Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8473910 | Journal of Molecular and Cellular Cardiology | 2016 | 24 Pages |
Abstract
Poldip2+/â MASMs exhibit higher β1-integrin expression and activity of the PI3K/Akt/mTOR signaling pathway, leading to increased ECM protein synthesis. These findings have important implications for vascular diseases in which ECM accumulation plays a role.
Keywords
Hsc70eIF4E4E-BP1eukaryotic initiation factor 4E binding protein 1ECMVSMCsATGp70S6KLC3BmTORPOLDIP2MMPPI3KPRAS40proline-rich AKT substrate of 40 kDaeukaryotic translation initiation factor 4EAktVascular smooth muscle cellsUbiquitin proteasome systemVascular smooth musclephosphatase and tensin homolog deleted from chromosome 10phosphoinositide-3-kinaseExtracellular matrixmatrix metalloproteinaseMechanistic target of rapamycinHeat shock cognate protein 70microtubule-associated protein 1A/1B-light chain 3protein kinase BPtenautophagy-related geneUPS
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Cell Biology
Authors
Masakazu Fujii, Angélica Amanso, Thalita B. Abrahão, Bernard Lassègue, Kathy K. Griendling,