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Identification Of A Post-Transcriptional Mechanism Regulating Epithelial-Mesenchymal Transition, George S. Hussey
Identification Of A Post-Transcriptional Mechanism Regulating Epithelial-Mesenchymal Transition, George S. Hussey
ETD Archive
No abstract provided.
Transforming Growth Factor-Beta (Tgfβ)-Mediated Post-Transcriptional Regulation Of Epithelial-Mesenchymal Transdifferentiation (Emt), Arindam Chaudhury
Transforming Growth Factor-Beta (Tgfβ)-Mediated Post-Transcriptional Regulation Of Epithelial-Mesenchymal Transdifferentiation (Emt), Arindam Chaudhury
ETD Archive
TGF├ƒ induces epithelial-mesenchymal transdifferentiation (EMT) accompanied by cellular differentiation and migration, a process fundamental during embryonic development and one that is reactivated in a variety of diseases including fibrosis and cancer. Despite extensive transcriptomic profiling, identification of TGF├ƒ-inducible, EMT-specific genes has met with limited success. Here, we report a novel post-transcriptional pathway by which TGF├ƒ modulates expression of EMT-specific proteins and EMT itself. We show that heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) binds a structural, 33 nucleotides (nt) TGF-beta-activated translation (BAT) element in the 3'-untranslated regions (UTRs) of disabled-2 (Dab2) and interleukin-like EMT inducer (ILEI) transcripts, and repress their translation. …
Transforming Growth Factor - Beta (Tgfß) Stimulated Isoform Specific Activation Of Akt2 Via Ras Mediates Epithelial-Mesenchymal Transition (Emt), Praveen Chander
Transforming Growth Factor - Beta (Tgfß) Stimulated Isoform Specific Activation Of Akt2 Via Ras Mediates Epithelial-Mesenchymal Transition (Emt), Praveen Chander
ETD Archive
TGFß induces epithelial-mesenchymal transdifferentiation (EMT) accompanied by cellular differentiation and migration. EMT has emerged as a fundamental process governing embryonic development, adult tissue homeostasis and metastatic progression. Our lab had earlier identified a post-transcriptional pathway by which TGFß modulates expression of EMT-specific proteins. It was shown that heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) binds a structural, 33 nucleotides (nt) TGF beta-activated translation (BAT) element in the 3'-UTR of disabled-2 (Dab2) and interleukin-like EMT inducer (ILEI)transcripts, and repress their translation. This inhibition is removed following hnRNP E1 phosphorylation by activated Akt2. We now show that specific activation of Akt2, and not …