๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Identification of metabolic model: Citrate production from glucose by Candida lipolytica

โœ Scribed by Shuichi Aiba; Masayoshi Matsuoka


Publisher
John Wiley and Sons
Year
1979
Tongue
English
Weight
560 KB
Volume
21
Category
Article
ISSN
0006-3592

No coin nor oath required. For personal study only.

โœฆ Synopsis


Abstract

The concept of mass balance was used to analyze the metabolic pathways of citrate production by Candida lipolytica from glucose. Specific rates of glucose consumption, citrate and isocitrate productions, carbon dioxide evolution, and cellular syntheses of protein and carbohydrate were observed in an NH~4~^+^โ€limited chemostat culture. These data permitted one to assess the carbon flux in vivo by solving simultaneous carbon balance equations with respect to intermediary metabolite pools in the steady State. Among the three models considered here, model I (which coordinates the pyruvate carboxylation with the tricarboxylic acid cycle, but disregards the glyoxylate cycle) was considered plausible because the carbon flux calculated so far was acceptable. On the other hand, models II and III (which overlook the pyruvate carboxylation and the 2โ€oxoglutarate dehydrogenation, respectively) were found to be most unlikely because of the unusual flux assessed from these models.


๐Ÿ“œ SIMILAR VOLUMES


Origin of end-products from the co-metab
โœ P. Schmitt; C. Diviรจs; R. Cardona ๐Ÿ“‚ Article ๐Ÿ“… 1992 ๐Ÿ› Springer ๐ŸŒ English โš– 591 KB

The addition of citrate to glucose broth led to an increase in specific growth rate and glucose catabolism, but a decrease in molar growth yield from glucose, in Leuconostoc rnesenteroides subsp, cremoris. Acetate and formate were produced during the stationary phase.of growth. According to the ferm

Chronic candidosis and oral cancer in AP
โœ Johanna Uittamo; Emilia Siikala; Pertti Kaihovaara; Mikko Salaspuro; Riina Raute ๐Ÿ“‚ Article ๐Ÿ“… 2009 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 79 KB

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare autosomal recessive disease caused by mutations of the AIRE (autoimmune regulator) gene. [1][2][3] It is associated with a limited T lymphocyte defect and an autoimmune response to various tissues, particularly endocri