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Prospective study demonstrated that AHRR (show CYP1A1 ELISA Kits) and F2RL3 methylation levels had inverse relationships with self-reported smoking status and accurately discriminated for both current- and former- smoking. Moreover, methylation markers distinguished former smokers from never-smokers with high accuracy and significantly associated with an increased risk of lung cancer.
F2RL3 variants have the potential to markedly alter platelet PAR4 (show PAWR ELISA Kits) reactivity particularly after exposure to therapeutic PAR1 (show MARK2 ELISA Kits) antagonists.
these findings are the first to show that internalization of activated PAR4 (show PAWR ELISA Kits) is linked to proper ERK1/2 (show MAPK1/3 ELISA Kits) and Akt (show AKT1 ELISA Kits) activation.
an intracellular PAR4 C-terminal motif that regulates calcium signaling and beta-arrestin interactions, was identified.
the contribution of PAR1 (show MARK2 ELISA Kits) and PAR4 (show PAWR ELISA Kits) to thrombin (show F2 ELISA Kits)-mediated activation of the platelet fibrin receptor (GPIIbIIIa), is reported.
Suppression of PAR4 (show PAWR ELISA Kits) expression has no significant effect on the proliferation of SW620 cells, but can inhibit the migration of the cells.
Both GPIbalpha (show GP1BA ELISA Kits) and PAR4 (show PAWR ELISA Kits) are required for thrombin (show F2 ELISA Kits)-induced reactive oxygen species formation in human platelets.
Bladder PAR (show JTB ELISA Kits) activation elicits urothelial MIF (show AMH ELISA Kits) release and urothelial MIF (show AMH ELISA Kits) receptor signaling at least partly through CXCR4 (show CXCR4 ELISA Kits) to result in abdominal hypersensitivity without overt bladder inflammation
protease-activated receptor 4 and Trefoil factor 2 (show TFF2 ELISA Kits) are expressed in human colorectal cancer
The PAR4 (show PAWR ELISA Kits) expression and activation via intracellular signaling pathways and the role of PAR4 (show PAWR ELISA Kits) signaling pathways in the development and maintenance of pain.
Findings indicate that the energy-sensing LKB1 (show STK11 ELISA Kits)-AMPK (show PRKAA1 ELISA Kits) pathway regulates IGF1 (show IGF1 ELISA Kits) secretion in mouse primary hepatocytes, which in turn regulates activation of the IGF1R (show IGF1R ELISA Kits)-PKB (show AKT2 ELISA Kits) pathway.
These data suggest that nutrient availability dictates the mode of division and that LKB1 (show STK11 ELISA Kits)-AMPK (show PRKAA1 ELISA Kits) mediates this nutrient-driven effect on intestinal epithelial stem cell proliferation.
this study identified the molecular mechanism of increased angiogenesis and tumor growth with LKB1 (show STK11 ELISA Kits) deficiency
These results suggest that although physiologic LKB1 (show STK11 ELISA Kits) expression exerts a potent pro-survival effect in lymphocytes, LKB1 (show STK11 ELISA Kits) inactivation nonetheless facilitates transformation of B, but not T, lymphocytes.
These results suggest that the LKB1 (show STK11 ELISA Kits)-AMPK (show PRKAA1 ELISA Kits)-FoxO1 (show FOXO1 ELISA Kits) signaling pathway is a critical mediator of the antioxidant properties of H2, further supporting the idea that H2 acts as a signaling molecule to serve various physiological functions.
Lkb1 (show STK11 ELISA Kits) activates the Notch (show NOTCH1 ELISA Kits) signaling pathway, which subsequently increases Pax7 (show PAX7 ELISA Kits) expression and promotes self-renewal and proliferation while inhibiting differentiation. Mechanistic studies reveal that Lkb1 (show STK11 ELISA Kits) regulates Notch (show NOTCH1 ELISA Kits) activation through AMPK (show PRKAA1 ELISA Kits)-mTOR (show FRAP1 ELISA Kits) pathway in myoblasts.
mitochondrial dysfunction triggers LKB1 (show STK11 ELISA Kits)-mediated AMPK (show PRKAA1 ELISA Kits) activation, which stimulates Sirt2 (show SIRT2 ELISA Kits) phosphorylation, leading to activation of mTOR (show FRAP1 ELISA Kits)-RAPTOR (show RPTOR ELISA Kits) and Glut1 (show SLC2A1 ELISA Kits)-mediated glucose uptake.
these data demonstrated that LKB1 (show STK11 ELISA Kits)/AMPK (show PRKAA1 ELISA Kits) signaling pathway activation improved the survival of diabetic mice complicated with endotoxemia. Thus, LKB1 (show STK11 ELISA Kits)/AMPK (show PRKAA1 ELISA Kits) signaling pathway may serve as a potentially useful therapeutic target for severe infection in diabetic patients.
Data show that the serine/threonine kinase (show CDK4 ELISA Kits) LKB1 (show STK11 ELISA Kits) regulates mitochondrial calcium uniporter (MCU (show MCU ELISA Kits))-expression, mitochondria-dependent Ca2 (show CA2 ELISA Kits)+ clearance, and thereby, presynaptic release properties.
LKB1 (show STK11 ELISA Kits) deficiency in LKB1 (show STK11 ELISA Kits)(Pax2 (show PAX2 ELISA Kits)) CKO mice disrupted hair cell planar polarity during embryonic development. The results suggest that LKB1 (show STK11 ELISA Kits) is required in planar cell polarity formation in cochlear hair cells in mice.
Coagulation factor II (thrombin) receptor-like 3 (F2RL3) is a member of the large family of 7-transmembrane-region receptors that couple to guanosine-nucleotide-binding proteins. F2RL3 is also a member of the protease-activated receptor family. F2RL3 is activated by proteolytic cleavage of its extracellular amino terminus. The new amino terminus functions as a tethered ligand and activates the receptor. F2RL3 is activated by thrombin and trypsin.
proteinase-activated receptor 4
, coagulation factor II (thrombin) receptor-like 3
, coagulation factor II (thrombin)
, protease-activated receptor-4
, thrombin receptor-like 3
, coagulation factor II receptor-like 3
, protease-activated receptor 4
, LKB1 short isoform
, liver kinase B1 homolog
, serine/threonine-protein kinase 11
, serine/threonine-protein kinase LKB1
, serine/threonine-protein kinase STK11