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1                                              SXR forms a heterodimer with RXR that can bind to and in
2                                              SXR functions as a xenobiotic sensor to coordinately reg
3 lated antineoplastic agent, did not activate SXR and displayed superior pharmacokinetic properties.
4 re weaker (saquinavir) or unable to activate SXR (nelfinavir, indinavir) thus defining analogs that f
5 monly used chemotherapeutic agent, activated SXR and enhanced P-glycoprotein-mediated drug clearance.
6 therapeutic agent that effectively activates SXR.
7 e to the wide variety of drugs that are also SXR agonists.
8   Two new nuclear hormone receptors, PXR and SXR, have been identified.
9 immunosuppressant effects of xenobiotics and SXR-responsive drugs.
10  thereby demonstrating a direct link between SXR and drug-mediated antagonism of NF-kappaB.
11 rus (HIV) protease inhibitor ritonavir binds SXR and activates its target genes.
12  toward steroids or xenobiotics exhibited by SXR/PXR.
13 s suggest that altered metabolism induced by SXR loss of function resulted in the accumulation of hyd
14 to activate CYP3A through previously defined SXR/PXR response elements.
15 nes whereas inhibition of NF-kappaB enhances SXR activity.
16                      Therefore, we establish SXR and PXR as bile acid receptors and a role for the xe
17  gene, CYP3A4, identifying it as a bona fide SXR ligand.
18 dentified naturally occurring antagonist for SXR (hPXR).
19       These results support a major role for SXR/PXR in protection against xenobiotic-induced oxidati
20 o displace transcriptional corepressors from SXR.
21 t that SFN is a specific antagonist of human SXR and that it inhibits SXR-mediated induction of drug
22 r) thus defining analogs that fail to induce SXR-regulated clearance pathways.
23        SFN can bind directly to SXR, inhibit SXR coactivator recruitment, and efficiently repress SXR
24                   Furthermore, SFN inhibited SXR-mediated CYP3A4 expression and CYP3A4-catalyzed mida
25 antagonist of human SXR and that it inhibits SXR-mediated induction of drug clearance.
26 , NF-kappaB activation reciprocally inhibits SXR and its target genes whereas inhibition of NF-kappaB
27                                     Instead, SXR inhibited VDR-mediated CYP24 promoter activity, and
28 nhibitors are distinct from previously known SXR ligands in that they are peptide mimetic compounds.
29                                    The known SXR activators rifampicin and hyperforin induced this pa
30 eparture from FXL to FXR (and apparently not SXR) is significant in only the malignant tumors, presum
31   However, here we showed that activation of SXR did not induce CYP24 expression in vitro and in vivo
32 ansgenic animals, we show that activation of SXR/PXR is necessary and sufficient to both induce CYP3A
33  demonstrate how the molecular activities of SXR can be manipulated to control drug clearance.
34     In transgenic mice, an activated form of SXR causes constitutive upregulation of CYP3A gene expre
35 1 transcription by acting as an inhibitor of SXR.
36 ery low in tissues containing high levels of SXR, including the small intestine.
37                                 This role of SXR could be generally applicable to other environmental
38 ut mice (SXRKO) and to elucidate the role of SXR in PCB-153 metabolism and promotion of its harmful e
39  have important implications for the role of SXR in regulating drug clearance and hepatic disorders a
40 hment in liver and intestine, major sites of SXR/PXR expression that are critical in xenobiotic metab
41       This expands the ligand specificity of SXR to include this unique chemical class whose pharmace
42 implication of this work is that a subset of SXR activators may function as effective therapeutic age
43  prevalent PCB congener in human tissues, on SXR knockout mice (SXRKO) and to elucidate the role of S
44 o the wide range of xenobiotics that are PXR/SXR ligands, including drugs, dietary constituents, and
45 rs that is consistent with activation of PXR/SXR by bile acids.
46 eceptor/steroid and xenobiotic receptor (PXR/SXR) closely paralleled each other but was markedly diff
47 to and activated the orphan nuclear receptor SXR and induced expression of the SXR target gene, CYP3A
48                  The orphan nuclear receptor SXR coordinately regulates drug clearance in response to
49                             Nuclear receptor SXR/PXR (steroid and xenobiotic receptor/pregnenolone X
50 monstrate that the human xenobiotic receptor SXR (steroid and xenobiotic receptor) and its rodent hom
51 tivation of steroid and xenobiotic receptor (SXR) also enhances the expression of CYP24, providing a
52 tion of the steroid and xenobiotic receptor (SXR) and regulation of oxidative stress, apoptosis, and
53 clear receptors steroid xenobiotic receptor (SXR) and the constitutive active receptor, CAR.
54 the nuclear steroid and xenobiotic receptor (SXR) by commonly used drugs in humans inhibits the activ
55  termed the steroid and xenobiotic receptor (SXR), which activates transcription in response to a div
56 ated by the steroid and xenobiotic receptor (SXR).
57  homologue, steroid and xenobiotic receptor (SXR).
58 e receptor, steroid and xenobiotic receptor (SXR; also called "hPXR").
59         The steroid and xenobiotic receptor [SXR; also known as the pregnane X receptor (PXR) and for
60 e mammalian steroid and xenobiotic receptor, SXR/PXR.
61 m could enter even the slow-exchange-regime (SXR).
62 tivator recruitment, and efficiently repress SXR activities.
63 ne, the pregnane X receptor (PXR in rodents, SXR in humans), regulates p-glycoprotein expression.
64                             We conclude that SXR/PXR genes encode the primary species-specific xeno-s
65                  Unexpectedly, we found that SXR can regulate CYP2B, both in cultured cells and in tr
66                            We show here that SXR also regulates drug efflux by activating expression
67 ver and intestine, our results indicate that SXR has a dual role in mediating vitamin D catabolism an
68                        Finally, we show that SXR ligands activate expression of multiple resistance p
69 in cells isolated from mice deficient in the SXR ortholog PXR.
70  significantly increased in mice lacking the SXR ortholog pregnane X receptor (PXR), thereby demonstr
71  expression was enhanced in mice lacking the SXR ortholog pregnane X receptor, and treatment of human
72 r receptor SXR and induced expression of the SXR target gene, CYP3A4, identifying it as a bona fide S
73 X receptor, and treatment of humans with the SXR agonist rifampicin had no effect on intestinal CYP24
74                                         This SXR/PXR-NF-kappaB axis provides a molecular explanation
75 tor of bone-specific genes that acts through SXR to favor the expression of osteoblastic markers.
76                                        Thus, SXR has a novel role as a mediator of bone homeostasis i
77                     SFN can bind directly to SXR, inhibit SXR coactivator recruitment, and efficientl