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https://www.selleckchem.com/products/cordycepin.html Copyright © 2020 by The Korean Society of Infectious Diseases, Korean Society for Antimicrobial Therapy, and The Korean Society for AIDS.BACKGROUND We investigated whether a heterozygous mutation that we newly identified in HTRA1 (high-temperature requirement serine protease A1 gene) in a pedigree with autosomal dominant hereditary cerebral small vessel disease (SVD) reduces the function of HTRA1 and affects the transforming growth factor-β1 (TGF-β1)/Smad signaling. METHODS Whole-exome sequence from the proband and her two sisters was examined using whole-exome enrichment and sequencing. Expression of HTRA1 and TGF-β1/Smad and HTRA1 activity were assayed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and western blotting analyses after transfecting wild-type and mutant HTRA1 genes into HEK293 cells. RESULTS A new heterozygous mutation (c.614C>Gp.Ser205Cys) in HTRA1 was identified in the sequence encoding the trypsin-like serine protease domain. The mutation was predicted to be deleterious by in silico tools. Moreover, in vitro activity and protein analyses revealed a loss-of-function effect of the mutation the proteolytic activity of mutant HTRA1 was decreased, and, notably, this was accompanied by an increase in TGF-β1/Smad protein levels. CONCLUSIONS The heterozygous mutation HTRA1 S205C causing diminished protease activity is associated with-and could represent a cause of-autosomal dominant hereditary cerebral SVD. Our results also indicate a relationship between HTRA1 and TGF-β1/Smad signaling. © 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.AIMS The aim of this study is to evaluate the contemporary use of a pulmonary artery catheter (PAC) in acute myocardial infarction-cardiogenic shock (AMI-CS). METHODS AND RESULTS A retrospective cohort of AMI-CS admissions using the National Inpatient Sample (2000-2014) was identified. Admissions with concomita

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