2007
DOI: 10.1073/pnas.0704315104
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Variant estrogen receptor–c-Src molecular interdependence and c-Src structural requirements for endothelial NO synthase activation

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Cited by 72 publications
(64 citation statements)
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“…2C). To confirm such is the case, however, we expressed inactivating FLAGtagged Myr (c-Src G2A ) (15,21), SH3 (c-Src W118K ) (7), and SH2 (c-SrcR 175L ) (7,27) point mutants in c-Src Ϫ/Ϫ splenocytes (see Fig. S3A in the supplemental material).…”
Section: Resultsmentioning
confidence: 99%
“…2C). To confirm such is the case, however, we expressed inactivating FLAGtagged Myr (c-Src G2A ) (15,21), SH3 (c-Src W118K ) (7), and SH2 (c-SrcR 175L ) (7,27) point mutants in c-Src Ϫ/Ϫ splenocytes (see Fig. S3A in the supplemental material).…”
Section: Resultsmentioning
confidence: 99%
“…Through this mechanism, estrogen activates eNOS via phosphatidylinositol 3-kinase/Akt, leading to phosphorylation of eNOS on serine 1177, enhancing NO production. This mechanism leads to the well described rapid effect of estrogen to enhance endothelial-dependent vasodilator responses mediated by NO, an effect that has been demonstrated both in vitro and in vivo (Williams et al, 1992;Stirone et al, 2005a;Li et al, 2007).…”
Section: B Rapid Effectsmentioning
confidence: 99%
“…These rapid responses include activation of different downstream signaling pathways, for example, the mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase (PI3K) pathways, eNOS activation, cyclic AMP production and intracellular calcium mobilization, which in turn can modulate nuclear transcriptional events in a variety of normal or transformed cell lines (reviewed in ref. [16][17][18][19][20][21][22][23][24][25][26]. How ER localizes to the cell membrane is not clear.…”
Section: Estrogen Receptors In the Testismentioning
confidence: 99%