3.4.21.108 medicine amyloid beta, a pivotal factor implicated in the pathogenesis of Alzheimer´s disease interacts with HtrA2/Omi 670400 3.4.21.108 medicine critical role of HtrA2 in a cytokine-induced cell death response. Inhibition by a viral protein 689289 3.4.21.108 medicine heterozygous G399S mutation in Parkinson's disease patients, which is absent in healthy controls, a A141S polymorphism is associated with Parkinson's disease, both mutations result in defective activation of Omi/HtrA2 and mitochondrial dysfunction associated with altered mitochondrial morphology 668876 3.4.21.108 medicine HtrA2 is linked to cancer and neurodegeneration, like Alzheimers disease, Parkinsons disease, Huntingtons disease, and brain, kidney and myocardial ischemia, reperfusion 697488 3.4.21.108 medicine HtrA2 is linked to Parkinsons disease 697176 3.4.21.108 medicine HtrA2 is regulated by Parkinson's disease-associated kinase PINK1. HtrA2 interacts with PINK1 and that both are components of the same stress-sensing pathway 689124 3.4.21.108 medicine HtrA2 knockout mice display features characteristic of a Parkinson syndrome, deletion of HtrA2 results in increased susceptibility to cell death stimuli, Smac/DIABOLO can compensate for the removal of HtrA2 in terms of neutralizing inhibitor of apoptosis proteins 670241 3.4.21.108 medicine HtrA2 under several different stress conditions induces cleavage of vimentin in wild-type as well as SH-SY5Y cells transfected with amyloid precursor protein with the Alzheimer disease-associated Swedish mutation. After stress treatment, inhibition of HtrA2 protease activity by the specific inhibitor, Ucf-101, reduces the cleavage of vimentin in wild-type cells 754775 3.4.21.108 medicine HtrA2-mediated proteolysis of WT1 may directly contribute to the effect of cytotoxic drugs warrants 717632 3.4.21.108 medicine HtrA2/Omi is associated with the pathogenesis of amyotrophic lateral sclerosis 710093 3.4.21.108 medicine involvement of HtrA2 in the etiology of Alzheimer's disease 670224 3.4.21.108 medicine link between HtrA2/Omi and Parkinson’s disease or Alzheimer’s disease 686002 3.4.21.108 medicine loss of HtrA2 function might contribute to the activation of a stress response of mitochondrial origin in the brain that promotes neurodegeneration 697178 3.4.21.108 medicine mutations in the OMI/HTRA2 gene are linked to Parkinsons disease 699689 3.4.21.108 medicine mutations of the OMI/HTRA2 gene are linked to Parkinsons disease 698176, 698185 3.4.21.108 medicine myocardial ischemia/reperfusion significantly increases cytosolic Omi/HtrA2 content and markedly increases apoptosis, ucf-101 can inhibit apoptosis 668267 3.4.21.108 medicine Omi/HtrA2 is involved in neuronal cell death following focal cerebral ischemia/reperfusion. Blocking the proteolytic activity of Omi/HtrA2 with specific inhibitors, such as the ucf-101, may be a way to afford neuroprotection and minimize cellular damage in cerebral ischemia/reperfusion 689170 3.4.21.108 medicine protease activity of HtrA2 is essential for the production of C161. Processing of amyloid precursor protein into C161 by HtrA2 is a natural event occurring under normal physiological conditions. Direct cleavage of mitochondrial beta-amyloid precursor protein by HtrA2 may prevent mitochondrial dysfunction caused by accumulation of amyloid precursor protein. Regulation of HtrA2 protease activity may be a therapeutic target in Alzheimer disease 687526 3.4.21.108 medicine role for HtrA2/Omi in apoptosis 686002 3.4.21.108 medicine the function of Omi/HtrA2 is linked to selective vulnerability of striatal neurons in Huntingtons disease 697749 3.4.21.108 medicine the identification of the role of HtrA2 in neurodegeneration will lead to an improved understanding of the pathogenesis of Parkinsons disease 695598 3.4.21.108 medicine the relation between p73 and HtrA2 may help to understand the behavior of the p73 protein in the responses of cancer cells to chemotherapy 697174 3.4.21.108 medicine the study does not support a role of HtrA2 variants in the pathogenesis of Parkinsons disease 700569 3.4.21.108 medicine therapeutic interventions that inhibit HtrA2 expression, translocation, or protease activity may provide attractive therapeutics in the treatment of cardiovascular diseases 697154 3.4.21.108 medicine therapeutic interventions that inhibit HtrA2/Omi expression, translocation, or protease activity may represent novel therapeutic strategies for retinal pigment epithelial cells and retinal pigment epithelial cells-related diseases 708821 3.4.21.108 medicine transfecting cells with siRNA molecules against Omi effectively eliminate Omi/HtrA2 protein expression 668267 3.4.21.108 medicine way to limit renal injury by specifically inhibiting its proteolytic activity -, 667167 3.4.21.108 additional information a role for Omi-mediated processing of WTS in negative regulation of cell cycle progression at interphase. Omi protease is not necessarily required for cell death 689287 3.4.21.108 additional information simple and rapid strategy for molecular cloning using a gel-free and antibiotic selection method, which allows for the complete elimination of DNA extraction by gel electrophoresis, and thus has several advantages over gel-based cloning methods, including a cloning efficiency that is approximately 10times higher due to the prevention of ethidium bromide ultraviolet-induced DNA damage and contamination with ligase inhibitors, the amount of plasmid DNA required is approximately five times less, and cloning time is several hours less 685760 3.4.21.108 additional information the bacterial protein quality control factor DegP is allosterically regulated by model peptides mimicking cellular stress signals. Strategy for the development of antimicrobials 683076