Here we show that the Prf complex is oligomeric, containing at least two molecules of Prf. Within the complex, Prf can associate with Pto or one of several Pto family members including Fen, Pth2, Pth3, or Pth5. The dimerization surface for Prf is the novel N-terminal domain,
which also coordinates an intramolecular interaction with the remainder of the selleck kinase inhibitor molecule, and binds Pto kinase or a family member. Thus, association of two Prf N-terminal domains brings the associated kinases into close promixity. Tomato lines containing Prf complexed with Pth proteins but not Pto possessed greater immunity against P. syringae than tomatoes lacking Prf. This demonstrates that incorporation of non-Pto kinases into the Prf complex extends the number of effector proteins that can be recognized.”
“Background: L-Arginine is an important precursor of nitric oxide (NO) and protein synthesis. Arginine is produced in the body (mainly kidney) by de novo production from citrulline and by protein breakdown. Arginine availability appears to be limited in sepsis.
Objective: The objective was to compare arginine and citrulline metabolism in septic patients and nonseptic control patients in an intensive care unit (ICU) and in healthy control
subjects.
Design: Ten patients with septic shock, 7 critically ill control patients, and 16 healthy elderly subjects were studied. Metabolism was measured by using a primed continuous (2 h) stable-isotope infusion protocol. NO production was calculated
as the conversion rate of arginine to RG7204 citrulline; de novo arginine production was calculated as the conversion rate of citrulline to arginine. Arterial blood (arterialized venous blood in healthy subjects) was collected SYN-117 molecular weight for the measurement of amino acid enrichment and concentrations. Data are reported as means +/- SDs.
Results: Whole-body citrulline production was significantly lower in septic patients (4.5 +/- 2.1 mu mol.kg(-1).h(-1)) than in ICU control patients (10.1 +/- 2.9 mu mol.kg(-1).h(-1); P < 0.01) and in healthy control subjects (13.7 +/- 4.1 mu mol.kg(-1).h(-1); P < 0.001). Accordingly, de novo arginine production was lower in patients with sepsis (3.3 +/- 3.7 mu mol.kg(-1).h(-1)) than in healthy controls (11.9 +/- 6.6 mu mol.kg(-1).h(-1); P < 0.01) and tended to be lower in septic patients than in ICU control patients (10.9 +/- 9.4 mu mol.kg(-1).h(-1); P = 0.05). NO production was lower in septic patients than in healthy control subjects (P < 0.01), whereas a larger part of arginine was converted to urea in sepsis.
Conclusions: Citrulline production is severely low in patients with sepsis and is related to diminished de novo arginine and NO production.