PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30536344-0	2018	Metformin promotes differentiation of human bone marrow derived mesenchymal stem cells into osteoblast via GSK3beta inhibition.	Metformin	0-9	glycogen synthase kinase 3 alpha	Homo sapiens	107-115	
30536344-4	2018	Therefore, the aim of this study is to evaluate the role of GSK3beta in metformin-induced osteogenic differentiation of mesenchymal stem cells (MSCs).	Metformin	72-81	glycogen synthase kinase 3 alpha	Homo sapiens	60-68	
30536344-7	2018	The expression of GSK3beta, beta-catenin and AMPK were measured by Western blotting in MSCs treated with metformin.	Metformin	105-114	glycogen synthase kinase 3 alpha	Homo sapiens	18-26	
30536344-9	2018	Next, we showed that GSK3beta and Wnt signaling pathway are involved in metformin-induced osteogenic differentiation of hBMSCs.	Metformin	72-81	glycogen synthase kinase 3 alpha	Homo sapiens	21-29	
30536344-10	2018	Furthermore, osteogenic differentiation of hBMSCs induced by metformin could be eliminated by inhibiting phosphorylation of GSK3beta.	Metformin	61-70	glycogen synthase kinase 3 alpha	Homo sapiens	124-132	
30536344-11	2018	CONCLUSIONS: The data suggested that metformin promoted the osteoblast differentiation of MSCs by, at least partly, inhibiting GSK3beta activity.	Metformin	37-46	glycogen synthase kinase 3 alpha	Homo sapiens	127-135	
30536344-12	2018	Additionally, we also found that AMPK plays an essential role in the inhibition of GSK3beta by metformin.	Metformin	95-104	glycogen synthase kinase 3 alpha	Homo sapiens	83-91	
34432352-0	2021	Pretreatment with metformin prevents microcystin-LR-induced tau hyperphosphorylation via mTOR-dependent PP2A and GSK-3beta activation.	Metformin	18-27	glycogen synthase kinase 3 alpha	Homo sapiens	113-122	
34432352-7	2021	In sum, the results suggested that metformin can ameliorate the MC-LR-induced AD-like phenotype by preventing tau phosphorylation at Ser202, which was mainly mediated by mTOR-dependent PP2A and GSK-3beta activation.	Metformin	35-44	glycogen synthase kinase 3 alpha	Homo sapiens	194-203	
34486387-8	2021	While 0.1mM/L metformin upregulated the expression of BECLIN1 and LC3 I/II gene and inhibited the expression of mTOR and GSK3beta, contribute to reverse the osteogenesis inhibition of ASCs caused by high glucose.	Metformin	14-23	glycogen synthase kinase 3 alpha	Homo sapiens	121-129	
34649197-6	2021	The selective glucose deprivation would not only disrupt tumor energy metabolism, but also upregulate the PP2A regulatory subunit B56delta and sensitize tumor cells to the metformin-induced CIP2A inhibition, leading to efficient apoptosis induction via PP2A-GSK3beta-MCL-1 axis with negligible side effects.	Metformin	172-181	glycogen synthase kinase 3 alpha	Homo sapiens	258-266	
35044756-5	2022	Additionally, combined metformin and anthocyanin treatment suppressed protein tyrosine phosphatase 1B expression and regulated the PI3K/AKT/GSK3beta pathway.	Metformin	23-32	glycogen synthase kinase 3 alpha	Homo sapiens	140-148	
33524789-6	2021	First, many studies showed that metformin could induce autophagy via a number of signaling pathways, including AMPK-related signaling pathways (e.g. AMPK/mTOR, AMPK/CEBPD, MiTF/TFE, AMPK/ULK1, and AMPK/miR-221), Redd1/mTOR, STAT, SIRT, Na+/H+ exchangers, MAPK/ERK, PK2/PKR/AKT/ GSK3beta, and TRIB3.	Metformin	32-41	glycogen synthase kinase 3 alpha	Homo sapiens	278-286	
35350904-0	2022	Plantamajoside promotes metformin-induced apoptosis, autophagy and proliferation arrest of liver cancer cells via suppressing Akt/GSK3beta signaling.	Metformin	24-33	glycogen synthase kinase 3 alpha	Homo sapiens	130-138	
33221742-8	2020	We suspected that metformin may play a neuroprotective role in early AD by increasing NEAT1 expression and through FZD3/GSK3beta/p-tau pathway.	Metformin	18-27	glycogen synthase kinase 3 alpha	Homo sapiens	120-128	
33918222-7	2021	Unexpectedly, Wnt/beta-catenin signaling remained activated in chronic HCV-infected cells after HCV eradication by DAA, but metformin reversed it through PKA/GSK-3beta-mediated beta-catenin degradation, inhibited colony-forming ability and proliferation, and increased apoptosis, suggesting that DAA therapy in combination with metformin may be a novel therapy to treat HCV-associated HCC where metformin suppresses Wnt/beta-catenin signaling for HCV-infected patients.	Metformin	124-133	glycogen synthase kinase 3 alpha	Homo sapiens	158-167