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Gene Information

Gene symbol: GSK3B

Gene name: glycogen synthase kinase 3 beta

HGNC ID: 4617

Related Genes

# Gene Symbol Number of hits
1 AKT1 1 hits
2 CAMK4 1 hits
3 HGF 1 hits
4 NPHS1 1 hits
5 TFEB 1 hits

Related Sentences

# PMID Sentence
1 20362052 AKT inhibition by PGE(2) was reversed following either siRNA-mediated EP(4) knockdown, PKA inhibition (H89), or phosphatase inhibition (orthovanadate).
2 20362052 Podocytes treated for 20min with H(2)O(2) (10(-4)M), which mimics reactive oxygen species generation by cells challenged by hyperglycemic or enhanced Pgc conditions, significantly increased the levels of active p38 MAPK, AKT, JNK and ERK1/2.
3 20362052 Interestingly, stretch and PGE(2) each significantly reduced H(2)O(2)-mediated AKT phosphorylation and was reversed by pretreatment with orthovanadate while stretch alone reduced GSK-3beta inhibitory phosphorylation at ser-9.
4 20362052 Finally, mechanical stretch alone or in combination with HG, induced ERK1/2 and JNK activation, via the EGF receptor since AG1478, a specific EGF receptor kinase inhibitor, blocked this activation.
5 20362052 These changes in MAPKs and AKT activities might impact cellular integrity required for a functional glomerular filtration barrier thereby contributing to the onset of proteinuria in DN.
6 32531122 Mechanistically, we found that CAMK4 phosphorylates GSK3β (glycogen synthase kinase 3 beta), activates the Wnt pathway and stabilizes the nephrin transcriptional repressor SNAIL.
7 32531122 Silencing neonatal Fc Receptor (FcRn) or CAMK4 prevented the podocyte-damaging effects of IgG from patients with TG.
8 32827692 HGF protected against diabetic nephropathy via autophagy-lysosome pathway in podocyte by modulating PI3K/Akt-GSK3β-TFEB axis.
9 32827692 Diabetic mice treated with HGF had markedly reduced ratio of kidney weight to body weight, urinary albumin excretion, podocyte loss and matrix expansion compared with that in the non-treated counterpart.
10 32827692 Simultaneously, HGF-treated diabetic mice exhibited increased autophagy activity as indicated by the decreased accumulation of sequestosome 1 (SQSTM1/ p62) and increased microtubule-associated proteins 1 light chains 3 (LC3) II/LC3I ratio.
11 32827692 These beneficial effects of HGF were blocked by HGF/c-Met inhibitor Crizotinib or phosphatidylinositide 3-kinases (PI3K) inhibitor LY294002.
12 32827692 Moreover, HGF treatment obviously prevented inactivation of the protein kinase B (Akt)-glycogen synthase kinase 3 beta (GSK3β)-transcription factor EB (TFEB) axis in high glucose-stimulated podocytes, which was associated with improved lysosome function and autophagy.
13 32827692 These results suggested that HGF protected against diabetic nephropathy through restoring podocyte autophagy, which at least partially involved PI3K/Akt-GSK3β-TFEB axis-mediated lysosomal function improvement.