PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23038264-2 2012 FGF19 inhibits bile acid synthesis in liver through transcriptional repression of cholesterol 7alpha-hydroxylase (CYP7A1) via a mechanism involving the nuclear receptor SHP. Bile Acids and Salts 15-24 nuclear receptor subfamily 0 group B member 2 Homo sapiens 169-172 22577560-3 2012 SHP is a transcriptional regulator affecting multiple key biological functions and metabolic processes including cholesterol, bile acid, and fatty acid metabolism, as well as reproductive biology and glucose-energy homeostasis. Bile Acids and Salts 126-135 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 22291651-2 2012 SHP is induced by bile acid-activated farnesoid X receptor (FXR) resulting in CYP7A1 gene suppression. Bile Acids and Salts 18-27 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 21566081-4 2011 We have examined whether 3Cl-AHPC acts as an agonist and increases SHP activity in the repression of bile acid biosynthetic CYP7A1 and CYP8B1 genes and delineated the underlying mechanisms. Bile Acids and Salts 101-110 nuclear receptor subfamily 0 group B member 2 Homo sapiens 67-70 21679700-2 2011 The efficacy of the different pathways to regulate bile acid synthesis through short heterodimer partner (SHP) dependent FXR modulation in liver, and SHP independent activation via FGF19 is demonstrated. Bile Acids and Salts 51-60 nuclear receptor subfamily 0 group B member 2 Homo sapiens 106-109 20970497-4 2011 In this review, we summarize studies concerning the structure and target genes of SHP and discuss recent progress in understanding the function of SHP in bile acid, cholesterol, triglyceride, glucose, and drug metabolism. Bile Acids and Salts 154-163 nuclear receptor subfamily 0 group B member 2 Homo sapiens 147-150 21566081-0 2011 Ligand-dependent regulation of the activity of the orphan nuclear receptor, small heterodimer partner (SHP), in the repression of bile acid biosynthetic CYP7A1 and CYP8B1 genes. Bile Acids and Salts 130-139 nuclear receptor subfamily 0 group B member 2 Homo sapiens 76-101 21566081-0 2011 Ligand-dependent regulation of the activity of the orphan nuclear receptor, small heterodimer partner (SHP), in the repression of bile acid biosynthetic CYP7A1 and CYP8B1 genes. Bile Acids and Salts 130-139 nuclear receptor subfamily 0 group B member 2 Homo sapiens 103-106 21262773-6 2011 Hepatic overexpression of SHP inhibited metabolic target genes, decreased bile acid and hepatic triglyceride levels, and increased glucose tolerance. Bile Acids and Salts 74-83 nuclear receptor subfamily 0 group B member 2 Homo sapiens 26-29 21262773-2 2011 In response to increased hepatic bile acids, SHP gene expression is induced and the SHP protein is stabilized. Bile Acids and Salts 33-43 nuclear receptor subfamily 0 group B member 2 Homo sapiens 45-48 21262773-2 2011 In response to increased hepatic bile acids, SHP gene expression is induced and the SHP protein is stabilized. Bile Acids and Salts 33-43 nuclear receptor subfamily 0 group B member 2 Homo sapiens 84-87 20233723-6 2010 Notably, vitamin A treatment reversed the effects of the bile acid sequestrant cholestyramine on Fgf15, Shp, and Cyp7a1 expression, suggesting a potential therapeutic benefit of vitamin A under conditions of bile acid malabsorption. Bile Acids and Salts 57-66 nuclear receptor subfamily 0 group B member 2 Homo sapiens 104-107 24212613-3 2011 SHP is a critical transcriptional regulator affecting diverse biological functions, including bile acid, cholesterol and lipid metabolism, glucose and energy homeostasis, and reproductive biology. Bile Acids and Salts 94-103 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 20444884-4 2010 The FXR-SHP pathway is critical in maintaining bile acid and fatty acid homeostasis. Bile Acids and Salts 47-56 nuclear receptor subfamily 0 group B member 2 Homo sapiens 8-11 22235657-5 2011 It is activated by other nuclear receptors like SHP, HNF-4alpha or LRH-1 and bile acids themselves, and represses CYP7A1 gene. Bile Acids and Salts 77-87 nuclear receptor subfamily 0 group B member 2 Homo sapiens 48-51 20375098-8 2010 Finally, we demonstrated that inhibition of SIRT1 activity significantly reversed SHP-mediated inhibition of bile-acid synthesis by LRH1 overexpression, thereby suggesting a novel mechanism of SHP-mediated inhibition of LRH1-dependent bile-acid homeostasis via recruitment of SIRT1 histone deacetylase protein. Bile Acids and Salts 109-118 nuclear receptor subfamily 0 group B member 2 Homo sapiens 82-85 20375098-8 2010 Finally, we demonstrated that inhibition of SIRT1 activity significantly reversed SHP-mediated inhibition of bile-acid synthesis by LRH1 overexpression, thereby suggesting a novel mechanism of SHP-mediated inhibition of LRH1-dependent bile-acid homeostasis via recruitment of SIRT1 histone deacetylase protein. Bile Acids and Salts 235-244 nuclear receptor subfamily 0 group B member 2 Homo sapiens 82-85 20375098-8 2010 Finally, we demonstrated that inhibition of SIRT1 activity significantly reversed SHP-mediated inhibition of bile-acid synthesis by LRH1 overexpression, thereby suggesting a novel mechanism of SHP-mediated inhibition of LRH1-dependent bile-acid homeostasis via recruitment of SIRT1 histone deacetylase protein. Bile Acids and Salts 235-244 nuclear receptor subfamily 0 group B member 2 Homo sapiens 193-196 18775915-0 2008 Bile acid induces expression of COX-2 through the homeodomain transcription factor CDX1 and orphan nuclear receptor SHP in human gastric cancer cells. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 92-119 19426389-3 2009 The activated FXR-SHP pathway regulates the enterohepatic recycling and biosynthesis of bile acids and underlies the down-regulation of hepatic fatty acid and triglyceride biosynthesis and very low density lipoprotein production mediated by sterol-regulatory element-binding protein-1c. Bile Acids and Salts 88-98 nuclear receptor subfamily 0 group B member 2 Homo sapiens 18-21 19185005-3 2009 Down-regulation of CYP7A1 under cholestatic conditions has been attributed to bile salt-mediated induction of the transcriptional repressor short heterodimer partner (SHP), because the interrupted enterohepatic cycle of bile salts is thought to abrogate intestinal FGF19 production and thus result in lowering of plasma FGF19 levels. Bile Acids and Salts 78-87 nuclear receptor subfamily 0 group B member 2 Homo sapiens 167-170 19185005-3 2009 Down-regulation of CYP7A1 under cholestatic conditions has been attributed to bile salt-mediated induction of the transcriptional repressor short heterodimer partner (SHP), because the interrupted enterohepatic cycle of bile salts is thought to abrogate intestinal FGF19 production and thus result in lowering of plasma FGF19 levels. Bile Acids and Salts 220-230 nuclear receptor subfamily 0 group B member 2 Homo sapiens 167-170 19805516-1 2009 Bile acid homeostasis is critical in maintaining health and is primarily regulated by the nuclear receptors farnesoid X receptor (FXR) and small heterodimer partner (SHP). Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 166-169 19805516-2 2009 Bile acid-activated FXR indirectly inhibits expression of cholesterol 7alpha hydroxylase (CYP7A1), a key enzyme in conversion of cholesterol to bile acids, by induction of SHP. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 172-175 19805516-2 2009 Bile acid-activated FXR indirectly inhibits expression of cholesterol 7alpha hydroxylase (CYP7A1), a key enzyme in conversion of cholesterol to bile acids, by induction of SHP. Bile Acids and Salts 144-154 nuclear receptor subfamily 0 group B member 2 Homo sapiens 172-175 19805516-5 2009 We have examined the role of these subunits in regulation of bile acid metabolism under physiological conditions by FXR and SHP. Bile Acids and Salts 61-70 nuclear receptor subfamily 0 group B member 2 Homo sapiens 124-127 19805516-8 2009 Our studies demonstrate that Brm and Brg-1 have distinct functions in the regulation of two key genes, CYP7A1 and SHP, within a single physiological pathway, feedback inhibition of bile acid biosynthesis, by differentially targeting SHP and FXR. Bile Acids and Salts 181-190 nuclear receptor subfamily 0 group B member 2 Homo sapiens 114-117 19805516-8 2009 Our studies demonstrate that Brm and Brg-1 have distinct functions in the regulation of two key genes, CYP7A1 and SHP, within a single physiological pathway, feedback inhibition of bile acid biosynthesis, by differentially targeting SHP and FXR. Bile Acids and Salts 181-190 nuclear receptor subfamily 0 group B member 2 Homo sapiens 233-236 18775915-5 2008 Furthermore, the induction of CDX1 by bile acid was mediated by the orphan nuclear receptor, small heterodimer partner (SHP). Bile Acids and Salts 38-47 nuclear receptor subfamily 0 group B member 2 Homo sapiens 93-118 18775915-5 2008 Furthermore, the induction of CDX1 by bile acid was mediated by the orphan nuclear receptor, small heterodimer partner (SHP). Bile Acids and Salts 38-47 nuclear receptor subfamily 0 group B member 2 Homo sapiens 120-123 18775915-7 2008 Collectively, these results reveal that bile acid induces an increase in the gene expression of COX-2 via the sequential transcriptional induction of SHP and CDX1 in precancerous lesions of human gastric cancer. Bile Acids and Salts 40-49 nuclear receptor subfamily 0 group B member 2 Homo sapiens 150-153 17145766-0 2007 Coordinated recruitment of histone methyltransferase G9a and other chromatin-modifying enzymes in SHP-mediated regulation of hepatic bile acid metabolism. Bile Acids and Salts 133-142 nuclear receptor subfamily 0 group B member 2 Homo sapiens 98-101 18307978-0 2008 Bile acid regulates c-Jun expression through the orphan nuclear receptor SHP induction in gastric cells. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 73-76 18307978-3 2008 In this study, we demonstrated that bile acid induced the expression of the SHP orphan nuclear receptor at the transcriptional level via c-Jun activation. Bile Acids and Salts 36-45 nuclear receptor subfamily 0 group B member 2 Homo sapiens 76-79 18307978-4 2008 Bile acid also enhanced the protein interaction of NF-kappaB and SHP, thereby resulting in an increase in c-Jun expression and the production of the inflammatory cytokine, TNFalpha. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 65-68 17601490-3 2007 Recently, SHP has been shown to mediate the bile acid-dependent down regulation of gluconeogenic gene expression in liver. Bile Acids and Salts 44-53 nuclear receptor subfamily 0 group B member 2 Homo sapiens 10-13 17895379-1 2007 Coordinated regulation of bile acid biosynthesis, the predominant pathway for hepatic cholesterol catabolism, is mediated by few key nuclear receptors including the orphan receptors liver receptor homolog 1 (LRH-1), hepatocyte nuclear factor 4alpha (HNF4alpha), small heterodimer partner (SHP), and the bile acid receptor FXR (farnesoid X receptor). Bile Acids and Salts 26-35 nuclear receptor subfamily 0 group B member 2 Homo sapiens 289-292 17145766-2 2007 Recently, we reported that SHP inhibits transcription of CYP7A1, a key gene in bile acid biosynthesis, by recruiting histone deacetylases (HDACs) and a Swi/Snf-Brm complex. Bile Acids and Salts 79-88 nuclear receptor subfamily 0 group B member 2 Homo sapiens 27-30 17145766-7 2007 G9a was recruited to and H3K9 was methylated at the CYP7A1 promoter in a SHP-dependent manner in bile acid-treated HepG2 cells. Bile Acids and Salts 97-106 nuclear receptor subfamily 0 group B member 2 Homo sapiens 73-76 17145766-11 2007 Our studies establish a critical role for G9a methyltransferase, histone deacetylases, and the Swi/Snf-Brm complex in the SHP-mediated inhibition of hepatic bile acid synthesis via coordinated chromatin modification at target genes. Bile Acids and Salts 157-166 nuclear receptor subfamily 0 group B member 2 Homo sapiens 122-125 15123650-11 2004 We propose a possible role of SREBP-1 in the species differential regulation of cholesterol and bile acid homeostasis via a novel mechanism of up-regulation of the hSHP gene expression. Bile Acids and Salts 96-105 nuclear receptor subfamily 0 group B member 2 Homo sapiens 164-168 16436500-11 2006 In addition, bile acid-inducible transcriptional repressor, small heterodimer partner (SHP), inhibited activation of the reporter-linked hOCT1 promoter and of the endogenous hOCT1 gene by HNF-4alpha. Bile Acids and Salts 13-22 nuclear receptor subfamily 0 group B member 2 Homo sapiens 60-85 16436500-11 2006 In addition, bile acid-inducible transcriptional repressor, small heterodimer partner (SHP), inhibited activation of the reporter-linked hOCT1 promoter and of the endogenous hOCT1 gene by HNF-4alpha. Bile Acids and Salts 13-22 nuclear receptor subfamily 0 group B member 2 Homo sapiens 87-90 16436500-12 2006 In conclusion, the hOCT1 gene, encoding an important drug transporter in the human liver, is activated by HNF-4alpha and suppressed by bile acids via SHP. Bile Acids and Salts 135-145 nuclear receptor subfamily 0 group B member 2 Homo sapiens 150-153 15796896-12 2005 Our results indicate that when bile acid synthesis is upregulated by cholestyramine treatment the SHP-independent pathway for controlling CYP7A1 transcription dominates over the SHP-dependent pathway. Bile Acids and Salts 31-40 nuclear receptor subfamily 0 group B member 2 Homo sapiens 98-101 15796896-12 2005 Our results indicate that when bile acid synthesis is upregulated by cholestyramine treatment the SHP-independent pathway for controlling CYP7A1 transcription dominates over the SHP-dependent pathway. Bile Acids and Salts 31-40 nuclear receptor subfamily 0 group B member 2 Homo sapiens 178-181 15314177-0 2004 Role of an mSin3A-Swi/Snf chromatin remodeling complex in the feedback repression of bile acid biosynthesis by SHP. Bile Acids and Salts 85-94 nuclear receptor subfamily 0 group B member 2 Homo sapiens 111-114 15314177-2 2004 SHP is central to feedback repression of cholesterol 7alpha hydroxylase gene (CYP7A1) expression by bile acids, which is critical for maintaining cholesterol homeostasis. Bile Acids and Salts 100-110 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 15314177-8 2004 Bile acid-induced recruitment of mSin3A/Brm, chromatin remodeling, and concomitant repression of endogenous CYP7A1 expression were impaired when SHP expression was inhibited by SHP small interfering RNA. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 145-148 15314177-8 2004 Bile acid-induced recruitment of mSin3A/Brm, chromatin remodeling, and concomitant repression of endogenous CYP7A1 expression were impaired when SHP expression was inhibited by SHP small interfering RNA. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 177-180 16168958-0 2005 Bile acids reduce SR-BI expression in hepatocytes by a pathway involving FXR/RXR, SHP, and LRH-1. Bile Acids and Salts 0-10 nuclear receptor subfamily 0 group B member 2 Homo sapiens 82-85 16168958-3 2005 Bile acid-activated FXR/RXR represses expression of CYP7A1, the rate-limiting enzyme during bile acid synthesis, by inducing the expression of SHP, which inhibits LXR/RXR and LRH-1-transactivation of CYP7A1. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 143-146 16168958-3 2005 Bile acid-activated FXR/RXR represses expression of CYP7A1, the rate-limiting enzyme during bile acid synthesis, by inducing the expression of SHP, which inhibits LXR/RXR and LRH-1-transactivation of CYP7A1. Bile Acids and Salts 92-101 nuclear receptor subfamily 0 group B member 2 Homo sapiens 143-146 15239098-9 2004 Antisense mediated knock-down of SHP in Caco-2 cells partially offset the bile acid mediated repression of ASBT promoter activity. Bile Acids and Salts 74-83 nuclear receptor subfamily 0 group B member 2 Homo sapiens 33-36 15239098-11 2004 Bile acids induce a negative feedback regulation of human ASBT via an FXR-mediated, SHP-dependent effect upon RAR/RXR activation of ASBT. Bile Acids and Salts 0-10 nuclear receptor subfamily 0 group B member 2 Homo sapiens 84-87 15047713-1 2004 Bile acid homeostasis is tightly controlled by the feedback mechanism in which an atypical orphan nuclear receptor (NR) small heterodimer partner (SHP) inactivates several NRs such as liver receptor homologue-1 and hepatocyte nuclear factor 4. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 147-150 15047713-3 2004 Here, we report that bile acids inhibit the expression of gluconeogenic genes, including glucose-6-phosphatase (G6Pase), phosphoenolpyruvate carboxykinase, and fructose 1,6-bis phosphatase in an SHP-dependent fashion. Bile Acids and Salts 21-31 nuclear receptor subfamily 0 group B member 2 Homo sapiens 195-198 15047713-7 2004 These findings reveal a novel mechanism by which bile acids regulate gluconeogenic gene expression via an SHP-dependent regulatory pathway. Bile Acids and Salts 49-59 nuclear receptor subfamily 0 group B member 2 Homo sapiens 106-109 12601360-2 2003 They are ligands of the farnesoid X receptor, which induces small heterodimer partner (SHP)-1, a transcriptional repressor of bile acid synthetic enzymes. Bile Acids and Salts 126-135 nuclear receptor subfamily 0 group B member 2 Homo sapiens 60-93 14672953-0 2004 Inhibitory effect of the small heterodimer partner on hepatocyte nuclear factor-4 mediates bile acid-induced repression of the human angiotensinogen gene. Bile Acids and Salts 91-100 nuclear receptor subfamily 0 group B member 2 Homo sapiens 25-50 14672953-9 2004 These results suggest that bile acids negatively regulate the human ANG gene through the inhibitory effect of SHP on HNF-4. Bile Acids and Salts 27-37 nuclear receptor subfamily 0 group B member 2 Homo sapiens 110-113 14699511-4 2004 A key regulator of hepatocellular bile salt homeostasis is the bile acid receptor/farnesoid X receptor FXR, which activates transcription of the BSEP and OATP8 genes and of the small heterodimer partner 1 (SHP). Bile Acids and Salts 34-43 nuclear receptor subfamily 0 group B member 2 Homo sapiens 177-204 14699511-4 2004 A key regulator of hepatocellular bile salt homeostasis is the bile acid receptor/farnesoid X receptor FXR, which activates transcription of the BSEP and OATP8 genes and of the small heterodimer partner 1 (SHP). Bile Acids and Salts 34-43 nuclear receptor subfamily 0 group B member 2 Homo sapiens 206-209 12805410-3 2003 SHP is up-regulated by primary bile acids, through the activation of their receptor farnesoid X receptor, leading to the repression of cholesterol 7alpha-hydroxylase (CYP7alpha) expression, the rate-limiting enzyme in bile acid production from cholesterol. Bile Acids and Salts 31-41 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 12805410-3 2003 SHP is up-regulated by primary bile acids, through the activation of their receptor farnesoid X receptor, leading to the repression of cholesterol 7alpha-hydroxylase (CYP7alpha) expression, the rate-limiting enzyme in bile acid production from cholesterol. Bile Acids and Salts 31-40 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 12805410-11 2003 These results reveal an elaborate regulatory cascade, tightly controlled by SHP, for both the maintenance of bile acid production and detoxification in the liver. Bile Acids and Salts 109-118 nuclear receptor subfamily 0 group B member 2 Homo sapiens 76-79 12559450-5 2003 An additional nuclear hormone receptor, small heterodimer partner (SHP), is required to inhibit the competence factor, liver receptor homolog-1 to achieve repression of bile acid synthesis in the liver and in so doing SHP autoregulates its own function. Bile Acids and Salts 169-178 nuclear receptor subfamily 0 group B member 2 Homo sapiens 40-65 12554795-4 2003 This repression is mediated, at least in part, through induction of the orphan nuclear receptor, short heterodimer partner (SHP), which is also induced by bile acids. Bile Acids and Salts 155-165 nuclear receptor subfamily 0 group B member 2 Homo sapiens 97-122 12554795-4 2003 This repression is mediated, at least in part, through induction of the orphan nuclear receptor, short heterodimer partner (SHP), which is also induced by bile acids. Bile Acids and Salts 155-165 nuclear receptor subfamily 0 group B member 2 Homo sapiens 124-127 12554795-5 2003 We demonstrate that SHP is regulated directly by LXRalpha through a DNA response element that overlaps with the previously characterized bile acid response element. Bile Acids and Salts 137-146 nuclear receptor subfamily 0 group B member 2 Homo sapiens 20-23 12559450-5 2003 An additional nuclear hormone receptor, small heterodimer partner (SHP), is required to inhibit the competence factor, liver receptor homolog-1 to achieve repression of bile acid synthesis in the liver and in so doing SHP autoregulates its own function. Bile Acids and Salts 169-178 nuclear receptor subfamily 0 group B member 2 Homo sapiens 67-70 12559450-5 2003 An additional nuclear hormone receptor, small heterodimer partner (SHP), is required to inhibit the competence factor, liver receptor homolog-1 to achieve repression of bile acid synthesis in the liver and in so doing SHP autoregulates its own function. Bile Acids and Salts 169-178 nuclear receptor subfamily 0 group B member 2 Homo sapiens 218-221 12198243-5 2002 Treatment of Caco-2 cells with bile acids, which activate farnesoid X receptor and subsequently induce SHP, leads to the repression of the human ABCG1 gene, an established LXR target gene. Bile Acids and Salts 31-41 nuclear receptor subfamily 0 group B member 2 Homo sapiens 103-106 11907135-5 2002 Bile acid activation of FXR has been shown to repress the expression of CYP7A1 via increasing the expression of small heterodimer partner (SHP), a non-DNA binding protein. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 112-137 11907135-5 2002 Bile acid activation of FXR has been shown to repress the expression of CYP7A1 via increasing the expression of small heterodimer partner (SHP), a non-DNA binding protein. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 139-142 11907135-8 2002 This "FXR/SHP-independent" pathway involves the interaction of bile acids with liver macrophages (i.e., Kupffer cells), which induces the expression, and secretion of cytokines. Bile Acids and Salts 63-73 nuclear receptor subfamily 0 group B member 2 Homo sapiens 10-13 11518759-5 2001 Bile acids and FXR repressed endogenous CYP7A1 but stimulated alpha-fetoprotein transcription factor (FTF) and small heterodimer partner (SHP) mRNA expression in HepG2 cells. Bile Acids and Salts 0-10 nuclear receptor subfamily 0 group B member 2 Homo sapiens 138-141 11668176-3 2002 This repression is thought to be based on the bile acid-dependent induction of expression of the orphan receptor small heterodimer partner (SHP) NR0B2, which inhibits the activity of LRH-1. Bile Acids and Salts 46-55 nuclear receptor subfamily 0 group B member 2 Homo sapiens 140-143 11668176-3 2002 This repression is thought to be based on the bile acid-dependent induction of expression of the orphan receptor small heterodimer partner (SHP) NR0B2, which inhibits the activity of LRH-1. Bile Acids and Salts 46-55 nuclear receptor subfamily 0 group B member 2 Homo sapiens 145-150 11535594-15 2001 Bile acids repress human CYP8B1 transcription by reducing the transactivation activity of HNF4alpha through interaction of HNF4alpha with SHP and reduction of HNF4alpha expression in the liver. Bile Acids and Salts 0-10 nuclear receptor subfamily 0 group B member 2 Homo sapiens 138-141 11574686-9 2001 FTF and not HNF-4 is the factor involved in regulation of 12alpha-hydroxylase promoter activity by bile acids through its interaction with SHP. Bile Acids and Salts 99-109 nuclear receptor subfamily 0 group B member 2 Homo sapiens 139-142 11518759-9 2001 Results revealed that FTF was a dominant negative factor that was induced by bile acid-activated FXR to inhibit both CYP7A1 and SHP transcription. Bile Acids and Salts 77-86 nuclear receptor subfamily 0 group B member 2 Homo sapiens 128-131 11518759-10 2001 Differential regulation of FTF and SHP expression by bile acids may explain the wide variation in CYP7A1 expression and the rate of bile acid synthesis and regulation in different species. Bile Acids and Salts 53-63 nuclear receptor subfamily 0 group B member 2 Homo sapiens 35-38 11518759-10 2001 Differential regulation of FTF and SHP expression by bile acids may explain the wide variation in CYP7A1 expression and the rate of bile acid synthesis and regulation in different species. Bile Acids and Salts 53-62 nuclear receptor subfamily 0 group B member 2 Homo sapiens 35-38 33692750-10 2020 However, following knockdown of FGF19, CDCA still independently decreased BA synthesis, presumably through the regulatory protein small heterodimer partner (SHP). Bile Acids and Salts 74-76 nuclear receptor subfamily 0 group B member 2 Homo sapiens 157-160 11030331-4 2000 Feedback repression of CYP7A1 is accomplished by the binding of bile acids to FXR, which leads to transcription of SHP. Bile Acids and Salts 64-74 nuclear receptor subfamily 0 group B member 2 Homo sapiens 115-118 11030332-0 2000 A regulatory cascade of the nuclear receptors FXR, SHP-1, and LRH-1 represses bile acid biosynthesis. Bile Acids and Salts 78-87 nuclear receptor subfamily 0 group B member 2 Homo sapiens 51-56 35156505-1 2022 Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules responsible for controlling serum bile acid levels. Bile Acids and Salts 120-129 nuclear receptor subfamily 0 group B member 2 Homo sapiens 40-65 35156505-1 2022 Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules responsible for controlling serum bile acid levels. Bile Acids and Salts 120-129 nuclear receptor subfamily 0 group B member 2 Homo sapiens 67-70 35156505-10 2022 Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules - responsible for controlling serum bile acid levels. Bile Acids and Salts 122-131 nuclear receptor subfamily 0 group B member 2 Homo sapiens 40-65 35156505-10 2022 Fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) are molecules - responsible for controlling serum bile acid levels. Bile Acids and Salts 122-131 nuclear receptor subfamily 0 group B member 2 Homo sapiens 67-70 32598580-2 2020 The small heterodimer partner (SHP) is a regulator of lipid and bile acid metabolism in the liver. Bile Acids and Salts 64-73 nuclear receptor subfamily 0 group B member 2 Homo sapiens 4-29 32598580-2 2020 The small heterodimer partner (SHP) is a regulator of lipid and bile acid metabolism in the liver. Bile Acids and Salts 64-73 nuclear receptor subfamily 0 group B member 2 Homo sapiens 31-34 31628911-8 2019 The upregulation of genes related to bile acid synthesis (CYP7A1 and CYP8B1) and the downregulation of genes related to conjugation (BAAT and BACS) and regulation (FXR and SHP) were detected in the liver, suggesting that hydrophobic bile acid production was increased and FXR signaling was impaired. Bile Acids and Salts 233-242 nuclear receptor subfamily 0 group B member 2 Homo sapiens 172-175 31905685-7 2019 For NR0B2, our results suggest a finely balanced expression optimum reached in highly permissive Huh7 cells, with even higher levels leading to a nearly complete breakdown of HCV replication, likely due to a dysregulation of bile acid and cholesterol metabolism. Bile Acids and Salts 225-234 nuclear receptor subfamily 0 group B member 2 Homo sapiens 4-9 30745141-5 2019 The activated Mst1/2 subsequently phosphorylates and stabilizes SHP to downregulate the key bile acid-synthesis enzyme Cyp7a1 expression, thereby limiting bile acid synthesis. Bile Acids and Salts 92-101 nuclear receptor subfamily 0 group B member 2 Homo sapiens 64-67 31767173-5 2019 The feedback-loop that terminates Cyp17a1-PPARalpha activity, and re-establishes anabolic liver metabolism during re-feeding is mapped to postprandial bile acid-signaling, involving the receptors FXR, SHP and LRH-1. Bile Acids and Salts 151-160 nuclear receptor subfamily 0 group B member 2 Homo sapiens 201-204 30745141-5 2019 The activated Mst1/2 subsequently phosphorylates and stabilizes SHP to downregulate the key bile acid-synthesis enzyme Cyp7a1 expression, thereby limiting bile acid synthesis. Bile Acids and Salts 155-164 nuclear receptor subfamily 0 group B member 2 Homo sapiens 64-67 28873070-3 2017 Accordingly, SHP1 is part of negative feedback loops of the transcriptional regulation of genes involved in drug metabolism and various metabolic pathways including bile acid and glucose homeostasis. Bile Acids and Salts 165-174 nuclear receptor subfamily 0 group B member 2 Homo sapiens 13-17 30419252-10 2019 The results showed 8-MOP could affect the CYP7A1, SHP and MRP3 expression via VDR, and such effects could be reversed by knockdown of VDR expression, suggesting a vital role of VDR involved in 8-MOP-regulated bile acid synthesis and transportation. Bile Acids and Salts 209-218 nuclear receptor subfamily 0 group B member 2 Homo sapiens 50-53 29849798-12 2018 Collectively, these results revealed that the activation of FXR and sequential direct transcriptional induction of SHP were involved in the expression of CDX2 induced by bile acid in gastric IM lesions. Bile Acids and Salts 170-179 nuclear receptor subfamily 0 group B member 2 Homo sapiens 115-118 28805978-6 2017 OCA dose-dependently increased fibroblast growth factor-19 (FGF-19) and small heterodimer partner (SHP) which, in turn, suppress mRNA levels of cholesterol 7-alpha-hydroxylase (CYP7A1), the rate-limiting enzyme for de novo synthesis of bile acids. Bile Acids and Salts 236-246 nuclear receptor subfamily 0 group B member 2 Homo sapiens 99-102 27770549-4 2017 Bioinformatics analysis revealed putative binding sites for PTBP1 within the coding region (CDS) of small heterodimer partner (SHP), a key repressor of BA biosynthesis. Bile Acids and Salts 152-154 nuclear receptor subfamily 0 group B member 2 Homo sapiens 100-134 24999016-11 2014 Intestinal and hepatic regulation of BA synthesis was characterised by a blunted intestinal FXR activation response and a failure of SHP to repress key hepatic targets. Bile Acids and Salts 37-39 nuclear receptor subfamily 0 group B member 2 Homo sapiens 133-136 26521940-4 2016 Chenodeoxycholic acid (CDCA), a major component of bile acids, represses CYP7A1 by activating a transcriptional repressor named small heterodimer partner (SHP). Bile Acids and Salts 51-61 nuclear receptor subfamily 0 group B member 2 Homo sapiens 128-153 26521940-4 2016 Chenodeoxycholic acid (CDCA), a major component of bile acids, represses CYP7A1 by activating a transcriptional repressor named small heterodimer partner (SHP). Bile Acids and Salts 51-61 nuclear receptor subfamily 0 group B member 2 Homo sapiens 155-158 26609171-13 2016 CONCLUSIONS: We conclude that the loss of APC function favors the silencing of FXR expression through CpG hypermethylation in mouse colonic mucosa and human colon cells, leading to reduced expression of downstream targets (SHP, IBABP) involved in BA homeostasis while increasing the expression of factors (COX-2, c-MYC) that contribute to inflammation and colon cancer. Bile Acids and Salts 229-231 nuclear receptor subfamily 0 group B member 2 Homo sapiens 223-226 26504773-2 2015 SHP is a transcriptional corepressor affecting diverse metabolic processes including bile acid synthesis, cholesterol and lipid metabolism, glucose and energy homeostasis, and reproductive biology via interaction with multiple NRs and transcriptional factors (TFs). Bile Acids and Salts 85-94 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3 24338587-8 2014 Furthermore, a leucine-enriched diet restored mammalian target of rapamycin (mTOR) activation, acetylation of FXR and histones, leading to an overall lower BA production through SHP-inhibition of Cyp7A1 and higher transport (BSEP) and detoxification (Sult2a1) leading to an improved liver regeneration. Bile Acids and Salts 156-158 nuclear receptor subfamily 0 group B member 2 Homo sapiens 178-181 25100060-0 2014 Another Shp on the horizon for bile acids. Bile Acids and Salts 31-41 nuclear receptor subfamily 0 group B member 2 Homo sapiens 8-11 24819989-5 2014 Bile acid induction of the FXR-alpha target gene, small heterodimer partner (SHP), is highly dependent on the activation PKCzeta, a branch of the insulin signaling pathway. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 50-75 24819989-5 2014 Bile acid induction of the FXR-alpha target gene, small heterodimer partner (SHP), is highly dependent on the activation PKCzeta, a branch of the insulin signaling pathway. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 77-80 23824184-5 2013 PKCzeta is coimmunopreciptitated with SHP and both are recruited to SHP target genes after bile acid or FGF19 treatment. Bile Acids and Salts 91-100 nuclear receptor subfamily 0 group B member 2 Homo sapiens 68-71 23824184-0 2013 Bile acid signal-induced phosphorylation of small heterodimer partner by protein kinase Czeta is critical for epigenomic regulation of liver metabolic genes. Bile Acids and Salts 0-9 nuclear receptor subfamily 0 group B member 2 Homo sapiens 44-69 23824184-3 2013 Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Bile Acids and Salts 79-81 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-25 23824184-3 2013 Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Bile Acids and Salts 79-81 nuclear receptor subfamily 0 group B member 2 Homo sapiens 27-30 23824184-3 2013 Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Bile Acids and Salts 192-194 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-25 23824184-3 2013 Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Bile Acids and Salts 192-194 nuclear receptor subfamily 0 group B member 2 Homo sapiens 27-30 23824184-3 2013 Small heterodimer partner (SHP) has been implicated as a key mediator of these BA signaling pathways by recruitment of chromatin modifying proteins, but the key question of how SHP transduces BA signaling into repressive histone modifications at liver metabolic genes remains unknown. Bile Acids and Salts 192-194 nuclear receptor subfamily 0 group B member 2 Homo sapiens 177-180 23824184-5 2013 PKCzeta is coimmunopreciptitated with SHP and both are recruited to SHP target genes after bile acid or FGF19 treatment. Bile Acids and Salts 91-100 nuclear receptor subfamily 0 group B member 2 Homo sapiens 38-41 24379397-1 2014 Small heterodimer partner (SHP) is an orphan nuclear receptor that functions as a transcriptional repressor to regulate bile acid and cholesterol homeostasis. Bile Acids and Salts 120-129 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-25 24379397-1 2014 Small heterodimer partner (SHP) is an orphan nuclear receptor that functions as a transcriptional repressor to regulate bile acid and cholesterol homeostasis. Bile Acids and Salts 120-129 nuclear receptor subfamily 0 group B member 2 Homo sapiens 27-30 24415870-10 2014 In addition, the transcription factors CDX1 and SHP synergistically enhanced bile acid-induced elevation of HDC gene expression. Bile Acids and Salts 77-86 nuclear receptor subfamily 0 group B member 2 Homo sapiens 48-51 24415870-12 2014 CONCLUSION: HDC production in the stomach is associated with bile acid exposure and its related transcriptional regulation network of FXR, SHP, and CDX1. Bile Acids and Salts 61-70 nuclear receptor subfamily 0 group B member 2 Homo sapiens 139-142 23824184-8 2013 Thr-55 phosphorylation increases interaction of SHP with chromatin modifiers and their occupancy at selective BA-responsive genes. Bile Acids and Salts 110-112 nuclear receptor subfamily 0 group B member 2 Homo sapiens 48-51 23299969-14 2013 FFA exposure prevented SHP-mediated repression of NTCP and Cyp7A1 expression, which lead to increased BA synthesis and uptake. Bile Acids and Salts 102-104 nuclear receptor subfamily 0 group B member 2 Homo sapiens 23-26