PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32597022-11	2020	Moreover, circ-AKT3/miR-296-3p/E-cadherin modulated the extracellular matrix of mouse mesangial cells in high-concentration (25 mmol/L) glucose, inhibiting the synthesis of related extracellular matrix protein.	Glucose	136-143	cadherin 1	Mus musculus	31-41	
33554651-4	2021	High glucose-induced degradation and endocytosis of E-cadherin of corneal epithelial cells reduce the formation of beta-catenin/E-cadherin complex and promote the nuclear translocation of beta-catenin.	Glucose	5-12	cadherin 1	Mus musculus	52-62	
33554651-4	2021	High glucose-induced degradation and endocytosis of E-cadherin of corneal epithelial cells reduce the formation of beta-catenin/E-cadherin complex and promote the nuclear translocation of beta-catenin.	Glucose	5-12	cadherin 1	Mus musculus	128-138	
33383483-16	2021	In high glucose induced HK-2 cells, expression levels of miR-30b-5p and E-cadherin were decreased, while SNAI1, a-SMA and Vimentin were increased.	Glucose	8-15	cadherin 1	Mus musculus	72-82	
33414476-4	2021	Knockdown of HDAC5 ameliorated high glucose-induced epithelial-mesenchymal transition (EMT) of HK2 cells, indicated in the increased E-cadherin and decreased alpha-SMA, via the downregulation of TGF-beta1.	Glucose	36-43	cadherin 1	Mus musculus	133-143	
31245789-1	2019	In leptin-deficient ob/ob mice, obesity and diabetes are associated with abnormal development of neurocircuits in the hypothalamic arcuate nucleus (ARC)1, a critical brain area for energy and glucose homeostasis2,3.	Glucose	192-199	cadherin 1	Mus musculus	148-153	
30741526-6	2019	We found that prolonged sevoflurane anesthesia significantly reduces the Cdh1 level in P7 mice compared to in the P21 ones; moreover, the decrease in Cdh1 level results in a switch in glucose metabolism from the PPP to neuronal glycolysis.	Glucose	184-191	cadherin 1	Mus musculus	150-154	
30741526-8	2019	As a result, sevoflurane induces neuroapoptosis through Cdh1-mediated glucose metabolism reprogramming.	Glucose	70-77	cadherin 1	Mus musculus	56-60	
28075049-7	2017	Again, either the M90-SHIP plasmid or the PI3K/Akt pathway inhibitor LY294002 could significantly prevent the high glucose-induced increase in TGF-beta1, alpha-SMA, and secreted Col 3 and decreased E-cadherin.	Glucose	115-122	cadherin 1	Mus musculus	198-208	
26956696-6	2016	High glucose (HG)/hypoxic conditions stimulated EMT in renal tubular cells as indicated by the significant decrease in epithelial marker E-cadherin and ZO-1 while the increase in mesenchymal markers alpha-smooth muscle actin (alpha-SMA).	Glucose	5-12	cadherin 1	Mus musculus	137-147	
18218692-4	2008	RNAi-mediated silencing of the adhesion molecule E-cadherin in confluent cells reduced glucose-stimulated secretion to the levels observed in isolated cells but had no impact on basal secretion.	Glucose	87-94	cadherin 1	Mus musculus	49-59	
18218692-8	2008	The increased basal insulin secretion of dispersed cells is due to spontaneous Ca(2+) transients that activate downstream Ca(2+) effectors, whereas engagement of cell adhesion molecules including E-cadherin contributes to the greater secretory response to glucose seen in cells with normal intercellular contacts.	Glucose	256-263	cadherin 1	Mus musculus	196-206	
11756330-5	2002	Blockade of E-cadherin-mediated cell adhesion in pancreatic islets abolished the glucose-stimulated increases in intracellular Ca(2+) levels and insulin secretion, suggesting that loss of E-cadherin in beta-cells is associated with impaired insulin secretion.	Glucose	81-88	cadherin 1	Mus musculus	12-22	
11756330-5	2002	Blockade of E-cadherin-mediated cell adhesion in pancreatic islets abolished the glucose-stimulated increases in intracellular Ca(2+) levels and insulin secretion, suggesting that loss of E-cadherin in beta-cells is associated with impaired insulin secretion.	Glucose	81-88	cadherin 1	Mus musculus	188-198