PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29140787-8	2018	Finally, the inhibition of these canonical and non-canonical pathways did not decrease the ROS increment, while the inhibition of ROS production entirely abolished the phosphorylation of Smad3, ERK1/2 and JNK1/2.	Reactive Oxygen Species	130-133	SMAD family member 3	Homo sapiens	187-192	
34687772-6	2021	Removal of ROS by N-acetylcysteine significantly reduced ER stress in prostate cancer cells, followed by the decrease of Smad3 phosphorylation and expression of nuclear Snail, resulting in the inhibition of EMT and malignant phenotypic changes of prostate cancer cells.	Reactive Oxygen Species	11-14	SMAD family member 3	Homo sapiens	121-126	
25858818-9	2015	Our results indicated that NOX4-derived ROS play pivotal roles in activating Src kinase activity leading to the activation of canonical (Smad3) and noncanonical (JNK) cascades that cooperate to attain maximum CCN2 expression.	Reactive Oxygen Species	40-43	SMAD family member 3	Homo sapiens	137-142	
26497676-4	2015	Mechanism study revealed that LTB4-mediated suppression of TGF-beta1-induced Smad3 activation and growth inhibition was due to enhanced phosphorylation of Smad3 linker region (pSmad3L) through activation of BLT1-NAD(P)H oxidase (NOX)-reactive oxygen species (ROS)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3-K)-extracellular signal-activated kinase1/2 (ERK1/2)-linked signaling cascade.	Reactive Oxygen Species	234-257	SMAD family member 3	Homo sapiens	77-82	
26497676-4	2015	Mechanism study revealed that LTB4-mediated suppression of TGF-beta1-induced Smad3 activation and growth inhibition was due to enhanced phosphorylation of Smad3 linker region (pSmad3L) through activation of BLT1-NAD(P)H oxidase (NOX)-reactive oxygen species (ROS)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3-K)-extracellular signal-activated kinase1/2 (ERK1/2)-linked signaling cascade.	Reactive Oxygen Species	234-257	SMAD family member 3	Homo sapiens	155-160	
26497676-4	2015	Mechanism study revealed that LTB4-mediated suppression of TGF-beta1-induced Smad3 activation and growth inhibition was due to enhanced phosphorylation of Smad3 linker region (pSmad3L) through activation of BLT1-NAD(P)H oxidase (NOX)-reactive oxygen species (ROS)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3-K)-extracellular signal-activated kinase1/2 (ERK1/2)-linked signaling cascade.	Reactive Oxygen Species	259-262	SMAD family member 3	Homo sapiens	77-82	
26497676-4	2015	Mechanism study revealed that LTB4-mediated suppression of TGF-beta1-induced Smad3 activation and growth inhibition was due to enhanced phosphorylation of Smad3 linker region (pSmad3L) through activation of BLT1-NAD(P)H oxidase (NOX)-reactive oxygen species (ROS)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3-K)-extracellular signal-activated kinase1/2 (ERK1/2)-linked signaling cascade.	Reactive Oxygen Species	259-262	SMAD family member 3	Homo sapiens	155-160	
24550076-3	2014	Elevated ROS impairs the transforming growth factor-beta (TGF-beta) pathway, through reduction of type II TGF-beta receptor (TbetaRII) and SMAD3 protein levels.	Reactive Oxygen Species	9-12	SMAD family member 3	Homo sapiens	139-144	
19553668-0	2009	Loss of NF-kappaB control and repression of Prdx6 gene transcription by reactive oxygen species-driven SMAD3-mediated transforming growth factor beta signaling.	Reactive Oxygen Species	72-95	SMAD family member 3	Homo sapiens	103-108	
23449528-3	2012	In this review, we discuss the pleiotropic effects of TGF-beta/Smad3 signaling on metabolism and energy homeostasis, all of which has an important part in the etiology and progression of obesity-linked diabetes; these include adipocyte differentiation, white to brown fat phenotypic transition, glucose and lipid metabolism, pancreatic function, insulin signaling, adipocytokine secretion, inflammation and reactive oxygen species production.	Reactive Oxygen Species	407-430	SMAD family member 3	Homo sapiens	63-68	
24714748-4	2014	We previously demonstrated that Nox4, a Nox family NADPH oxidase, is a TGF-beta/SMAD3-inducible source of reactive oxygen species (ROS) affecting cell migration and fibronectin expression, an EMT marker, in normal and metastatic breast epithelial cells.	Reactive Oxygen Species	106-129	SMAD family member 3	Homo sapiens	80-85	
24714748-4	2014	We previously demonstrated that Nox4, a Nox family NADPH oxidase, is a TGF-beta/SMAD3-inducible source of reactive oxygen species (ROS) affecting cell migration and fibronectin expression, an EMT marker, in normal and metastatic breast epithelial cells.	Reactive Oxygen Species	131-134	SMAD family member 3	Homo sapiens	80-85	
16002781-0	2005	Activation of transforming growth factor-beta1/p38/Smad3 signaling in stromal cells requires reactive oxygen species-mediated MMP-2 activity during bone marrow damage.	Reactive Oxygen Species	93-116	SMAD family member 3	Homo sapiens	51-56