Relationship of the 20S Proteasome and the Proteasome Activator PA28 to Atherosclerosis and Intimal Hyperplasia in the Human Vascular System
REFERENCES (20)
- et al.
Catalytic properties of 26S and 20S proteasomes and radio-labeling of MB1, LMP7 and C7 subunits associated with trypsin-like and chymotrypsin-like activities
J Biol Chem
(1997) - et al.
The interferon gamma inducible 11S regulator (PA 28) and the LMP2/LMP7 sub-units govern the peptide production by the 20S proteasome in vitro
J Biol Chem
(1995) - et al.
Isolation of genes differentially expressed at the downstream anastomosis of prosthetic arterial grafts with use of mRNA differential display
J Vasc Surg
(1995) - et al.
Smooth muscle cell migration and proliferation are mediated by distinct phases of activation of the intracellular messenger mitogen-activated protein kinase
J Vasc Surg
(1998) - et al.
Antisense basic fibroblast growth factor gene transfer reduces neointimal thickening after arterial injury
J Vasc Surg
(1997) - et al.
Enzymes catalyzing ubiquitination and proteolytic processing of the p105 precursor of nuclear factor KB1
J Biol Chem
(1998) - et al.
Differential inhibition of three peptidase activities of the proteasome in human lens epithelium by heat and oxidation
Exp Eye Res
(1999) The 26S proteasome
- et al.
New insights into the mechanisms and importance off the proteasome in intracellular protein degradation
Biol Chem
(1997) Proteasomes: structure and biology
J BioChem (Tokyo)
(1998)
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2022, Journal of Heart and Lung TransplantationCitation Excerpt :The circulating 20s proteasome is modulated by proteasome activator (PA28) subunits such as proteasome activator subunit 2. Abnormalities of this modulation contribute to increased intimal hyperplasia and atherosclerosis.31 Of note is that 7 proteins found in univariate analysis on acute rejection with hemodynamic compromise were not clearly related to the top pathways observed in brain-dead donors.
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2013, Journal of Vascular SurgeryCitation Excerpt :Neointimal hyperplasia has also been linked to proteasome activity. Faries et al stained biopsy specimens of atherosclerotic and normal vessels, as well as patent and occluded grafts, for 11S proteasome activator (PA28) expression and observed that areas of vessels with less PA28 staining (lower proteasome activity) had increased levels of atherosclerosis and neointimal hyperplasia.25 Finally, Stone et al observed reduced expression of ubiquitin, E2 enzymes, ubiquitin ligase enzymes, and proteasomal subunits at the anastomoses of vein grafts in the carotid arteries of mongrel dogs.26
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