PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26264613-8	2016	However, treatment with neutralizing TGF-beta1 antibody partially abrogated FoxP3-induced NIS repression.	Nickel	90-93	transforming growth factor beta 1	Homo sapiens	37-46	
32171946-0	2020	Exogenous hydrogen sulfide donor NaHS alleviates nickel-induced epithelial-mesenchymal transition and the migration of A549 cells by regulating TGF-beta1/Smad2/Smad3 signaling.	Nickel	49-55	transforming growth factor beta 1	Homo sapiens	144-153	
30055191-0	2018	Reversal of Sp1 transactivation and TGFbeta1/SMAD1 signaling by H2S prevent nickel-induced fibroblast activation.	Nickel	76-82	transforming growth factor beta 1	Homo sapiens	36-44	
30055191-9	2018	Moreover, H2S incubation reversed nickel-stimulated TGFbeta1/SMAD1 signal and blocked TGFbeta1-initiated expressions of alphaSMA and fibronectin.	Nickel	34-40	transforming growth factor beta 1	Homo sapiens	52-60	
30055191-10	2018	Nickel inhibited the interaction of Sp1 with CSE promoter but strengthened the binding of Sp1 with TGFbeta1 promoter, which was reversed by exogenously applied NaHS.	Nickel	0-6	transforming growth factor beta 1	Homo sapiens	99-107	
26264613-0	2016	FoxP3 in papillary thyroid carcinoma induces NIS repression through activation of the TGF-beta1/Smad signaling pathway.	Nickel	45-48	transforming growth factor beta 1	Homo sapiens	86-95	
26264613-9	2016	These findings suggest that FoxP3 could compromise NIS expression by inducing TGF-beta1.	Nickel	51-54	transforming growth factor beta 1	Homo sapiens	78-87	
26044615-10	2015	The identification of genes modified by the toxic effects of nickel on THP-1 cells (EPOR, RELB, FIGF, SPI-1, TGF-beta1, CXCL16 and CRLF2) may aid in the development of interventional measures for the treatment/prevention of nickel ion-associated toxic effects during the treatment of congenital heart disease.	Nickel	61-67	transforming growth factor beta 1	Homo sapiens	109-118	
23119075-9	2012	IMAC of purified TGF-beta1 and the latency associated peptide showed that these proteins bound to the immobilized nickel ions.	Nickel	114-120	transforming growth factor beta 1	Homo sapiens	17-26	
23119075-9	2012	IMAC of purified TGF-beta1 and the latency associated peptide showed that these proteins bound to the immobilized nickel ions.	Nickel	114-120	transforming growth factor beta 1	Homo sapiens	35-61	
23119075-10	2012	These data clearly demonstrate that TGF-beta1 was co-purified by specific interactions with nickel, and not by specific interactions with fibrillin-1 fragments.	Nickel	92-98	transforming growth factor beta 1	Homo sapiens	36-45	
9675033-4	1998	The peptide Leu155-Val260 immobilized by the polyhistidine tag on a nickel chelate column bound TGF-beta1 and -beta2 almost as effectively as the largest fragment (Asp45-Lys359) studied.	Nickel	68-74	transforming growth factor beta 1	Homo sapiens	96-116	
21473897-3	2011	In this in vitro study, we found that nickel, as nickel chloride, could significantly enhance the invasive potential of human lung cancer cells, accompanied by elevated expression of IL-8, TGF-beta, MMP2 and MMP9 in human lung cancer cells.	Nickel	38-44	transforming growth factor beta 1	Homo sapiens	189-197	
19861538-3	2009	Here, we show a mechanism through which BRAF induces NIS repression and promotes epithelial to mesenchimal transition and invasion based on the operation of an autocrine transforming growth factor (TGF)beta loop.	Nickel	53-56	transforming growth factor beta 1	Homo sapiens	198-206	
19861538-4	2009	BRAF induces secretion of functional TGFbeta and blocking TGFbeta/Smad signaling at multiple levels rescues BRAF-induced NIS repression.	Nickel	121-124	transforming growth factor beta 1	Homo sapiens	37-44	
19861538-4	2009	BRAF induces secretion of functional TGFbeta and blocking TGFbeta/Smad signaling at multiple levels rescues BRAF-induced NIS repression.	Nickel	121-124	transforming growth factor beta 1	Homo sapiens	58-65	
19861538-8	2009	Interestingly, TGFbeta is overexpressed in the invasive front, whereas NIS is preferentially expressed in the central regions of the tumors, suggesting that this negative correlation between TGFbeta and NIS occurs locally inside the tumor.	Nickel	71-74	transforming growth factor beta 1	Homo sapiens	191-198	
19861538-9	2009	Our study describes a novel mechanism of NIS repression in thyroid cancer and provides evidence that TGFbeta may play a key role in promoting radioiodide resistance and tumor invasion during PTC progression.	Nickel	41-44	transforming growth factor beta 1	Homo sapiens	101-108