Phasin proteins activate Aeromonas caviae polyhydroxyalkanoate (PHA) synthase but not Ralstonia eutropha PHA synthase.
In this study, we performed in vitro and in vivo activity assays of polyhydroxyalkanoate (PHA) synthase (PhaCs) in the presence of protein phasin (PhaPs), which revealed that PhaPs are activators of PHAC derived from Aeromonas caviae (PhaCAc). In an in vitro study, among the three PhaCs tested, PhaCAc significantly activated when PhaPs added at the beginning of polymerization (prepolymerization PhaCAc), while prepolymerization PhaCRe (derived from Cupriavidus necator) and PhaCDa (Delftia acidovorans) showed decreased activity with PhaPs.
The PhaCAc Phap-enabled show a slight shift in substrate preference towards 3-hydroxyhexanoyl-CoA (C6). PhaPAc also enabled PhaCAc when added during the polymerization (polymer-elongating PhaCAc), while this effect was not observed for PhaCRe.
In an in vivo test using Escherichia coli strain Caprine Recombinant Proteins TOP10 as the host, the effect of PhaPAc expression on PHA synthesis by PhaCAc or PhaCRe examined. As PhaPAc expression increases, PHA production increased by 2.3-fold in PhaCAc-expressing strain, while it increased slightly in PhaCRe-expressing strain. Taken together, these studies provide evidence that PhaPs serves as an activator for PhaCAc both in vitro and in vivo but not activate PhaCRe. This activating effect may be associated with the new role PhaPs in polymerization reactions by PhaCAc.
bacterial peritonitis in the inferior vena cava liver disease: a hypothesis to explain the cause of infection in high-protein ascites.
IVC liver disease (HVD), a disease caused by complete obstruction or stenosis of the near-atrial junction cava inferior vena cava (IVC) is endemic in Nepal. It is a chronic disease characterized by upper abdominal pain, hepatomegaly, splenomegaly and dilated surface veins in the trunk of the body. Ascites generally, with a high protein Cavia Recombinant Proteins content is a feature of acute and subacute phase and during acute exacerbations of chronic disease.
We assess the occurrence of bacterial peritonitis among patients with ascites HVD. One hundred sixty-seven consecutive patients with ascites, including 91 patients with HVD examined for the presence of bacterial peritonitis. Ascites fluid examined for total and differential WBC counting. Fluid and blood were cultured for aerobic microorganisms at the bedside inoculation in blood culture bottles. HVD is a common cause of non-cirrhotic ascites the high protein content in Nepal.
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