PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26264186-5	2015	In addition, inhibition of ZEB1 expression potentiated redifferentiation induced by a combination of soluble factors, as judged by an improved response to glucose stimulation and a 3-fold increase in the fraction of C-peptide-positive cells to 60% of BCD cells.	Glucose	155-162	zinc finger E-box binding homeobox 1	Homo sapiens	27-31	
33193839-7	2020	ZEB1-AS1 in lung cells was downregulated by high glucose treatment, and overexpression of ZEB1-AS1 resulted in inhibited lung cancer cell apoptosis and downregulated p53.	Glucose	49-56	zinc finger E-box binding homeobox 1	Homo sapiens	0-4	
33215445-0	2020	NORAD regulates proliferation and apoptosis in cardiomyocytes under high-glucose treatment through miRNA-150-5p/ZEB1 axis.	Glucose	73-80	zinc finger E-box binding homeobox 1	Homo sapiens	112-116	
31209937-6	2019	Our results demonstrated that network pharmacology could provide a guidance role for traditional Chinese medicine research, and mulberry leaves could be of benefit in preventing high glucose-induced EMT in HK-2 cells, which proved that it was related to the upregulation of miR-302a by targeting ZEB1 and the inhibition of NADPH oxidase/ROS/ERK1/2 pathway.	Glucose	183-190	zinc finger E-box binding homeobox 1	Homo sapiens	296-300	
32294702-0	2020	lncRNA ZEB1-AS1 inhibits high glucose-induced EMT and fibrogenesis by regulating the miR-216a-5p/BMP7 axis in diabetic nephropathy.	Glucose	30-37	zinc finger E-box binding homeobox 1	Homo sapiens	7-11	
32294702-14	2020	lncRNA ZEB1-AS1 inhibited high glucose-induced EMT and fibrogenesis via regulating miR-216a-5p/BMP7 axis in diabetic nephropathy, providing a potential target for DN therapy.	Glucose	31-38	zinc finger E-box binding homeobox 1	Homo sapiens	7-11	
29227974-9	2018	In vitro, miR-302a-3p expression in HG group increased at 6 h and ascended to the highest level at 12 and 24 h and then gradually decreased from 48 to 72 h. More interesting, ZEB1 protein expression had an opposite change, which gradually decreased from 6 to 24 h and then gradually increased from 48 to 72 h. Moreover, overexpression of miR-302a-3p suppressed expression of ZEB1 in the post-transcriptional level and reversed high glucose-mediated downregulation of E-cadherin and upregulation of vimentin.	Glucose	432-439	zinc finger E-box binding homeobox 1	Homo sapiens	175-179	
28412735-4	2017	We further show that ZEB1 induced NNMT, rendered cells resistant to glucose deprivation and recapitulated metabolic adaptations and mesenchymal gene expression observed in glucose-restricted cells.	Glucose	68-75	zinc finger E-box binding homeobox 1	Homo sapiens	21-25	
28111379-0	2017	Knocking down TCF8 inhibits high glucose- and angiotensin II-induced epithelial to mesenchymal transition in podocytes.	Glucose	33-40	zinc finger E-box binding homeobox 1	Homo sapiens	14-18	
28111379-6	2017	Moreover, a high concentration of glucose and angiotensin II promoted TCF8 expression.	Glucose	34-41	zinc finger E-box binding homeobox 1	Homo sapiens	70-74	
28111379-7	2017	Inhibiting TCF8 expression with siRNA reversed EMT in podocytes in the presence of a high concentration of glucose and angiotensin.	Glucose	107-114	zinc finger E-box binding homeobox 1	Homo sapiens	11-15	
28111379-9	2017	Therefore, glucose and angiotensin II may promote EMT in podocytes via TCF8.	Glucose	11-18	zinc finger E-box binding homeobox 1	Homo sapiens	71-75