Proteomics reveals Rictor as a noncanonical TGF-β signaling target during aneurysm progression in Marfan mice.

ABSTRACT: The objective of the present study was to 1) analyze the ascending aortic proteome within a mouse model of Marfan syndrome (MFS; Fbn1^C1041G/+) at early and late stages of aneurysm and 2) subsequently test a novel hypothesis formulated on the basis of this unbiased proteomic screen that links changes in integrin composition to transforming growth factor (TGF)-β-dependent activation of the rapamycin-independent component of mammalian target of rapamycin (Rictor) signaling pathway. Ingenuity Pathway Analysis of over 1,000 proteins quantified from the in vivo MFS mouse aorta by data-independent acquisition mass spectrometry revealed a predicted upstream regulator, Rictor, that was selectively activated in aged MFS mice. We validated this pattern of Rictor activation in vivo by Weste

SUBMITTER: Parker SJ 

PROVIDER: S-EPMC6335018 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature