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Data Supplement from Src Kinase Is a Novel Therapeutic Target in Lymphangioleiomyomatosis
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<p>Increased phospho-Src in LAM lungs (Figure S1); Enhanced activation of Src, STAT3 and Snail in human LAM cells (Figure S2); mTOR activation in TSC2-deficient cells (Figure S3); Src kinase is activated in TSC2-deficient cells (Figure S4); Knockdown of TSC2 in Hela cells up-regulates mTOR activity (Figure S5); Autophagy inhibition results in Src kinase activation (Figure S6); Effects of Src inhibition on migration activity of EEF cells (Figure S7); Src kinase inhibitors decrease proliferation of TSC2-/- cells (Figure S8); Proposed model of Src role in LAM (Figure S9).</p>
American Association for Cancer Research (AACR)
Title: Data Supplement from Src Kinase Is a Novel Therapeutic Target in Lymphangioleiomyomatosis
Description:
<p>Increased phospho-Src in LAM lungs (Figure S1); Enhanced activation of Src, STAT3 and Snail in human LAM cells (Figure S2); mTOR activation in TSC2-deficient cells (Figure S3); Src kinase is activated in TSC2-deficient cells (Figure S4); Knockdown of TSC2 in Hela cells up-regulates mTOR activity (Figure S5); Autophagy inhibition results in Src kinase activation (Figure S6); Effects of Src inhibition on migration activity of EEF cells (Figure S7); Src kinase inhibitors decrease proliferation of TSC2-/- cells (Figure S8); Proposed model of Src role in LAM (Figure S9).
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<div>Abstract<p>Lymphangioleiomyomatosis (LAM) is a progressive cystic lung disease affecting some women with tuberous sclerosis complex (TSC). Sporadic LAM can develop...