A Salt-Induced Kinetic Intermediate Is on a New Parallel Pathway of Lysozyme Folding†

Biochemistry ◽  
1999 ◽  
Vol 38 (38) ◽  
pp. 12460-12470 ◽  
Author(s):  
Oliver Bieri ◽  
Gudrun Wildegger ◽  
Annett Bachmann ◽  
Clemens Wagner ◽  
Thomas Kiefhaber
2011 ◽  
Vol 100 (3) ◽  
pp. 237a
Author(s):  
Steve Meisburger ◽  
Krista Brooks ◽  
Suzette Pabit ◽  
Li Li ◽  
Joshua Blose ◽  
...  

1976 ◽  
Vol 230 (6) ◽  
pp. 1708-1721 ◽  
Author(s):  
W Perl ◽  
F Silverman ◽  
AC Delea ◽  
FP Chinard

Bolus injection of T-1824-albumin, test indicator, and tritiated water into a jugular vein of the anesthetized dog and sequential sampling of blood from a carotid artery yielded multiple-indicator outflow patterns for the lung. Permeability-surface products of the test indicator for the lung endothelial barrier were obtained by comparison of test indicator with T-1824-albumin on the upslope of the test-indicator curve and correction for backdiffusion. The derived endothelial permeability coefficients, based on surface area/wet lung weight-500 cm2/g (mean +/- 2 SE, 10(-5) cm s(-1)), were: sodium ion, 2.9 +/- 0.8; ethylene glycol, 7.3 +/- 1.5; 1, 3-propranediol, 7.9 +/- 3.2; 1, 2-propanediol, 10 +/- 4; 1, 4-butanediol, 14 +/- 8; 1, 5-pentanediol, 21 +/- 6; 1, 6-hexanediol, 41 +/- 11; formamide, 16 +/- 9; acetamide, 13 +/- 4; propionamide, 31 +/- 12; butyramide, 42 +/- 24; valeramide, 79 +/- 12; tritiated water, 150 +/- 50. The backdiffusion correction varies from 8% for sodium to 75% for valeramide. A parallel-pathway model of blood-tissue passive exchange of small nonelectrolyte solutes is compatible with these results, with a lipid pathway through endothelial cells and an aqueous pathway possibly through interendothelial clefts.


2017 ◽  
Vol 6 (1) ◽  
pp. 015006 ◽  
Author(s):  
Elena V Nemtseva ◽  
Olesya O Lashchuk ◽  
Marina A Gerasimova ◽  
Tatiana N Melnik ◽  
Galina S Nagibina ◽  
...  

2000 ◽  
Vol 11 (5) ◽  
pp. 1631-1643 ◽  
Author(s):  
Changjiang Zeng ◽  
Christophe Anjard ◽  
Karsten Riemann ◽  
Angelika Konzok ◽  
Wolfgang Nellen

Discoidin I expression was used as a marker to screen for mutants affected in the growth–differentiation transition (GDT) ofDictyostelium. By REMI mutagenesis we have isolated mutant 2-9, an overexpressor of discoidin I. It displays normal morphogenesis but shows premature entry into the developmental cycle. The disrupted gene was denominated gdt1. The mutant phenotype was reconstructed by disruptions in different parts of the gene, suggesting that all had a complete loss of function.gdt1 was expressed in growing cells; the levels of protein and mRNA appear to increase with cell density and rapidly decrease with the onset of development. gdt1 encodes a 175-kDa protein with four putative transmembrane domains. In the C terminus, the derived amino acid sequence displays some similarity to the catalytic domain of protein kinases. Mixing experiments demonstrate that the gdt1 −phenotype is cell autonomous. Prestarvation factor is secreted at wild-type levels. The response to folate, a negative regulator of discoidin expression, was not impaired in gdt1 mutants. Cells that lack the G protein α2 display a loss of discoidin expression and do not aggregate.gdt1 −/Gα2 −double mutants show no aggregation but strong discoidin expression. This suggests that gdt1 is a negative regulator of the GDT downstream of or in a parallel pathway to Gα2.


Biochemistry ◽  
2009 ◽  
Vol 48 (32) ◽  
pp. 7584-7594 ◽  
Author(s):  
Alexander Kyrychenko ◽  
Yevgen O. Posokhov ◽  
Mykola V. Rodnin ◽  
Alexey S. Ladokhin

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