uPA Human ELISA Kit

Amyloid beta peptide (A beta) accumulation is the major event in the brain of cases with Alzheimer's disease (AD). The serine protease plasmin, which is generated from the inactive zymogen plasminogen, could accelerate A beta degradation, and thus may play a role in AD pathogenesis. It has been reported that the increasing of plasminogen activator inhibitor-1 (PAI-1) inhibits the activity of plasminogen activator and thus reduces the generation of plasmin in vivo. For seeking the correlation of the PAI-1 promoter with sporadic AD (SAD), we performed a case-control study in a group of Chinese Han population. In the study, we detected two polymorphisms, a G/A single base substitution polymorphism at -844 bp (rs2227631) and a single guanosine deletion/insertion 4G/5G polymorphism at -675 bp (rs1799889) upstream from the start of transcription. Direct sequencing was used for genotyping in 324 SAD patients and 278 controls. We failed to find any associations between these two polymorphisms and SAD even after stratified by age of onset, gender and apolipoprotein E (APOE) epsilon 4 status. Our data do not support that there is an association between the PAI-1 promoter polymorphisms and SAD in the Chinese Han population. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Ribosome-inactivating stresses possess a potent regulatory activity against tumor cell progression. In this study, we demonstrated that macrophage inhibitory cytokine-1 (MIC-1) and its associated signals determined the colon cancer cell response to the chemical ribotoxic stress. The ribotoxic stress agent anisomycin-induced MIC-I gene expression which was involved in the ribotoxin-induced apoptotic pathway. MIC-I was also a critical inducer of apoptosis-related gene products such as activated urokine-type plasminogen activator (PLAU) and PLAU receptor (uPAR). When MIC-1 or PLAU action was repressed in the tumor cells, the chemical ribotoxic stress triggered a survival-related MAP kinase such as ERK. Mechanistically, gene expression of apoptosis-mediator MIC-I was enhanced by activating transcription factor 3 (ATF-3) via the p38 MAP kinase signaling pathway. Moreover, both promoter activity and mRNA stability of MIC-1 gene were up-regulated by ribotoxic anisomycin via the p38 MAP kinase signaling pathway. In conclusion, ribotoxic anisomycin-induced MIC-I expression via p38-ATF3 pathway and subsequent apoptosis while suppressing survival ERK signal in the colon cancer cells. The results of this study provide mechanistic insight into tumor cell decision for death or survival pathways in response to ribosome-disrupting stresses from chemotherapeutics. (C) 2009 Elsevier Inc. All rights reserved.