Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.25.1 (proteasome)
 28,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of platelet-derived microparticles (PDMPs), platelet activation markers (P-selectin, CD63, and PAC-1 on activated platelets), and C-C chemokines (monocyte chemotactic peptide [MCP]-1 and regulated on activation normally T-cell expressed and secreted [RANTES] were measured and compared in patients with acute myocardial infarction (AMI) or stable pectoris angina. These substances are thought to paricipate in the development of complications in patients with AMI. The percentage binding of anti-P-selectin, CD63, and PAC-1 antibody to platelets, and the levels of PDMPs (per 10(4) platelets) were higher in the patients with AMI than in those with stable pectoris angina (P-selectin, 23.1% +/- 2.1% vs. 10.3% +/- 1.2%, p < 0.001; CD63, 24.6% +/- 3.3% vs. 11.2% +/- 3.1%, p < 0.01; PAC-1, 14.1% +/- 1.7% vs. 9.3% +/- 2.1%, p < 0.05; PDMPs, 613 +/- 71 vs. 413 +/- 55, p < 0.01). There were no differences in platelet levels of GPIIb/IIIa and GPIb between groups. Levels of MCP-1 and RANTES were higher in the patients with AMI than in patients with stable pectoris angina (MCP-1, 430 +/- 35 vs. 265 +/- 23, p<0.01; RANTES, 175 +/- 32 vs. 88 +/- 29, p<0.001). The effects of percutaneous transluminal coronary angioplasty (PTCA) on the levels of these agents in patients with AMI were studied. Platelet activation markers were significantly decreased in patients with AMI after PTCA. RANTES level was also significantly decreased after treatment, but MCP-1 level was not changed. In addition, this tendency was clearer in STENT patients. These findings suggest that in patients with AMI PTCA, particularly STENT, may prevent the development of complications in which activated platelet and RANTES participate.
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PMID:Association of platelet-derived microparticles with C-C chemokines on vascular complication in patients with acute myocardial infarction. 1236 Dec 7

In addition to its role in the removal of damaged and unneeded proteins, the ubiquitin-proteasome system (UPS) may play a key role in coronary artery disease (CAD). To investigate the expression of ubiquitin in monocytes and lymphocytes isolated from patients at different stages of CAD, 120 patients with CAD (40 with acute myocardial infarction [AMI], 40 with unstable angina pectoris [UAP] and 40 with stable angina pectoris [SAP]) were selected; 40 patients with normal coronary arteries served as controls. At both the mRNA and protein levels, ubiquitin expression was higher in patients with CAD than in controls, and patients with AMI had a much higher expression of ubiquitin (at both the mRNA and protein levels) than those with SAP and UAP. These data indicate that ubiquitin expression increased with increasing severity of CAD, suggesting that ubiquitin may play a critical role in the development and progression of CAD.
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PMID:Expression of ubiquitin in peripheral inflammatory cells from patients with coronary artery disease. 1909 31

A 79-year-old female patient with multiple myeloma who had no prior cardiac disease history developed an acute myocardial infarction on day 5 after receiving bortezomib and dexamethasone (BD). After treatment of coronary stenoses by stents, she received another course of BD therapy and developed angina pectoris on day 5 after the therapy. Bortezomib's antitumor effect is due to the inhibition of proteasome activity. This inhibition may increase endothelial progenitor cell apoptosis and decrease endothelial nitric oxide synthase/nitric oxide (eNOS/NO), thus leading to coronary spasm. It is, therefore, important to carefully monitor patients being treated with bortezomib for the potential occurrence of ischemic heart disease.
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PMID:Ischemic heart disease associated with bortezomib treatment combined with dexamethasone in a patient with multiple myeloma. 2045 63