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These proteins are important in neuronal differentiation, and regeneration proteins like ACTB, GSK3B, CREB1, and CTNNB1 have physical interaction with coexpressed proteins .
MicroRNA Samples Diseases Target Effects on CD UC autophagy miR-142-3p * HCT116 + - ATG16L1, Inhibit NOD2 miR-320 HT-29 + + NOD2, Inhibit NF-[kappa]B miR-192 * HCT116 + - NOD2, Inhibit NF-[kappa]B miR-122 HT-29 + - NOD2, Inhibit NF-[kappa]B miR-93; Human colon + - ATG16L1 Inhibit miR-106B tissues, HCT116 PTEN miR-30C; Human intestinal + - ATG5, Inhibit miR-130a epithelial T84 ATG16L1 cells/mice mTOR enterocytes miR-346 Human intestinal + + Vitamin D Upregulate epithelial cells receptor (VDR) GSK3B miR-20a Human colonic + - BECN1, Inhibit mucosal tissues ATG16L1, SQSTM1 MiR-196 * Human epithelial + - LC3-II, Inhibit cells IRGM miR-665 Human/mice + + XBP1, Induce colonic mucosal ORMDL3 tissues.
In preadipocytes, both insulin and Wnt3a lead to phosphorylation of LRP 6, GSK3b, Akt, and extracellular signal-regulated kinase (ERK1/2).
By blocking the so-called SMAD signaling pathway and inhibiting glycogen synthase kinase 3 beta (GSK3B), they increased the transformational efficiency by several times--and were thus able to even simplify the means of extraction.
The level of [beta]-catenin is regulated by the adenomatous polyposis coli (APC)gene product, by cooperating with glycogen synthase kinase 3 [beta] (GSK3B) to phosphorylate multiple serine threonine residues coded by exon 3 of the [beta]-catenin gene.
Activated Akt also promotes cell cycle transition through the regulation of CDKN1B [encoded by cyclin-dependent kinase inhibitor 1B (CDKN1B)], GSK3B [encoded by glycogen synthase kinase 3 beta (GSK3B)], and mTOR [encoded by mammalian target of rapamycin (MTOR)] signaling.
By activating AKt multipurpose like phosphorylation of Bad, Bax, caspase 9, GSK3B, potential constant mitochondrial membrane and ATP synthesis that all belonging to the anti - apoptotic effects starts to appear.
CE decreased the expression of further genes encoding insulin-signaling pathway proteins including GSK3B, IGF1R, IGF2R, and PIK3R1.
La fosforilacion de la Tau por la GSK3b ocasionada por la isquemia, altera la estabilidad de los microtubulos, el transporte a traves de los axones y hace a las neuronas mas susceptibles a la proteolisis.
Irreversibly reduced expression of another gene, GSK3B, in smokers could account for an exaggerated inflammatory response and contribute to the development of lung cancer, said the scientists.
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- GSK-3 alpha
- GSK3beta isoform
- GSL medicine