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Data suggest both PXR (show NR1I2 Proteins) and CAR are expressed in testis/Sertoli cells; exposure of Sertoli cells (in vitro model of blood-testis barrier) to PXR (show NR1I2 Proteins) or CAR ligands (including antiretroviral drugs) up-regulates expression of Pgp/ABCB1 (show ABCB4 Proteins), BCRP, and MRP4 (show ABCC4 Proteins). (PXR (show NR1I2 Proteins) = pregnane X receptor (show NR1I2 Proteins); CAR = constitutive androstane receptor (show NR1I3 Proteins); Pgp/ABCB1 (show ABCB4 Proteins) = P-glycoprotein ABCB1 (show ABCB1 Proteins); BCRP = breast cancer resistance protein; MRP4 (show ABCC4 Proteins) =multidrug resistance protein 4)
Genetic variations in PXR (show NR1I2 Proteins) affect induction of Bupropion hydroxylation by sodium ferulate.
The pregnane X receptor (show NR1I2 Proteins) down-regulates organic cation transporter 1 (SLC22A1) in human hepatocytes by competing for ("squelching") SRC-1 (show SRC Proteins) coactivator.
This study revealed for the first time the involvement of NR1I2 (show NR1I2 Proteins) in the pharmacogenetics of irinotecan and suggest that it may help to predict the toxicity of low-dose irinotecan.
EPCR (show PROCR Proteins) occupancy recruits G-protein coupled receptor kinase 5 (show GRK5 Proteins), thereby inducing beta-arrestin-2 (show ARRB2 Proteins) biased PAR1 (show MARK2 Proteins) signaling by both APC (show APC Proteins) and thrombin (show F2 Proteins). In
In intrahepatic cholestasis of pregnancy, gene silencing of miR (show MLXIP Proteins)-148a upregulated PXR (show NR1I2 Proteins) expression which was inhibited by estradiol in liver cells. miR (show MLXIP Proteins)-148a may be involved in the estrogen induction in ICP via PXR (show NR1I2 Proteins) signaling. MRP3 (show ABCC3 Proteins) may be involved.
Data suggest that the abrogation of protease-activated receptor 1 (PAR1)-dependent signaling pathways may prove a promising strategy for gliomas.
these data indicate that KLKB1 (show KLKB1 Proteins) induces inflammatory reactions in human dental tissues via protease-activated receptor 1
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (show F2 Proteins)-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1 (show RUNX1 Proteins)/Cbfb (show CBFB Proteins)-deleted MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) cells. Similar to the effect of Runx1 (show RUNX1 Proteins)/Cbfb (show CBFB Proteins) deletion, PAR-1 (show MARK2 Proteins) overexpression induced CDKN1A/p21 (show CDKN1A Proteins) expression and attenuated proliferation in MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) cells
this study shows that PXR (show NR1I2 Proteins) augments Mycobacterium tuberculosis survival inside the host macrophages by promoting the foamy macrophage formation and abrogating phagolysosomal fusion, inflammation, and apoptosis
PAR1 in its inactive unligated state functions as a scaffold for TGFbetaRII to downregulate TGF-beta (show TGFB1 Proteins) signaling, and thereby promote embryonic stem cell transition to functional endothelial cells.
this study shows that poly I:C treated PAR-1 (show MARK2 Proteins)-/- mice given the thrombin (show F2 Proteins) inhibitor dabigatran etexilate exhibited less IFNbeta and CXCL10 (show CXCL10 Proteins) expression in the spleen and plasma
Brain water content in the ipsilateral hemisphere and the tumor mass were significantly lower in PAR-1 (show MARK2 Proteins) KO than WT mice at day 12 after implantation of glioma cells.
The results of this study suggested that polarized microglia occur dynamically after ICH (show ACE Proteins) and that PAR-1 (show MARK2 Proteins) plays a role in the microglia activation and polarization.
our findings define a detrimental role of thrombin (show F2 Proteins)-activated PAR-1 (show MARK2 Proteins) in wound healing in mice with spinal cord injuries.
thrombin (show F2 Proteins)/PAR-1 (show MARK2 Proteins) interaction regulated MCP-1 (show CPT1B Proteins), TF, MCSF (show CSF1 Proteins) and IL-6 (show IL6 Proteins) production.
Thrombin (show F2 Proteins) upregulates LCN2 (show LCN2 Proteins) through protease-activated receptor-1 activation and causes brain damage.
Matrix metalloproteinases (MMP) are effectors of hippocampal neuroplasticity in the adult central nervous system and that the MMP-1 (show MMP1 Proteins)/protease-activated receptor-1 axis may play a role in neurogenesis following physiological and/or pathological stimuli.
Data indicate an involvement of protease-activated receptor-1 in the neuroinflammation mediated by Eomes (show EOMES Proteins)(+) CD4 (show CD4 Proteins)(+) T cells.
MMP-1 (show MMP1 Proteins) promotes VEGFR2 (show KDR Proteins) expression and proliferation of endothelial cells through stimulation of PAR-1 and activation of NF-kappaB (show NFKB1 Proteins)
PAR1 and PAR2 regulate endothelial NO synthase phosphorylation and activity through G(12/13) and G(q), delineating the signaling pathways by which the proteases act on protease-activated receptors to modulate endothelial functions.
Thrombin stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1, RhoA, and myocardin.
Thrombin (show F2 Proteins) induces a sustained contraction in the normal pulmonary artery, by activating PAR(1) and thereby increasing the sensitivity of the myofilament to Ca(2 (show CA2 Proteins)+).
Coagulation factor II receptor is a 7-transmembrane receptor involved in the regulation of thrombotic response. Proteolytic cleavage leads to the activation of the receptor. F2R is a G-protein coupled receptor family member.
protease-activated receptor 1
, proteinase-activated receptor 1
, Thrombin receptor
, coagulation factor II receptor
, thrombin receptor
, protease-activated receptor-1
, coagulation factor II (thrombin) receptor