PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12891557-5	2003	RESULTS: In mice, treatment with the FXR agonist taurocholic acid strongly decreased serum triglyceride levels, an effect associated with reduced Apo CIII serum and liver messenger RNA levels.	Taurocholic Acid	49-65	nuclear receptor subfamily 1, group H, member 4	Mus musculus	37-40	
30409838-5	2019	The accumulation of TCA was associated with activation of intestinal FXR, which can mediate bile acid, lipid, and glucose metabolism.	Taurocholic Acid	20-23	nuclear receptor subfamily 1, group H, member 4	Mus musculus	69-72	
11927623-5	2002	In human apoA-I transgenic mice, treatment with the FXR agonist taurocholic acid strongly decreased serum concentrations and liver mRNA levels of human apoA-I, which was associated with reduced serum HDL levels.	Taurocholic Acid	64-80	nuclear receptor subfamily 1, group H, member 4	Mus musculus	52-55	
32003602-9	2020	Importantly, TA (but not DCA) effects were largely lost in FXR knockout mice.	Taurocholic Acid	13-15	nuclear receptor subfamily 1, group H, member 4	Mus musculus	59-62	
30556042-4	2018	More than 90% of 20-month-old whole-body Fxr-null mice had hepatic tumors with enhanced hepatic expression of myelocytomatosis oncogene (Myc) and cyclin-dependent kinase 4 (Cdk4) messenger RNAs (mRNAs) and elevated serum taurocholate (TCA) and tauromuricholate (TMCA) and their respective unconjugated derivatives.	Taurocholic Acid	235-238	nuclear receptor subfamily 1, group H, member 4	Mus musculus	41-44	
30556042-4	2018	More than 90% of 20-month-old whole-body Fxr-null mice had hepatic tumors with enhanced hepatic expression of myelocytomatosis oncogene (Myc) and cyclin-dependent kinase 4 (Cdk4) messenger RNAs (mRNAs) and elevated serum taurocholate (TCA) and tauromuricholate (TMCA) and their respective unconjugated derivatives.	Taurocholic Acid	221-233	nuclear receptor subfamily 1, group H, member 4	Mus musculus	41-44	
30556042-7	2018	Treatment with TCA induced Myc expression in Fxr-null cultured primary mouse hepatocytes but not in wild-type (WT) mouse hepatocytes, demonstrating that the combination of hepatocyte FXR disruption with elevated TCA is required for Myc induction and ensuing age-dependent hepatocarcinogenesis in Fxr-null mice.	Taurocholic Acid	15-18	nuclear receptor subfamily 1, group H, member 4	Mus musculus	45-48	
30556042-7	2018	Treatment with TCA induced Myc expression in Fxr-null cultured primary mouse hepatocytes but not in wild-type (WT) mouse hepatocytes, demonstrating that the combination of hepatocyte FXR disruption with elevated TCA is required for Myc induction and ensuing age-dependent hepatocarcinogenesis in Fxr-null mice.	Taurocholic Acid	15-18	nuclear receptor subfamily 1, group H, member 4	Mus musculus	183-186	
30556042-7	2018	Treatment with TCA induced Myc expression in Fxr-null cultured primary mouse hepatocytes but not in wild-type (WT) mouse hepatocytes, demonstrating that the combination of hepatocyte FXR disruption with elevated TCA is required for Myc induction and ensuing age-dependent hepatocarcinogenesis in Fxr-null mice.	Taurocholic Acid	15-18	nuclear receptor subfamily 1, group H, member 4	Mus musculus	296-299	
28505368-6	2017	Treatment of Fxr-null hepatocytes with TCA, but not T-beta-MCA, significantly increased c-Jun-N-terminal kinase (JNK) activation and Ccl2 mRNA levels, and up-regulation of Ccl2 mRNA was attenuated by co-treatment with a JNK inhibitor SP600125, indicating that TCA directly amplifies hepatocyte inflammatory signaling mainly mediated by JNK under FXR-deficiency.	Taurocholic Acid	39-42	nuclear receptor subfamily 1, group H, member 4	Mus musculus	13-16	
28505368-6	2017	Treatment of Fxr-null hepatocytes with TCA, but not T-beta-MCA, significantly increased c-Jun-N-terminal kinase (JNK) activation and Ccl2 mRNA levels, and up-regulation of Ccl2 mRNA was attenuated by co-treatment with a JNK inhibitor SP600125, indicating that TCA directly amplifies hepatocyte inflammatory signaling mainly mediated by JNK under FXR-deficiency.	Taurocholic Acid	260-263	nuclear receptor subfamily 1, group H, member 4	Mus musculus	13-16	
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Taurocholic Acid	105-121	nuclear receptor subfamily 1, group H, member 4	Mus musculus	154-157	
23051670-0	2012	Enterobacteria-mediated deconjugation of taurocholic acid enhances ileal farnesoid X receptor signaling.	Taurocholic Acid	41-57	nuclear receptor subfamily 1, group H, member 4	Mus musculus	73-93	
25870546-9	2015	FXR deletion increased serum concentrations of many bile acids, including taurodehydrocholic acid, taurocholic acid, deoxycholic acid (DCA), glycocholic acid (GCA), tauro-alpha-muricholic acid, tauro-omega-muricholic acid, and hyodeoxycholic acid (HDCA).	Taurocholic Acid	99-115	nuclear receptor subfamily 1, group H, member 4	Mus musculus	0-3	
21464203-1	2011	It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation.	Taurocholic Acid	123-126	nuclear receptor subfamily 1, group H, member 4	Mus musculus	154-157	
21464203-11	2011	Repression of human apoA-I expression by TCA in transgenic mice is probably mediated through FXR-independent mechanisms.	Taurocholic Acid	41-44	nuclear receptor subfamily 1, group H, member 4	Mus musculus	93-96	
16284190-6	2006	In all of the mice studied, dietary taurocholate increased ileal expression of FGF15, a FXR-inducible murine homologue of human FGF19.	Taurocholic Acid	36-48	nuclear receptor subfamily 1, group H, member 4	Mus musculus	88-91