GSK3B (Glycogen Synthase Kinase 3 Beta)

The journal retracts the article, "GSK-3β-Targeting Fisetin Promotes Melanogenesis in B16F10 Melanoma Cells and Zebrafish Larvae through β-Catenin Activation" [...].

Genetic ablation of β-catenin under GSK3-deficient conditions reduced stem and Paneth cell populations while restoring tuft and enteroendocrine cells, thereby ameliorating niche abnormalities and improving absorptive and peristaltic functions. This study indicates the essential role of GSK3/β-catenin signaling in maintaining intestinal niche integrity and digestive physiology, highlighting potential therapeutic targets for intestinal and digestive disorders.

Although APP expression is increased by palmitate exposure, there was no increase in secreted or intracellular Aβ, and tau phosphorylation was reduced, implying that these defects are separate from the classical hallmarks of AD. We conclude that long-term, chronic exposure of differentiating neurones induces pathological changes that may explain the link between T2DM and LOAD.

Like β-catenin, SREBP2 is stabilized by extracellular Wnt ligands; unlike β-catenin, its regulation is independent of GSK3β and CK1α and requires the entire APC mutational cluster region (MCR), whereas β-catenin turnover can operate with only a partial MCR. These findings define a β-catenin-independent branch of Wnt signaling that couples APC to sterol metabolism, providing a mechanistic rationale to target the mevalonate/SREBP2 axis in APC-mutant colorectal cancer.

Mechanistic studies revealed that assembly of the oncogenic BDC is scaffolded by its own substrate β-catenin, establishing an autoregulatory mechanism that represents an unexploited vulnerability in cancers harboring common APC truncations. Our comprehensive mutational resource provides a foundation for understanding WNT/β-catenin signaling mechanisms in health and disease, while revealing strategies for therapeutic intervention in WNT-driven cancers.

We demonstrated that pioglitazone and minocycline protected against glutamate-induced axonal injury, rotenone-induced neuronal death and promoted oligodendrocyte differentiation. In summary, our findings demonstrate that human preclinical IPSC platforms can be used to characterize the neuroprotective properties of compounds and thus may aid the selection of drugs for clinical trials. Moreover, the platform's flexibility allows for the easy incorporation of additional disease-specific phenotypic assays.

Targeted re-analysis of publicly available single-cell RNA-sequencing datasets from COVID pneumonia patients revealed elevated CDC6 expression alongside reduced MYC and ODC1 levels in alveolar epithelial cells exhibiting markers of senescence. Collectively, these findings identify putrescine as a metabolic checkpoint in replication stress-induced senescence and reveal a MYC-orchestrated signaling-metabolic circuit that temporally integrates oncogene activation with cell fate decisions.

Clinical and bioinformatic analyses revealed that circ_GLS was significantly downregulated in NSCLC tissues, while miR-410-3p was significantly upregulated and GSK3beta downregulated, correlating with diagnosis and prognosis, though independent validation is needed. In conclusion, this study demonstrates for the first time in NSCLC that this axis regulates malignancy, suggesting their potential as therapeutic targets and biomarkers, although challenges in targeting circRNAs remain.

This study demonstrates that although all four methods can isolate GELNs, UC is recommended for fundamental research due to its high protein yield, excellent stability, and potent in vitro anti-lung cancer activity. Furthermore, the anti-lung cancer activity of GELNs may be attributed to the regulation of GSK3B, PGR, and SRC by 10-Gingerol, Hexahydrocurcumin, and [6]-Dehydrogingerdione.

Nonetheless, GLN therapy significantly alleviated testicular impairments via regulating aforementioned biochemical and histological abnormalities. These findings suggest he palliative efficacy of GLN against DPN induced testicular damages thereby recommending the use of GLN to promote reproductive health in male.

Additionally, HAR, HAL, and P. harmala's alkaloid extract markedly decreased GSK3β expression and increased BAX expression. These results may offer therapeutic potential in oxaliplatin-resistant phenotypes.

Cancer-induced EndMT affects tumors and surrounding TME-promoting tumor growth and metastasis, expanding cancer stem cell-like cells, driving macrophage differentiation, and redistributing pericytes-and is closely associated with poor survival and therapy resistance. Finally, we indicate each study's stance: some frame cancer-induced EndMT as a source of CAFs, whereas others, from an endothelial perspective, emphasize barrier weakening and promotion of metastasis.