PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33095806-11 2020 Moreover, LOXL1 expression was positively correlated with the EMT (epithelial-mesenchymal transition) gene set in GSEA. gsea 114-118 lysyl oxidase like 1 Homo sapiens 10-15 14742670-2 2004 In this study, using transgenic mice bearing conditional expression of the activated constitutive androstane receptor (CAR), we demonstrate that activation of CAR is both necessary and sufficient to confer resistance to the hepatotoxicity of lithocholic acid (LCA). Lithocholic Acid 242-258 nuclear receptor subfamily 1, group I, member 3 Mus musculus 119-122 14742670-2 2004 In this study, using transgenic mice bearing conditional expression of the activated constitutive androstane receptor (CAR), we demonstrate that activation of CAR is both necessary and sufficient to confer resistance to the hepatotoxicity of lithocholic acid (LCA). Lithocholic Acid 242-258 nuclear receptor subfamily 1, group I, member 3 Mus musculus 159-162 14742670-2 2004 In this study, using transgenic mice bearing conditional expression of the activated constitutive androstane receptor (CAR), we demonstrate that activation of CAR is both necessary and sufficient to confer resistance to the hepatotoxicity of lithocholic acid (LCA). Lithocholic Acid 260-263 nuclear receptor subfamily 1, group I, member 3 Mus musculus 85-117 14742670-2 2004 In this study, using transgenic mice bearing conditional expression of the activated constitutive androstane receptor (CAR), we demonstrate that activation of CAR is both necessary and sufficient to confer resistance to the hepatotoxicity of lithocholic acid (LCA). Lithocholic Acid 260-263 nuclear receptor subfamily 1, group I, member 3 Mus musculus 159-162 14742670-3 2004 Surprisingly, the CAR-mediated protection is not attributable to the expected and previously characterized CYP3A pathway; rather, it is associated with a robust induction of SULT gene expression and increased LCA sulfation. Lithocholic Acid 209-212 nuclear receptor subfamily 1 group I member 3 Homo sapiens 18-21 15206167-11 2003 The selective binding of lithocholic acid to AR supports the hypothesis that diet-related endoluminal substances may play a role in cancer development model where molecular alterations such as DNA damage or mutation is the 1st event. Lithocholic Acid 25-41 androgen receptor Homo sapiens 45-47 14990919-10 2004 SIGNIFICANCE: A higher percentage of IIX MyHC is expected to impart a high speed of shortening to the TA and LCA muscles. Lithocholic Acid 109-112 myosin heavy chain 6 Homo sapiens 41-45 14525957-2 2004 Recently, secondary bile acids such as lithocholic acid (LCA) were identified as endogenous VDR agonists. Lithocholic Acid 39-55 vitamin D receptor Homo sapiens 92-95 14525957-2 2004 Recently, secondary bile acids such as lithocholic acid (LCA) were identified as endogenous VDR agonists. Lithocholic Acid 57-60 vitamin D receptor Homo sapiens 92-95 14525957-3 2004 To identify structural determinants required for VDR activation by 1alpha,25(OH)2D3 and LCA, we generated VDR mutants predicted to modulate ligand response based on sequence homology to pregnane X receptor, another bile acid-responsive nuclear receptor. Lithocholic Acid 88-91 nuclear receptor subfamily 1 group I member 2 Homo sapiens 186-205 14525957-4 2004 In both vitamin D response element activation and mammalian two-hybrid assays, we found that VDR-S278V is activated by 1alpha,25(OH)2D3 but not by LCA, whereas VDR-S237M can respond to LCA but not to 1alpha,25(OH)2D3. Lithocholic Acid 185-188 vitamin D receptor Homo sapiens 93-96 14525957-4 2004 In both vitamin D response element activation and mammalian two-hybrid assays, we found that VDR-S278V is activated by 1alpha,25(OH)2D3 but not by LCA, whereas VDR-S237M can respond to LCA but not to 1alpha,25(OH)2D3. Lithocholic Acid 185-188 vitamin D receptor Homo sapiens 160-163 14525957-5 2004 Competitive ligand binding analysis reveals that LCA, but not 1alpha,25(OH)2D3, effectively binds to VDR-S237M and both 1alpha,25(OH)2D3 and LCA bind to VDR-S278V. Lithocholic Acid 49-52 vitamin D receptor Homo sapiens 101-104 14525957-5 2004 Competitive ligand binding analysis reveals that LCA, but not 1alpha,25(OH)2D3, effectively binds to VDR-S237M and both 1alpha,25(OH)2D3 and LCA bind to VDR-S278V. Lithocholic Acid 49-52 vitamin D receptor Homo sapiens 153-156 14525957-5 2004 Competitive ligand binding analysis reveals that LCA, but not 1alpha,25(OH)2D3, effectively binds to VDR-S237M and both 1alpha,25(OH)2D3 and LCA bind to VDR-S278V. Lithocholic Acid 141-144 vitamin D receptor Homo sapiens 153-156 14525957-6 2004 We propose a docking model for LCA binding to VDR that is supported by mutagenesis data. Lithocholic Acid 31-34 vitamin D receptor Homo sapiens 46-49 14525957-7 2004 Comparative analysis of the VDR-LCA and VDR-1alpha,25(OH)2D3 structure-activity relationships should be useful in the development of bile acid-derived synthetic VDR ligands that selectively target VDR function in cancer and immune disorders without inducing adverse hypercalcemic effects. Lithocholic Acid 32-35 vitamin D receptor Homo sapiens 28-31 12875239-8 2003 However, hepatic lithocholic acid (LCA) levels are lower in LCA-fed FXR-null female mice compared to those in wild-type female mice. Lithocholic Acid 17-33 nuclear receptor subfamily 1, group H, member 4 Mus musculus 68-71 12875239-8 2003 However, hepatic lithocholic acid (LCA) levels are lower in LCA-fed FXR-null female mice compared to those in wild-type female mice. Lithocholic Acid 35-38 nuclear receptor subfamily 1, group H, member 4 Mus musculus 68-71 12875239-8 2003 However, hepatic lithocholic acid (LCA) levels are lower in LCA-fed FXR-null female mice compared to those in wild-type female mice. Lithocholic Acid 60-63 nuclear receptor subfamily 1, group H, member 4 Mus musculus 68-71 12875239-9 2003 Furthermore, FXR-null female mice are less susceptible to liver damage by LCA compared with female wild-type mice. Lithocholic Acid 74-77 nuclear receptor subfamily 1, group H, member 4 Mus musculus 13-16 12875239-10 2003 Marked increases in hepattic LCA-sulfating activity and hepatic hydroxysteroid sulfotransferase and biliary sulfated bile acid levels are detected in FXR-null female mice, suggesting the protective role of hydroxysteroid sulfotransferase in LCA-induced liver damage. Lithocholic Acid 29-32 nuclear receptor subfamily 1, group H, member 4 Mus musculus 150-153 12875239-10 2003 Marked increases in hepattic LCA-sulfating activity and hepatic hydroxysteroid sulfotransferase and biliary sulfated bile acid levels are detected in FXR-null female mice, suggesting the protective role of hydroxysteroid sulfotransferase in LCA-induced liver damage. Lithocholic Acid 241-244 nuclear receptor subfamily 1, group H, member 4 Mus musculus 150-153 12637555-0 2003 Protective role of hydroxysteroid sulfotransferase in lithocholic acid-induced liver toxicity. Lithocholic Acid 54-70 sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 2 Mus musculus 19-50 12637555-9 2003 These transporter levels are higher in FXR-null mice than wild-type mice after 1% LCA supplement. Lithocholic Acid 82-85 nuclear receptor subfamily 1, group H, member 4 Mus musculus 39-42 12637555-11 2003 These results indicate hydroxysteroid sulfotransferase-mediated LCA sulfation as a major pathway for protection against LCA-induced liver damage. Lithocholic Acid 64-67 sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 2 Mus musculus 23-54 12637555-1 2003 Supplement of 1% lithocholic acid (LCA) in the diet for 5-9 days resulted in elevated levels of the marker for liver damage aspartate aminotransferase and alkaline phosphatase activities in both farnesoid X receptor (FXR)-null and wild-type female mice. Lithocholic Acid 17-33 nuclear receptor subfamily 1, group H, member 4 Mus musculus 217-220 12637555-11 2003 These results indicate hydroxysteroid sulfotransferase-mediated LCA sulfation as a major pathway for protection against LCA-induced liver damage. Lithocholic Acid 120-123 sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 2 Mus musculus 23-54 12637555-1 2003 Supplement of 1% lithocholic acid (LCA) in the diet for 5-9 days resulted in elevated levels of the marker for liver damage aspartate aminotransferase and alkaline phosphatase activities in both farnesoid X receptor (FXR)-null and wild-type female mice. Lithocholic Acid 35-38 nuclear receptor subfamily 1, group H, member 4 Mus musculus 217-220 12637555-3 2003 Consistent with liver toxicity marker activities, serum and liver levels of bile acids, particularly LCA and taurolithocholic acid, were clearly higher in wild-type mice than in FXR-null mice after 1% LCA supplement. Lithocholic Acid 201-204 nuclear receptor subfamily 1, group H, member 4 Mus musculus 178-181 12637555-4 2003 Marked increases in hepatic sulfating activity for LCA (5.5-fold) and hydroxysteroid sulfotransferase (St) 2a (5.8-fold) were detected in liver of FXR-null mice. Lithocholic Acid 51-54 nuclear receptor subfamily 1, group H, member 4 Mus musculus 147-150 12637555-5 2003 A 7.4-fold higher 3alpha-sulfated bile acid concentration was observed in bile of FXR-null mice fed an LCA diet compared with that of wild-type mice. Lithocholic Acid 103-106 nuclear receptor subfamily 1, group H, member 4 Mus musculus 82-85 12637555-7 2003 In contrast, microsomal LCA 6beta-hydroxylation was not increased and was in fact lower in FXR-null mice compared in wild-type mice. Lithocholic Acid 24-27 nuclear receptor subfamily 1, group H, member 4 Mus musculus 91-94 12637555-8 2003 Clear decreases in mRNA encoding sodium taurocholate cotransporting polypeptide, organic anion transporting polypeptide 1, and liver-specific organic anion transporter-1 function in bile acid import were detected in LCA-fed mice. Lithocholic Acid 216-219 solute carrier organic anion transporter family, member 1b2 Mus musculus 127-169 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 117-133 nuclear receptor subfamily 1 group I member 2 Homo sapiens 21-24 12149270-5 2002 Both deoxycholic acid and lithocholic acid as well as CDCA, but not ursodeoxycholic acid, increase the mRNA level for the LDL receptor, even when Hep G2 cells are cultured with 25-hydroxycholesterol, a potent suppressor of gene expression for the LDL receptor. Lithocholic Acid 26-42 low density lipoprotein receptor Homo sapiens 122-134 12149270-5 2002 Both deoxycholic acid and lithocholic acid as well as CDCA, but not ursodeoxycholic acid, increase the mRNA level for the LDL receptor, even when Hep G2 cells are cultured with 25-hydroxycholesterol, a potent suppressor of gene expression for the LDL receptor. Lithocholic Acid 26-42 low density lipoprotein receptor Homo sapiens 247-259 12360401-6 2002 Lithocholic acid, chenodeoxycholic acid, cholic acid and deoxycholic acid stimulated cellular invasion of SRC- and RhoA-transformed PCmsrc and MDCKT23-RhoAV14 cells, and of HCT-8/E11 cells originating from a sporadic tumor, but were ineffective in premalignant PC/AA/C1 and MDCKT23 cells. Lithocholic Acid 0-16 ras homolog family member A Homo sapiens 115-119 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 117-133 nuclear receptor subfamily 1 group I member 2 Homo sapiens 26-45 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 117-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-212 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 135-138 nuclear receptor subfamily 1 group I member 2 Homo sapiens 21-24 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 135-138 nuclear receptor subfamily 1 group I member 2 Homo sapiens 26-45 12370413-1 2002 The nuclear receptor PXR (pregnane X receptor) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by inducing expression of the hydroxylating cytochrome P450 enzyme CYP3A and promoting detoxification. Lithocholic Acid 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-212 12370413-2 2002 We found that activation of PXR also increases the activity and gene expression of the phase II conjugating enzyme dehydroepiandrosterone sulfotransferase (STD) known to sulfate LCA to facilitate its elimination. Lithocholic Acid 178-181 nuclear receptor subfamily 1 group I member 2 Homo sapiens 28-31 12052824-0 2002 Lithocholic acid decreases expression of bile salt export pump through farnesoid X receptor antagonist activity. Lithocholic Acid 0-16 ATP binding cassette subfamily B member 11 Homo sapiens 41-62 12296454-2 2002 Lithocholic acid can bind to the intestinal vitamin D receptor and thereby induce the cytochrome CYP3A, which detoxifies lithocholic acid by catabolic reactions. Lithocholic Acid 0-16 vitamin D receptor Homo sapiens 44-62 12296454-2 2002 Lithocholic acid can bind to the intestinal vitamin D receptor and thereby induce the cytochrome CYP3A, which detoxifies lithocholic acid by catabolic reactions. Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 12296454-2 2002 Lithocholic acid can bind to the intestinal vitamin D receptor and thereby induce the cytochrome CYP3A, which detoxifies lithocholic acid by catabolic reactions. Lithocholic Acid 121-137 vitamin D receptor Homo sapiens 44-62 12296454-2 2002 Lithocholic acid can bind to the intestinal vitamin D receptor and thereby induce the cytochrome CYP3A, which detoxifies lithocholic acid by catabolic reactions. Lithocholic Acid 121-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 12052824-0 2002 Lithocholic acid decreases expression of bile salt export pump through farnesoid X receptor antagonist activity. Lithocholic Acid 0-16 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 81-91 12052824-9 2002 In contrast to CDCA and GW4064, lithocholate (LCA), a hydrophobic bile acid and a potent inducer of cholestasis, strongly decreased BSEP expression. Lithocholic Acid 32-44 ATP binding cassette subfamily B member 11 Homo sapiens 132-136 12052824-10 2002 Previous studies did not identify LCA as an FXR antagonist ligand in cells, but we show here that LCA is an FXR antagonist with partial agonist activity in cells. Lithocholic Acid 98-101 nuclear receptor subfamily 1 group H member 4 Homo sapiens 108-111 12052824-9 2002 In contrast to CDCA and GW4064, lithocholate (LCA), a hydrophobic bile acid and a potent inducer of cholestasis, strongly decreased BSEP expression. Lithocholic Acid 46-49 ATP binding cassette subfamily B member 11 Homo sapiens 132-136 12052824-11 2002 In an in vitro co-activator association assay, LCA decreased CDCA- and GW4064-induced FXR activation with an IC(50) of 1 microm. Lithocholic Acid 47-50 nuclear receptor subfamily 1 group H member 4 Homo sapiens 86-89 12052824-12 2002 In HepG2 cells, LCA also effectively antagonized GW4064-enhanced FXR transactivation. Lithocholic Acid 16-19 nuclear receptor subfamily 1 group H member 4 Homo sapiens 65-68 12016314-2 2002 We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. Lithocholic Acid 74-90 vitamin D receptor Homo sapiens 13-16 12052824-13 2002 These data suggest that the toxic and cholestatic effect of LCA in animals may result from its down-regulation of BSEP through FXR. Lithocholic Acid 60-63 ATP binding cassette subfamily B member 11 Homo sapiens 114-118 12052824-13 2002 These data suggest that the toxic and cholestatic effect of LCA in animals may result from its down-regulation of BSEP through FXR. Lithocholic Acid 60-63 nuclear receptor subfamily 1 group H member 4 Homo sapiens 127-130 12060116-5 2002 LCA was mediated in vitro by CD56+/CD8alpha+/CD3- natural killer cells. Lithocholic Acid 0-3 CD8a molecule Homo sapiens 35-43 12016314-2 2002 We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. Lithocholic Acid 92-95 vitamin D receptor Homo sapiens 13-16 12016314-3 2002 VDR is an order of magnitude more sensitive to LCA and its metabolites than are other nuclear receptors. Lithocholic Acid 47-50 vitamin D receptor Homo sapiens 0-3 12016314-4 2002 Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. Lithocholic Acid 21-24 vitamin D receptor Homo sapiens 14-17 12016314-4 2002 Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. Lithocholic Acid 21-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 12016314-4 2002 Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. Lithocholic Acid 116-119 vitamin D receptor Homo sapiens 14-17 12016314-4 2002 Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. Lithocholic Acid 116-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 70-86 nuclear receptor subfamily 1 group I member 2 Homo sapiens 43-46 11939783-0 2002 Photoaffinity labeling of human retinoid X receptor beta (RXRbeta) with 9-cis-retinoic acid: identification of phytanic acid, docosahexaenoic acid, and lithocholic acid as ligands for RXRbeta. Lithocholic Acid 152-168 retinoid X receptor beta Homo sapiens 58-65 11939783-0 2002 Photoaffinity labeling of human retinoid X receptor beta (RXRbeta) with 9-cis-retinoic acid: identification of phytanic acid, docosahexaenoic acid, and lithocholic acid as ligands for RXRbeta. Lithocholic Acid 152-168 retinoid X receptor beta Homo sapiens 184-191 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 70-86 nuclear receptor subfamily 1 group I member 2 Homo sapiens 102-105 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 70-86 nuclear receptor subfamily 1 group I member 2 Homo sapiens 102-105 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 228-244 nuclear receptor subfamily 1 group I member 2 Homo sapiens 43-46 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 228-244 nuclear receptor subfamily 1 group I member 2 Homo sapiens 102-105 11893771-3 2002 Among the chemicals that bind and activate PXR is the toxic bile acid lithocholic acid; activation of PXR, in turn, protects against the severe liver damage caused by this bile acid.Thus, PXR serves as a physiological sensor of lithocholic acid and perhaps other bile acids and coordinately regulates genes involved in their detoxification. Lithocholic Acid 228-244 nuclear receptor subfamily 1 group I member 2 Homo sapiens 102-105 11814779-0 2002 Biotinylated lithocholic acids for affinity chromatography of mammalian DNA polymerases alpha and beta. Lithocholic Acid 13-30 DNA polymerase alpha 1, catalytic subunit Homo sapiens 72-93 11400191-0 2001 Enantioselective inhibition of the binding of rac-profens to human serum albumin induced by lithocholate. Lithocholic Acid 92-104 albumin Homo sapiens 73-80 11686928-1 2001 The molecular action of lithocholic acid (LCA), a selective inhibitor of mammalian DNA polymerase beta (pol beta), was investigated. Lithocholic Acid 24-40 DNA polymerase beta Homo sapiens 104-112 11686928-1 2001 The molecular action of lithocholic acid (LCA), a selective inhibitor of mammalian DNA polymerase beta (pol beta), was investigated. Lithocholic Acid 42-45 DNA polymerase beta Homo sapiens 83-102 11686928-1 2001 The molecular action of lithocholic acid (LCA), a selective inhibitor of mammalian DNA polymerase beta (pol beta), was investigated. Lithocholic Acid 42-45 DNA polymerase beta Homo sapiens 104-112 11686928-4 2001 Therefore, LCA should be classified as an inhibitor of both pol beta and topo II. Lithocholic Acid 11-14 DNA polymerase beta Homo sapiens 60-68 11686928-5 2001 Here, we report the molecular interaction of LCA with pol beta and topo II. Lithocholic Acid 45-48 DNA polymerase beta Homo sapiens 54-62 11686928-6 2001 By three-dimensional structural model analysis and by comparison with the spatial positioning of specific amino acids binding to LCA on pol beta (Lys60, Leu77, and Thr79), we obtained supplementary information that allowed us to build a structural model of topo II. Lithocholic Acid 129-132 DNA polymerase beta Homo sapiens 136-144 11686928-9 2001 These results suggested that the LCA binding domains of pol beta and topo II are three-dimensionally very similar. Lithocholic Acid 33-36 DNA polymerase beta Homo sapiens 56-64 11686928-0 2001 Three-dimensional structural model analysis of the binding site of lithocholic acid, an inhibitor of DNA polymerase beta and DNA topoisomerase II. Lithocholic Acid 67-83 DNA polymerase beta Homo sapiens 101-120 11686928-1 2001 The molecular action of lithocholic acid (LCA), a selective inhibitor of mammalian DNA polymerase beta (pol beta), was investigated. Lithocholic Acid 24-40 DNA polymerase beta Homo sapiens 83-102 11400191-1 2001 The reversible binding of lithocholate to human serum albumin determines a decrease of the binding of rac-ketoprofen. Lithocholic Acid 26-38 albumin Homo sapiens 54-61 11400191-7 2001 The difference in circular dichroism spectroscopy was also used to characterize the binding of lithocholate to human serum albumin. Lithocholic Acid 95-107 albumin Homo sapiens 123-130 11248085-2 2001 In this study, we demonstrate that PXR is activated by the toxic bile acid lithocholic acid (LCA) and its 3-keto metabolite. Lithocholic Acid 75-91 nuclear receptor subfamily 1 group I member 2 Homo sapiens 35-38 11248085-0 2001 The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity. Lithocholic Acid 30-46 nuclear receptor subfamily 1 group I member 2 Homo sapiens 21-24 11248085-2 2001 In this study, we demonstrate that PXR is activated by the toxic bile acid lithocholic acid (LCA) and its 3-keto metabolite. Lithocholic Acid 93-96 nuclear receptor subfamily 1 group I member 2 Homo sapiens 35-38 11248085-4 2001 Finally, we demonstrate that activation of PXR protects against severe liver damage induced by LCA. Lithocholic Acid 95-98 nuclear receptor subfamily 1 group I member 2 Homo sapiens 43-46 11248085-5 2001 Based on these data, we propose that PXR serves as a physiological sensor of LCA, and coordinately regulates gene expression to reduce the concentrations of this toxic bile acid. Lithocholic Acid 77-80 nuclear receptor subfamily 1 group I member 2 Homo sapiens 37-40 11248086-3 2001 In particular, the secondary bile acid derivative lithocholic acid (LCA) is highly hepatotoxic and, as we show here, a metabolic substrate for CYP3A hydroxylation. Lithocholic Acid 50-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 11248086-3 2001 In particular, the secondary bile acid derivative lithocholic acid (LCA) is highly hepatotoxic and, as we show here, a metabolic substrate for CYP3A hydroxylation. Lithocholic Acid 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 11248086-4 2001 By using combinations of knockout and transgenic animals, we show that activation of SXR/PXR is necessary and sufficient to both induce CYP3A enzymes and confer resistance to toxicity by LCA, as well as other xenotoxicants such as tribromoethanol and zoxazolamine. Lithocholic Acid 187-190 nuclear receptor subfamily 1 group I member 2 Homo sapiens 85-88 11248086-4 2001 By using combinations of knockout and transgenic animals, we show that activation of SXR/PXR is necessary and sufficient to both induce CYP3A enzymes and confer resistance to toxicity by LCA, as well as other xenotoxicants such as tribromoethanol and zoxazolamine. Lithocholic Acid 187-190 nuclear receptor subfamily 1 group I member 2 Homo sapiens 89-92 11027140-0 2000 Structure of lithocholic acid binding to the N-terminal 8-kDa domain of DNA polymerase beta. Lithocholic Acid 13-29 DNA polymerase beta Homo sapiens 72-91 11027140-1 2000 The purpose of this study was to investigate the molecular action of lithocholic acid (LCA), known as a selective inhibitor of DNA polymerase beta (pol beta). Lithocholic Acid 69-85 DNA polymerase beta Homo sapiens 127-146 11027140-1 2000 The purpose of this study was to investigate the molecular action of lithocholic acid (LCA), known as a selective inhibitor of DNA polymerase beta (pol beta). Lithocholic Acid 69-85 DNA polymerase beta Homo sapiens 148-156 11027140-1 2000 The purpose of this study was to investigate the molecular action of lithocholic acid (LCA), known as a selective inhibitor of DNA polymerase beta (pol beta). Lithocholic Acid 87-90 DNA polymerase beta Homo sapiens 127-146 11027140-1 2000 The purpose of this study was to investigate the molecular action of lithocholic acid (LCA), known as a selective inhibitor of DNA polymerase beta (pol beta). Lithocholic Acid 87-90 DNA polymerase beta Homo sapiens 148-156 11027140-5 2000 On (1)H-(15)N HMQC NMR analysis of pol beta with LCA, the 8-kDa domain bound to LCA as a 1:1 complex with a dissociation constant (K(D)) of 1.56 mM. Lithocholic Acid 49-52 DNA polymerase beta Homo sapiens 35-43 11027140-5 2000 On (1)H-(15)N HMQC NMR analysis of pol beta with LCA, the 8-kDa domain bound to LCA as a 1:1 complex with a dissociation constant (K(D)) of 1.56 mM. Lithocholic Acid 80-83 DNA polymerase beta Homo sapiens 35-43 11027140-8 2000 This region was composed mainly of three amino acid residues (Lys60, Leu77, and Thr79) of pol beta on the LCA interaction interface. Lithocholic Acid 106-109 DNA polymerase beta Homo sapiens 90-98 11022826-5 2000 Treatment with chenodeoxycholic acid, cholic acid, deoxycholic acid, hyodeoxycholic acid and lithocholic acid at a concentration of 100 micromol/L for 48 h significantly enhanced the mRNA expression of UGT2B1, a UGT isoform responsible for the glucuronidation of bile acids. Lithocholic Acid 93-109 UDP glucuronosyltransferase family 2 member B17 Rattus norvegicus 202-208 11033072-5 2000 In Caco-2 cells exposed to 250 microM CDCA for 1 h a maximal increase of c-fos mRNA ( approximately 2.5-fold induction over the control) was observed; deoxycholic acid (DCA; 250 microM) and lithocholic acid (LCA; 250 microM) were less effective (approximately 2-fold induction over the control). Lithocholic Acid 208-211 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 11033072-9 2000 Thus it appears that PKC, as well as other signalling pathways, is involved in CDCA-, DCA- and LCA-induced c-fos gene expression. Lithocholic Acid 95-98 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 107-112 10604327-8 2000 The treatment difference in fecal lithocholic acid output related to the difference in serum PSA (r = 0.57, p = 0.035). Lithocholic Acid 34-50 kallikrein related peptidase 3 Homo sapiens 93-96 10726960-1 2000 AIMS/BACKGROUND: Dehydroepiandrosterone sulphotransferase (DHEA ST) is the enzyme responsible for sulphation of lithocholic acid and other potentially hepatotoxic steroids. Lithocholic Acid 112-128 sulfotransferase family 2A member 1 Homo sapiens 17-57 10726960-1 2000 AIMS/BACKGROUND: Dehydroepiandrosterone sulphotransferase (DHEA ST) is the enzyme responsible for sulphation of lithocholic acid and other potentially hepatotoxic steroids. Lithocholic Acid 112-128 sulfotransferase family 2A member 1 Homo sapiens 59-66 10604327-9 2000 CONCLUSIONS: A small but statistically significantly lower serum PSA was seen in healthy men consuming soluble fiber, which was not related to changes in serum sex hormones but was related to the increased lithocholic acid output as a possible marker of increased fecal steroid elimination. Lithocholic Acid 206-222 kallikrein related peptidase 3 Homo sapiens 65-68 10499066-8 1999 The adductor muscles--TA, LCA, and IA--have a higher percentage of type IIB MHC and a lower percentage of type I when compared with the abductor--PCA. Lithocholic Acid 26-29 major histocompatibility complex, class I, C Homo sapiens 76-79 10499066-9 1999 The rank file order for type IIB MHC composition (TA > LCA > or = IA > PCA) is the same in all specimens. Lithocholic Acid 58-61 major histocompatibility complex, class I, C Homo sapiens 33-36 10334993-2 1999 Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. Lithocholic Acid 75-91 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 138-148 10357775-2 1999 In the present study, using two human colon carcinoma cell lines, HT-29 and HCT 116, transiently transfected with the AP-1-luciferase reporter construct, we showed that the bile acids, deoxycholate, chenodeoxycholate, ursodeoxycholate and lithocholate, induced AP-1-dependent gene transcription in a dose-dependent manner, whereas cholate was without effect. Lithocholic Acid 239-251 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122 10334993-2 1999 Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. Lithocholic Acid 75-91 nuclear receptor subfamily 1 group H member 4 Homo sapiens 150-153 10334993-2 1999 Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. Lithocholic Acid 75-91 nuclear receptor subfamily 1 group H member 4 Homo sapiens 155-160 10216279-13 1999 From the present results, it can be concluded that CYP3A4 is active in the 6alpha-hydroxylation of both taurochenodeoxycholic acid and lithocholic acid in human liver. Lithocholic Acid 135-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 10216279-0 1999 6alpha-hydroxylation of taurochenodeoxycholic acid and lithocholic acid by CYP3A4 in human liver microsomes. Lithocholic Acid 55-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 9547277-4 1998 CYP3A10/6beta-hydroxylase is a male-specific P450 that catalyzes 6beta-hydroxylation of lithocholic acid, and the pattern of GH secretion is directly responsible for male-specific expression of this gene. Lithocholic Acid 88-104 growth hormone 1 Homo sapiens 125-127 10216279-3 1999 Recombinant expressed CYP3A4 was the only enzyme that was active towards these bile acids and the enzyme catalyzed an efficient 6alpha-hydroxylation of both taurochenodeoxycholic acid and lithocholic acid. Lithocholic Acid 188-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 9914784-0 1998 Lithocholic acid, a putative tumor promoter, inhibits mammalian DNA polymerase beta. Lithocholic Acid 0-16 DNA polymerase beta Homo sapiens 64-83 9914784-5 1998 Among eukaryotic DNA polymerases alpha, beta, delta, epsilon, and gamma, pol beta was the most sensitive to inhibition by LCA. Lithocholic Acid 122-125 DNA polymerase alpha 1, catalytic subunit Homo sapiens 17-71 9914784-5 1998 Among eukaryotic DNA polymerases alpha, beta, delta, epsilon, and gamma, pol beta was the most sensitive to inhibition by LCA. Lithocholic Acid 122-125 DNA polymerase beta Homo sapiens 73-81 9679709-5 1998 The SAR distribution from a single LCA was measured by E-field scanning and thermographic (TG) imaging, and compared with the GB-predicted SAR distribution. Lithocholic Acid 35-38 sarcosine dehydrogenase Homo sapiens 4-7 9679709-11 1998 The average SAR differences with and without water as intermedium were 7% respectively 11%, indicating that the GBM can provide good qualitative information about the SAR distribution of dual LCA-arrays. Lithocholic Acid 192-195 sarcosine dehydrogenase Homo sapiens 167-170 8761540-16 1996 Median PTH levels remained stable at about two times the upper limit of normal over the 2 years of study with LCa. Lithocholic Acid 110-113 parathyroid hormone Homo sapiens 7-10 9514645-0 1998 The in vitro effect of lithocholic acid on the polymerization properties of PiZ alpha-1-antitrypsin. Lithocholic Acid 23-39 serpin family A member 1 Homo sapiens 80-99 9514645-1 1998 We describe here an in vitro effect of lithocholic acid (LA), a secondary, hydrophobic bile acid, on the rate of polymerization of mutant, Z and wild-type, M alpha-1-antitrypsin (AAT). Lithocholic Acid 39-55 serpin family A member 1 Homo sapiens 158-177 9514645-1 1998 We describe here an in vitro effect of lithocholic acid (LA), a secondary, hydrophobic bile acid, on the rate of polymerization of mutant, Z and wild-type, M alpha-1-antitrypsin (AAT). Lithocholic Acid 39-55 serpin family A member 1 Homo sapiens 179-182 9595468-2 1998 ET-1 (75 pmol) was administered into the left coronary artery (LCA) in anesthetized closed-chest dogs with and without prior infusion of TMP (80 mg/kg). Lithocholic Acid 63-66 endothelin 1 Canis lupus familiaris 0-4 9595468-8 1998 Intracoronary injection of ET-1 resulted in a significant vasoconstriction of the entire vascular bed of the LCA, with a decrease in CAD of 35.9 +/- 5.7% (n = 5; p < 0.01) and ischemic changes on ECG and in tissues of endocardium, myocardium, coronary endothelial cells, and capillary vessels. Lithocholic Acid 109-112 endothelin-1 Oryctolagus cuniculus 27-31 9003356-5 1996 Of the bile salts examined, lithocholate and taurolithocholate sulphate showed the greatest binding to L-FABP. Lithocholic Acid 28-40 fatty acid binding protein 1 Rattus norvegicus 103-109 9390170-8 1997 The formation of chenodeoxycholyl-CoA by rBAL was strongly inhibited by hydrophobic bile acids (the C24 monohydroxy bile acid lithocholic acid and 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid, the C27 homolog of cholic acid), but only weakly by cholic acid. Lithocholic Acid 126-142 solute carrier family 27 member 5 Rattus norvegicus 41-45 8761540-17 1996 However, 23% of the patients on LCa developed severe hyperparathyroidism, with PTH levels exceeding ten times the upper limit of normal compared to only 10.3% of the patients on SCa. Lithocholic Acid 32-35 parathyroid hormone Homo sapiens 79-82 8761540-25 1996 Thus, LCa dialysis requires close and continuous monitoring of PTH and bone metabolism. Lithocholic Acid 6-9 parathyroid hormone Homo sapiens 63-66 7498648-5 1995 In contrast, reductions in mass and proportions of lithocholate and deoxycholate occurred after administering the C-7 sulfates. Lithocholic Acid 51-63 complement C7 Rattus norvegicus 114-117 8573067-4 1996 The results show that DD1 encoded by C9 possesses prostaglandin F synthase activity but low affinity for lithocholic acid, whereas DD2, showing differences of six amino acid residues from the DD1 sequence, exhibited high-affinity binding for the bile acid. Lithocholic Acid 105-121 aldo-keto reductase family 1 member C1 Homo sapiens 22-25 7498648-6 1995 The fecal lithocholate/deoxycholate ratio, a risk marker for colon cancer, increased markedly after administration of ursodeoxycholate and its C-3 sulfate, but did not change after administering the C-7 sulfates. Lithocholic Acid 10-22 complement C3 Rattus norvegicus 143-146 7498648-7 1995 Unlike ursodeoxycholate or its C-3 sulfate, which increased liver concentrations of lithocholate and ursodeoxycholate, the C-7 sulfates had the opposite effect, which was consistent with poor absorption. Lithocholic Acid 84-96 complement C3 Rattus norvegicus 31-34 7766669-4 1995 Additionally, DD3 was shown to catalyze the dehydrogenation of bile acids (lithocholic acid, taurolithocholic acid and taurochenodeoxycholic acid) having no 12-hydroxy groups with low Km values (17 +/- 0.65, 33 +/- 1.9 and 890 +/- 73 microM, respectively). Lithocholic Acid 75-91 aldo-keto reductase family 1 member C3 Homo sapiens 14-17 8550804-3 1995 Using high performance liquid chromatography and immobilized 3 alpha-hydroxysteroid dehydrogenase in column form, significant increases in the proportion of chenodeoxycholic acid and significant decreases in the proportion of deoxycholic acid and lithocholic acid were found in the bile of patients with colorectal adenoma or carcinoma compared with the control subjects. Lithocholic Acid 247-263 aldo-keto reductase family 1 member C3 Homo sapiens 61-97 7649186-8 1995 The purified cytochrome P-450 fraction catalysed in addition omega- and omega-1 hydroxylation of lauric acid and 6 alpha-hydroxylation of 3 alpha-hydroxy-5 beta-cholanoic acid (lithocholic acid). Lithocholic Acid 138-175 cytochrome P450 family 2 subfamily D member 6 Sus scrofa 13-29 7649186-8 1995 The purified cytochrome P-450 fraction catalysed in addition omega- and omega-1 hydroxylation of lauric acid and 6 alpha-hydroxylation of 3 alpha-hydroxy-5 beta-cholanoic acid (lithocholic acid). Lithocholic Acid 177-193 cytochrome P450 family 2 subfamily D member 6 Sus scrofa 13-29 7852916-1 1995 BACKGROUND AND OBJECTIVES: Interactions between hydrophobic compounds like cholesterol and lithocholic acid and alpha-1-antitrypsin (alpha-1-AT) have previously been described. Lithocholic Acid 91-107 serpin family A member 1 Homo sapiens 112-131 7794524-1 1995 We have previously shown that the interaction between alpha 1-antitrypsin (AAT) and lithocholic acid (LA) results in changes of AAT properties leading to its polymerization and inactivation. Lithocholic Acid 84-100 serpin family A member 1 Homo sapiens 54-73 7794524-1 1995 We have previously shown that the interaction between alpha 1-antitrypsin (AAT) and lithocholic acid (LA) results in changes of AAT properties leading to its polymerization and inactivation. Lithocholic Acid 84-100 serpin family A member 1 Homo sapiens 75-78 7794524-1 1995 We have previously shown that the interaction between alpha 1-antitrypsin (AAT) and lithocholic acid (LA) results in changes of AAT properties leading to its polymerization and inactivation. Lithocholic Acid 84-100 serpin family A member 1 Homo sapiens 128-131 7852916-1 1995 BACKGROUND AND OBJECTIVES: Interactions between hydrophobic compounds like cholesterol and lithocholic acid and alpha-1-antitrypsin (alpha-1-AT) have previously been described. Lithocholic Acid 91-107 serpin family A member 1 Homo sapiens 133-143 1461170-6 1992 Lithocholic acid is suggested to be more inhibitory to glutathione S-transferase than the other major colonic secondary bile acid, deoxycholic acid, on the basis of inhibition-structure relationships. Lithocholic Acid 0-16 glutathione S-transferase kappa 1 Homo sapiens 55-80 8077896-1 1994 Previous studies have demonstrated such hydrophobic compounds as cholesterol and lithocholic acid, to interact with alpha 1-antitrypsin (alpha 1-AT). Lithocholic Acid 81-97 serpin family A member 1 Homo sapiens 116-135 8077896-1 1994 Previous studies have demonstrated such hydrophobic compounds as cholesterol and lithocholic acid, to interact with alpha 1-antitrypsin (alpha 1-AT). Lithocholic Acid 81-97 serpin family A member 1 Homo sapiens 137-147 1461170-2 1992 A factor in the increased risk is hypothesised to result from the inhibition of isoforms of a colonic epithelial cell enzyme that detoxifies genotoxins, glutathione S-transferase, by one of the major secondary bile acids produced in the colon by fat digestion, lithocholic acid. Lithocholic Acid 261-277 glutathione S-transferase kappa 1 Homo sapiens 153-178 1461170-4 1992 Elements in the hypothesis include the ability of relatively low concentrations of lithocholic acid to inhibit isoforms of glutathione S-transferase found in colon epithelial cells, entry of lithocholic acid into the epithelial cells, and the correlation of neoplasia-associated colon pathology with high levels of lithocholic acid in fecal water. Lithocholic Acid 83-99 glutathione S-transferase kappa 1 Homo sapiens 123-148 7929584-6 1994 Treatment of couplets with glycine derivatives of lithocholate and ursodeoxycholate, but not cholate or chenodeoxycholate, led to a marked relocalization of annexin II, which initially became concentrated at the basolateral membrane, then moved to a perinuclear distribution and finally to the apical membrane as the incubation progressed. Lithocholic Acid 50-62 annexin A2 Homo sapiens 157-167 7923585-2 1994 The unconjugated and conjugated forms of cholic (CA), chenodeoxycholic (CDCA), deoxycholic (DCA) and lithocholic acid (LCA) were added to calf thymus DNA followed by 1 h of incubation at 37 degrees C. After the incubation the mixture was analyzed by the nuclease P1 modification of 32P-postlabeling. Lithocholic Acid 101-117 clathrin light chain A Bos taurus 119-122 8196671-9 1994 LCA decreased the rate of transcription of HLA-B (64%) and HLA-C (87%) but not HLA-A; DCA had a similar but less pronounced effect. Lithocholic Acid 0-3 major histocompatibility complex, class I, B Homo sapiens 43-48 8095246-2 1993 In a short-term assay in which DCA and LCA were given in the diet for 3 weeks in conjunction with partial hepatectomy midway followed by the selection regimen, DCA dose-dependently induced gamma-glutamyltranspeptidase (gamma-GTP)-positive foci, but the results for LCA were less unequivocal and no dose-dependency was evident. Lithocholic Acid 39-42 gamma-glutamyltransferase 1 Rattus norvegicus 189-228 8095246-5 1993 In contrast, both DCA and LCA treatments enhanced the development of glutathione S-transferase placental form (GST-P)-positive foci with or without subsequent PB promotion. Lithocholic Acid 26-29 glutathione S-transferase pi 1 Rattus norvegicus 69-116 2112579-12 1990 Lithocholate (100 microM) by itself had only marginal effects on release of lysozyme or beta-glucuronidase from PMNs. Lithocholic Acid 0-12 glucuronidase, beta Rattus norvegicus 88-106 1619484-2 1992 We therefore examined the effect of LPD on lithocholic acid (LCA)-induced intrahepatic cholestasis. Lithocholic Acid 43-59 acyl-CoA synthetase bubblegum family member 1 Rattus norvegicus 36-39 1619484-9 1992 Studies of LCA metabolism in rats fed a LPD indicated lower hepatic LCA hydroxylation, a greater percent contribution of glyco conjugates and lower levels of tauro conjugates. Lithocholic Acid 11-14 acyl-CoA synthetase bubblegum family member 1 Rattus norvegicus 40-43 1619484-9 1992 Studies of LCA metabolism in rats fed a LPD indicated lower hepatic LCA hydroxylation, a greater percent contribution of glyco conjugates and lower levels of tauro conjugates. Lithocholic Acid 68-71 acyl-CoA synthetase bubblegum family member 1 Rattus norvegicus 40-43 1417875-7 1992 FABP may therefore specifically alter hepatotoxicity of lithocholate and its metabolites. Lithocholic Acid 56-68 glutamic-oxaloacetic transaminase 2 Homo sapiens 0-4 1813743-2 1991 For the reconstruction of the coronary vessels, the left coronary artery (LCA) is automatically labelled on standard RAO and LAO projections, using anatomical models of the LCA. Lithocholic Acid 74-77 interleukin 4 induced 1 Homo sapiens 125-128 2146214-7 1990 Capping of the LCA appeared to correlate with the ability of the CD45 mAb to block killing, suggesting that cross-linking of LCA molecular isoforms on the NK cell surface is required for CD45 mAb to inhibit non-MHC-restricted cytolysis. Lithocholic Acid 15-18 protein tyrosine phosphatase receptor type C Homo sapiens 65-69 2146214-7 1990 Capping of the LCA appeared to correlate with the ability of the CD45 mAb to block killing, suggesting that cross-linking of LCA molecular isoforms on the NK cell surface is required for CD45 mAb to inhibit non-MHC-restricted cytolysis. Lithocholic Acid 15-18 protein tyrosine phosphatase receptor type C Homo sapiens 187-191 2146214-7 1990 Capping of the LCA appeared to correlate with the ability of the CD45 mAb to block killing, suggesting that cross-linking of LCA molecular isoforms on the NK cell surface is required for CD45 mAb to inhibit non-MHC-restricted cytolysis. Lithocholic Acid 125-128 protein tyrosine phosphatase receptor type C Homo sapiens 65-69 2146214-7 1990 Capping of the LCA appeared to correlate with the ability of the CD45 mAb to block killing, suggesting that cross-linking of LCA molecular isoforms on the NK cell surface is required for CD45 mAb to inhibit non-MHC-restricted cytolysis. Lithocholic Acid 125-128 protein tyrosine phosphatase receptor type C Homo sapiens 187-191 1974829-1 1990 The initiating potential of the secondary bile acids, deoxycholic acid (DCA) and lithocholic acid (LCA), for rat hepatocarcinogenesis was investigated using the development of hyperplastic nodules and/or glutathione S-transferase placental form (GST-P)-positive liver foci as the end point. Lithocholic Acid 81-97 glutathione S-transferase pi 1 Rattus norvegicus 204-251 2112579-13 1990 However, lithocholate (100 microM) inhibited beta-glucuronidase release from FMLP-stimulated PMNs to near-baseline levels. Lithocholic Acid 9-21 glucuronidase, beta Rattus norvegicus 45-63 1690592-5 1990 The AFP from one case had a small LCA-reactive fraction similar to that of HCC. Lithocholic Acid 34-37 alpha fetoprotein Homo sapiens 4-7 2153675-5 1990 Using equilibrium dialysis, the major lithocholate-binding activity was found to coelute with 3 beta-HSD, completely separate from 3 alpha-HSD. Lithocholic Acid 38-50 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 94-104 2317526-6 1990 NADPH inhibited the binding of lithocholic acid (3 alpha-hydroxy-5 beta-cholanic acid) by 3 alpha-hydroxysteroid dehydrogenase. Lithocholic Acid 31-47 aldo-keto reductase family 1, member C14 Rattus norvegicus 90-126 2317526-6 1990 NADPH inhibited the binding of lithocholic acid (3 alpha-hydroxy-5 beta-cholanic acid) by 3 alpha-hydroxysteroid dehydrogenase. Lithocholic Acid 49-85 aldo-keto reductase family 1, member C14 Rattus norvegicus 90-126 34808237-5 2022 Intravenous administration of LCA at a much lower dosage (compared to oral treatment) showed a comparable anti-psoriatic effect and markedly suppressed the IL-17A response. Lithocholic Acid 30-33 interleukin 17A Mus musculus 156-162 34558841-9 2021 Pearson"s correlation coefficients identified strong associations between serum ALP and metabolic ratios of CDCA-3G (r2 = 0.62, P < 0.0001), deoxycholic acid (DCA)-3G (r2 = 0.48, P < 0.0001), and LCA-3G (r2 = 0.40, P < 0.001), in ursodiol monotherapy versus control. Lithocholic Acid 198-201 alkaline phosphatase, placental Homo sapiens 80-83 34816756-9 2022 Stools from patients who weaned from PN were enriched in secondary BAs including deoxycholic acid and lithocholic acid. Lithocholic Acid 102-118 U6 snRNA biogenesis phosphodiesterase 1 Homo sapiens 37-39 34808237-6 2022 Ex vivo experiments revealed that LCA reduced IL-17A production in IL-23-stimulated murine T cells in the absence of BA receptors TGR5 or FXR. Lithocholic Acid 34-37 interleukin 17A Mus musculus 46-52 34808237-6 2022 Ex vivo experiments revealed that LCA reduced IL-17A production in IL-23-stimulated murine T cells in the absence of BA receptors TGR5 or FXR. Lithocholic Acid 34-37 interleukin 23, alpha subunit p19 Mus musculus 67-72 34351780-4 2021 The other insulin analogue, linked to the sterol lithocholic acid, formed n-hexamers with n ranging from 1 to 15, increasing with NaCl concentration and insulin concentration, indicating attractive forces in competition with the electrostatic repulsion and solution entropy. Lithocholic Acid 49-65 insulin Homo sapiens 10-17 34698602-8 2021 Lithocholic acid, inhibited the production of CDCA 24-acyl-beta-D-glucuronide with IC50 values of 1.68, 1.84, and 12.42 microM in HLM, rUGT1A3, and HIM, respectively.4. Lithocholic Acid 0-16 UDP glycosyltransferase 1 family, polypeptide A3 Rattus norvegicus 135-142 34339974-0 2021 Design, synthesis and evaluation of side-chain hydroxylated derivatives of lithocholic acid as potent agonists of the vitamin D receptor (VDR). Lithocholic Acid 75-91 vitamin D receptor Homo sapiens 118-136 34339974-0 2021 Design, synthesis and evaluation of side-chain hydroxylated derivatives of lithocholic acid as potent agonists of the vitamin D receptor (VDR). Lithocholic Acid 75-91 vitamin D receptor Homo sapiens 138-141 34685598-5 2021 LCA feeding led to strong liver damage and activation of NLRP3 inflammasome. Lithocholic Acid 0-3 NLR family, pyrin domain containing 3 Mus musculus 57-62 34638550-0 2021 Lithocholic Acid Induces miR21, Promoting PTEN Inhibition via STAT3 and ERK-1/2 Signaling in Colorectal Cancer Cells. Lithocholic Acid 0-16 microRNA 21 Homo sapiens 25-30 34638550-0 2021 Lithocholic Acid Induces miR21, Promoting PTEN Inhibition via STAT3 and ERK-1/2 Signaling in Colorectal Cancer Cells. Lithocholic Acid 0-16 phosphatase and tensin homolog Homo sapiens 42-46 34638550-0 2021 Lithocholic Acid Induces miR21, Promoting PTEN Inhibition via STAT3 and ERK-1/2 Signaling in Colorectal Cancer Cells. Lithocholic Acid 0-16 signal transducer and activator of transcription 3 Homo sapiens 62-67 34638550-0 2021 Lithocholic Acid Induces miR21, Promoting PTEN Inhibition via STAT3 and ERK-1/2 Signaling in Colorectal Cancer Cells. Lithocholic Acid 0-16 mitogen-activated protein kinase 3 Homo sapiens 72-79 34638550-2 2021 Our study using real-time PCR assay found that a secondary bile acid, lithocholic acid (LCA), stimulated the expression of miR21 in the CRC cell lines. Lithocholic Acid 70-86 microRNA 21 Homo sapiens 123-128 34638550-2 2021 Our study using real-time PCR assay found that a secondary bile acid, lithocholic acid (LCA), stimulated the expression of miR21 in the CRC cell lines. Lithocholic Acid 88-91 microRNA 21 Homo sapiens 123-128 34638550-3 2021 Promoter activity assay showed that LCA strongly stimulated miR21 promoter activity in HCT116 cells in a time- and dose-dependent manner. Lithocholic Acid 36-39 microRNA 21 Homo sapiens 60-65 34638550-4 2021 Studies of chemical inhibitors and miR21 promoter mutants indicated that Erk1/2 signaling, AP-1 transcription factor, and STAT3 are major signals involved in the mechanism of LCA-induced miR21 in HCT116 cells. Lithocholic Acid 175-178 microRNA 21 Homo sapiens 35-40 34638550-4 2021 Studies of chemical inhibitors and miR21 promoter mutants indicated that Erk1/2 signaling, AP-1 transcription factor, and STAT3 are major signals involved in the mechanism of LCA-induced miR21 in HCT116 cells. Lithocholic Acid 175-178 mitogen-activated protein kinase 3 Homo sapiens 73-79 34638550-4 2021 Studies of chemical inhibitors and miR21 promoter mutants indicated that Erk1/2 signaling, AP-1 transcription factor, and STAT3 are major signals involved in the mechanism of LCA-induced miR21 in HCT116 cells. Lithocholic Acid 175-178 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-95 34638550-4 2021 Studies of chemical inhibitors and miR21 promoter mutants indicated that Erk1/2 signaling, AP-1 transcription factor, and STAT3 are major signals involved in the mechanism of LCA-induced miR21 in HCT116 cells. Lithocholic Acid 175-178 signal transducer and activator of transcription 3 Homo sapiens 122-127 34638550-4 2021 Studies of chemical inhibitors and miR21 promoter mutants indicated that Erk1/2 signaling, AP-1 transcription factor, and STAT3 are major signals involved in the mechanism of LCA-induced miR21 in HCT116 cells. Lithocholic Acid 175-178 microRNA 21 Homo sapiens 187-192 34638550-6 2021 This study is the first to report that LCA affects miR21 expression in CRC cells, providing us with a better understanding of the cancer-promoting mechanism of bile acids that have been described as the very first promoters of CRC progression. Lithocholic Acid 39-42 microRNA 21 Homo sapiens 51-56 34351780-4 2021 The other insulin analogue, linked to the sterol lithocholic acid, formed n-hexamers with n ranging from 1 to 15, increasing with NaCl concentration and insulin concentration, indicating attractive forces in competition with the electrostatic repulsion and solution entropy. Lithocholic Acid 49-65 insulin Homo sapiens 153-160 34415766-6 2021 Given that bile acids are the essential signal factors for regulating lipid metabolism via the farnesoid-X-receptor (FXR), we conducted serum bile acid profile analysis and found that the levels of high-affinity agonists deoxycholic acid and lithocholic acid were decreased in the iotaCTs group, showing that iotaCTs failed to activate FXR. Lithocholic Acid 242-258 nuclear receptor subfamily 1, group H, member 4 Mus musculus 117-120 34174520-6 2021 Deoxycholic acid and lithocholic acid promoted intracellular lipid accumulation, reduced triglyceride concentration in media, and suppressed expression of PNPLA3 and MTTP in HepG2 human hepatoma cells. Lithocholic Acid 21-37 patatin like phospholipase domain containing 3 Homo sapiens 155-161 34174520-6 2021 Deoxycholic acid and lithocholic acid promoted intracellular lipid accumulation, reduced triglyceride concentration in media, and suppressed expression of PNPLA3 and MTTP in HepG2 human hepatoma cells. Lithocholic Acid 21-37 microsomal triglyceride transfer protein Homo sapiens 166-170 34174520-7 2021 These findings suggest that deoxycholic acid and lithocholic acid promote HLA by inhibiting the expression of PNPLA3, ACOX1, and MTTP that are involved in lipid metabolism. Lithocholic Acid 49-65 patatin like phospholipase domain containing 3 Homo sapiens 110-116 34174520-7 2021 These findings suggest that deoxycholic acid and lithocholic acid promote HLA by inhibiting the expression of PNPLA3, ACOX1, and MTTP that are involved in lipid metabolism. Lithocholic Acid 49-65 acyl-Coenzyme A oxidase 1, palmitoyl Mus musculus 118-123 34174520-7 2021 These findings suggest that deoxycholic acid and lithocholic acid promote HLA by inhibiting the expression of PNPLA3, ACOX1, and MTTP that are involved in lipid metabolism. Lithocholic Acid 49-65 microsomal triglyceride transfer protein Homo sapiens 129-133 35605478-3 2022 Studies using bile duct ligation or lithocholic acid modeling have shown that the alleviating effect of OA on cholerosis is related to the regulation of nuclear factor erythroid 2 related factor (Nrf2) or farnesoid X receptor (Fxr). Lithocholic Acid 36-52 NFE2 like bZIP transcription factor 2 Rattus norvegicus 196-200 34096956-9 2021 Curcumin altered bile acid (BA) metabolism with increased fractions of circulating deoxycholic acid (DCA) and lithocholic acid (LCA), which are the two most potent ligands for TGR5. Lithocholic Acid 110-126 G protein-coupled bile acid receptor 1 Mus musculus 176-180 34096956-9 2021 Curcumin altered bile acid (BA) metabolism with increased fractions of circulating deoxycholic acid (DCA) and lithocholic acid (LCA), which are the two most potent ligands for TGR5. Lithocholic Acid 128-131 G protein-coupled bile acid receptor 1 Mus musculus 176-180 34357066-6 2021 Changes in TGR5 expression were investigated with lithocholic acid (LCA) as the agonist. Lithocholic Acid 50-66 G protein-coupled bile acid receptor 1 Rattus norvegicus 11-15 35605478-3 2022 Studies using bile duct ligation or lithocholic acid modeling have shown that the alleviating effect of OA on cholerosis is related to the regulation of nuclear factor erythroid 2 related factor (Nrf2) or farnesoid X receptor (Fxr). Lithocholic Acid 36-52 nuclear receptor subfamily 1, group H, member 4 Rattus norvegicus 205-225 35605478-3 2022 Studies using bile duct ligation or lithocholic acid modeling have shown that the alleviating effect of OA on cholerosis is related to the regulation of nuclear factor erythroid 2 related factor (Nrf2) or farnesoid X receptor (Fxr). Lithocholic Acid 36-52 nuclear receptor subfamily 1, group H, member 4 Rattus norvegicus 227-230 35441471-12 2022 CONCLUSION: LCA exacerbates NEC by inhibiting intestinal cell proliferation through downregulating the Wnt/beta-catenin pathway. Lithocholic Acid 12-15 catenin beta 1 Homo sapiens 107-119 35500691-7 2022 Both LCA conjugated micelles decreased lipogenic activity and increased expressions of Bax (1.3 fold) and p53 (1.2 fold) apoptotic genes. Lithocholic Acid 5-8 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 35500691-7 2022 Both LCA conjugated micelles decreased lipogenic activity and increased expressions of Bax (1.3 fold) and p53 (1.2 fold) apoptotic genes. Lithocholic Acid 5-8 tumor protein p53 Homo sapiens 106-109 35586114-1 2022 Objective: This study aimed to investigate the ability of serum cholic acid (CA) and lithocholic acid (LCA) in the diagnosis and perinatal prognosis assessment of intrahepatic cholestasis of pregnancy (ICP), and the relationship between both indicators and hypoxia-inducible factor-1alpha (HIF-1alpha). Lithocholic Acid 85-101 clathrin light chain A Homo sapiens 103-106 35586114-1 2022 Objective: This study aimed to investigate the ability of serum cholic acid (CA) and lithocholic acid (LCA) in the diagnosis and perinatal prognosis assessment of intrahepatic cholestasis of pregnancy (ICP), and the relationship between both indicators and hypoxia-inducible factor-1alpha (HIF-1alpha). Lithocholic Acid 85-101 hypoxia inducible factor 1 subunit alpha Homo sapiens 257-288 35586114-1 2022 Objective: This study aimed to investigate the ability of serum cholic acid (CA) and lithocholic acid (LCA) in the diagnosis and perinatal prognosis assessment of intrahepatic cholestasis of pregnancy (ICP), and the relationship between both indicators and hypoxia-inducible factor-1alpha (HIF-1alpha). Lithocholic Acid 85-101 hypoxia inducible factor 1 subunit alpha Homo sapiens 290-300 35351776-7 2022 The canine CYP3A isoforms have lower activity than human isoforms toward T 6beta-hydroxylation and LCA 6alpha-hydroxylation and both substrates undergo non-CYP3A catalyzed side reactions. Lithocholic Acid 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 35441471-0 2022 The inhibition of enterocyte proliferation by lithocholic acid exacerbates necrotizing enterocolitis through downregulating the Wnt/beta-catenin signalling pathway. Lithocholic Acid 46-62 catenin beta 1 Homo sapiens 132-144 35441471-10 2022 Specifically, LCA supplementation caused higher levels of FITC-labelled dextran in serum, reduced PCNA expression and inhibited the activity of Wnt/beta-catenin pathway in enterocytes. Lithocholic Acid 14-17 proliferating cell nuclear antigen Homo sapiens 98-102 35441471-10 2022 Specifically, LCA supplementation caused higher levels of FITC-labelled dextran in serum, reduced PCNA expression and inhibited the activity of Wnt/beta-catenin pathway in enterocytes. Lithocholic Acid 14-17 catenin beta 1 Homo sapiens 148-160