TRIM11 as a pro-oncogenic factor and suggest that it is a potential functional driver of EC. - Source: PubMed
Publication date: 2026/05/14
Li WeiLan QingzhiLu ShiminDong Weiguo - Gestational diabetes mellitus (GDM) is a chronic metabolic disease occur during the pregnancy which is characterized via insulin resistance, hyperglycemia, inflammation and oxidative stress. Gigantol, a naturally occurring bibenzyl phytoconstituents showed the anti-inflammatory and antioxidant potential against various disease. The aim of the current study was to investigate the protective effect of gigantol against streptozotocin (STZ) induced GDM in female rats. Intraperitoneal administration of STZ (25 mg/kg) was used for induction the GDM in the rats and rats were received the oral administration of different doses of gigantol. The body weight, fetal weight, placental weight and placental index. The oral glucose tolerance test (OGTT), insulin tolerance test (ITT) estimated and calculate the area the under curve (AUC). Antioxidant parameters, inflammatory cytokines, inflammatory and apoptosis parameters were estimated. The mRNA expressions were also estimated. Gigantol treatment significantly improved the body weight, fetal weight and suppressed the placental weight and index. Gigantol remarkably altered the fasting blood glucose, plasma insulin, HOMA-IR and HOMA-β. Its also suppressed the blood glucose level during OGTT and ITT. Gigantol remarkably altered the level of AGE, visfatin, adiponectin, leptin, ICAM-1, VCAM-1, HO-1, Nrf2; antioxidant parameters, lipid parameters, inflammatory cytokines, inflammatory parameters and apoptosis parameters. Gigantol significantly altered the mRNA expression of Akt, MyD88, NF-κB, PI3K, TRL4, GSK-3β, Nrf2 and HO-1. Gigantol exhibited a protective effect against GDM via alterations in the Nrf2/HO-1, TLR4/MyD88/NF-κB, and PI3K/Akt/GSK-3β signaling pathways. - Source: PubMed
Su YeqingXing JiejieZheng Xian - Cobalt exposure, increasingly encountered in industrial and medical contexts, represents a rising neurotoxic threat, yet its underlying mechanisms and effective treatments remain poorly characterized. Here, we investigated the neuroprotective effects of Lyoniresinol, a natural lignan with antioxidant and anti-inflammatory properties, in a rat model of cobalt-induced neurodegeneration. Rats were exposed to cobalt chloride (CoCl₂, 40 mg/kg/day, intraperitoneally) for 14 days, with a subset receiving co-treatment with Lyoniresinol (30 mg/kg/day). Behavioral assessments demonstrated that Lyoniresinol significantly improved spatial memory, recognition memory, anxiety-like behavior, and motor coordination, as evaluated by the Morris water maze, novel object recognition, elevated plus maze, and rotarod test, respectively. Biochemical analyses revealed that Lyoniresinol enhanced antioxidant defense [increased superoxide dismutase (SOD) and reduced glutathione (GSH), reduced Malondialdehyde (MDA)], suppressed pro-inflammatory cytokines [Interlukin-1β (IL-1β), IL-6, tumour necrosis factor-α (TNF-α), C-reactive protein (CRP)], and normalized neurotransmitter levels [dopamine, serotonin, and Gamma-aminobutyric acid (GABA)], indicating restored redox homeostasis and neurochemical balance. Histopathological analysis confirmed preservation of hippocampal neuronal architecture in treated animals. Molecular investigations further demonstrated that Lyoniresinol significantly downregulated the overactivation of Nuclear Factor kappa B (NF-κB), Glycogen synthase kinase-3 beta (GSK3β), and c-Jun N-terminal kinase (JNK) signaling pathways at both mRNA and protein levels, as evidenced by qPCR and Western blot analyses. These findings suggest that Lyoniresinol exerts a broad-spectrum neuroprotective effect against cobalt-induced neurotoxicity by concurrently ameliorating behavioral impairments, oxidative and inflammatory stress, neurotransmitter disruptions, and intracellular signaling dysregulation. - Source: PubMed
Zhang YumingWang JunHuo QifanYao BoSu JinyaoXue Fei - Curcumin exhibits potent neuroprotective activity but is limited by poor solubility and limited bioavailability. Conjugation with hyaluronic acid (HA), a biocompatible polysaccharide, may improve the stability, therapeutic efficacy and bioavailability of curcumin. - Source: PubMed
Publication date: 2026/05/11
Gayathri S VManjunatha P MPai PrasannaMuzzammil Bahawuddeen Khalwathi MJana PrithwirajAkhila A VPriya AnnuPrerna Satvik Marwein Arjune SinghNchimbi Abubakar HamzaAtem Atem Edward MachokSharma Uday RajHari Babu T - Macroautophagy/autophagy is a critical process for maintaining cellular homeostasis and has emerging implications in cancer biology. DRAM2 (DNA damage regulated autophagy modulator 2), a transmembrane protein enriched at lysosomal membranes, has been implicated in autophagy regulation; however, the upstream mechanisms governing its trafficking and function remain unclear. In this study, we identified RPS6KA3/RSK2, a stress-responsive kinase downstream of the MAPK pathway, as a novel upstream kinase of DRAM2. RPS6KA3/RSK2 interacted with and phosphorylated DRAM2 at Ser263 within its cytosolic tail. This phosphorylation was required for AP3D1/AP-3-dependent trafficking of DRAM2 to the late endosomal-lysosomal pathway, thereby facilitating autolysosome formation and sustaining autophagic flux. In contrast, the non-phosphorylatable DRAM2 mutant failed to bind AP3D1/AP-3, exhibited defective lysosomal trafficking, and was partially redistributed toward plasma membrane-proximal compartments, where it enhanced exosome secretion. Bioinformatic analyses revealed a strong positive correlation between RPS6KA3/RSK2 and DRAM2 expression in melanoma tissues, and elevated DRAM2 expression was associated with poor patient prognosis. Depletion of RPS6KA3/RSK2 or DRAM2 impaired autophagic flux and inhibited melanoma cell proliferation. Similarly, expression of the DRAM2 mutant suppressed melanoma progression in vitro and in vivo by disrupting autophagy. Moreover, DRAM2 protein levels were elevated in skin cancer tissues compared to normal tissues. Collectively, our findings uncover a phosphorylation-dependent trafficking switch that bifurcates DRAM2 function between autophagy and exosome secretion, and establish the RPS6KA3/RSK2-DRAM2 axis as a critical regulator of melanoma progression. This signaling pathway may represent a promising therapeutic target for autophagy-associated malignancies. AGC: protein kinase A, G, and C families; AP-3: adaptor protein 3; CD: cytosolic domain; CSNK2/CK2: casein kinase 2; co-IP: co-immunoprecipitation; CQ: chloroquine; CREB: cAMP responsive element binding protein; CTKD: C-terminal kinase domain; DRAM2: DNA damage regulated autophagy modulator 2; EBSS: Earle's balanced salt solution; ESCRT: endosomal sorting complexes required for transport; GEPIA: gene expression profiling interactive analysis; GPS: global positioning system; GRK7: G protein-coupled receptor kinase 7; GSK3B: glycogen synthase kinase 3 beta; IP-MS: immunoprecipitation-mass spectrometry; LAMP1: lysosome associated membrane protein 1; LAMP2: lysosome associated membrane protein 2; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAPK: mitogen-activated protein kinase; MVB: multivesicular body; NTA: nanoparticle tracking analysis; NTKD: N-terminal kinase domain; PI4K2: phosphatidylinositol 4-kinase type 2 alpha; PRKAA2: protein kinase AMP-activated catalytic subunit alpha 2; RPS6KA3/RSK2: ribosomal protein S6 kinase A3; SKCM: skin cutaneous melanoma; SQSTM1: sequestosome 1. - Source: PubMed
Publication date: 2026/05/03
Lee Ga-EunNam Soo-BinMoon EunyoungHuh Yang HoonPark Hye SunNa SeungjinKim Jin YoungHan Eun HeeCho HanaChoi Jung HoonCho Yong-YeonBang GeulLee Cheol-Jung