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CXCR6 → TLR4-NOX4-AP-1: " TLR4-NOX4-AP-1 signaling mediates lipopolysaccharide induced CXCR6 expression in human aortic smooth muscle cells "
CXCR6 → TLR4-NOX4-AP-1: " TLR4-NOX4-AP-1 signaling mediates lipopolysaccharide induced CXCR6 expression in human aortic smooth muscle cells "
CXCR6 → TLR4: " Inhibition of TLR4 with neutralizing antibodies or specific siRNA interference blocked LPS mediated CXCR6 expression "
CXCR6 → LPS: " Inhibition of TLR4 with neutralizing antibodies or specific siRNA interference blocked LPS mediated CXCR6 expression "
CXCR6 ⊣ LPS: " LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression "
CXCR6 → AP-1: " LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression "
AP-1 → LPS: " LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression "
NF-kappaB → AP-1: " LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression "
NF-kappaB → LPS: " LPS stimulated both AP-1 ( c-Fos, c-Jun ) and NF-kappaB ( p50 and p65 ) activation, but only inhibition of AP-1 attenuated LPS induced CXCR6 expression "
AP-1 → LPS: " Using dominant negative expression vectors and siRNA interference, we demonstrate that LPS induces AP-1 activation via MyD88, TRAF6, ERK1/2, and JNK signaling pathways "
CXCR6 → AP-1: " Furthermore, the flavoprotein inhibitor diphenyleniodonium chloride significantly attenuated LPS mediated AP-1 dependent CXCR6 expression, as did inhibition of NOX4 NADPH oxidase by siRNA "
CXCR6 → LPS: " Furthermore, the flavoprotein inhibitor diphenyleniodonium chloride significantly attenuated LPS mediated AP-1 dependent CXCR6 expression, as did inhibition of NOX4 NADPH oxidase by siRNA "
LPS-TLR4-NOX4-AP-1 → CXCR6: " These results demonstrate that LPS-TLR4-NOX4-AP-1 signaling can induce CXCR6 expression in ASMC, and suggest that the CXCL16-CXCR6 axis may be an important proinflammatory pathway in the pathogenesis of atherosclerosis "
CXCR6 → LPS-TLR4-NOX4-AP-1: " These results demonstrate that LPS-TLR4-NOX4-AP-1 signaling can induce CXCR6 expression in ASMC, and suggest that the CXCL16-CXCR6 axis may be an important proinflammatory pathway in the pathogenesis of atherosclerosis "
CXCR6 → LPS-TLR4-NOX4-AP-1: " These results demonstrate that LPS-TLR4-NOX4-AP-1 signaling can induce CXCR6 expression in ASMC, and suggest that the CXCL16-CXCR6 axis may be an important proinflammatory pathway in the pathogenesis of atherosclerosis "
CXCR6 → LPS-TLR4-NOX4-AP-1: " These results demonstrate that LPS-TLR4-NOX4-AP-1 signaling can induce CXCR6 expression in ASMC, and suggest that the CXCL16-CXCR6 axis may be an important proinflammatory pathway in the pathogenesis of atherosclerosis "