Ueber Isofenchylalkohol

Bertram, J.; Helle, J.

doi:10.1002/prac.19000610126

Cited by 22 publications

(5 citation statements)

References 3 publications

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“…4 bridgehead H, broad, 2.65 ppm; 2-exo H, quartet, 2.97 ppm; no. 1 bridgehead H, broad, 3.13 ppm; 6-olefin H, broad, 5.55 ppm; carboxylic H, 12 ppm. 5-emfo-MethyI-5-hydroxy-2-e/7i/o-norbomanecarboxylic Acid (5).…”

Section: Bf-ch+mentioning

confidence: 99%

Molecular rearrangements. XXX. Applications of an algebraic-graphical model for analyzing rearrangements of bicyclo[2.2.1]heptyl cations

Collins¹,

Johnson²,

Raaen³

1974

J. Am. Chem. Soc.

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The algebraic model, coset graphs, and computer program previously describedlb•2 have been applied to two specific chemical problems: (1) the rearrangements,6•7 in sulfuric acid, of 1 -methyl-7,2-carbolactone (1) and of 5-methyl-2-e«£fo-norbornenecarboxylic acid (4), and (2) the rearrangements,9 in S02C1F-FS03H, of the fenchyl cation. The use of coset graphs is illustrated. In each study described, important mechanistic information resulted from the use of the model and computer program. We also discuss how the method can be used in the design of isotopic tracer experiments.

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Section: Bf-ch+mentioning

confidence: 99%

Molecular rearrangements. XXX. Applications of an algebraic-graphical model for analyzing rearrangements of bicyclo[2.2.1]heptyl cations

Collins¹,

Johnson²,

Raaen³

1974

J. Am. Chem. Soc.

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“…On fait rdagir, dans les conditions decrites pour le camphbne [l]. 100 g (0,73 mole) defenchbnes [9] avec 140 g (1,48 mole) de phenol en presence de 10 g de BF, B 35% dans AcOH. et distille les terpenylphinols ainsi produits: fr.…”

Section: Partie Experimentaleunclassified

Synthèses et relations entre constitution chimique et odeur dans la série des terpényl‐3‐cyclohexanols

Demole¹,

Stoll²

1964

Helvetica Chimica Acta

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“…As the archetypical metabolic pathway of mammalian cells, these initial steps of glycolysis have been well-characterized biochemically, which has lead to the proposal that PFK1 activity is oscillatory in beta-cells, and governs downstream oscillations in metabolism (mitochondrial NADH and O 2 , ATP/ADP), electrical activity (K ATP and Ca 2+ channel activity), and finally, pulsatile insulin release [1].Based on this hypothesis we have developed a computational model of the beta-cell, termed ( Fig. 1), in which slow oscillations in insulin secretion reflect slow oscillations in glycolytic PFK1 activity, which then interact with fast oscillations arising from membrane electrical activity and Ca 2+ [2]. Here, we have compared specific glycolytic behaviors in the DOM with timelapse imaging of islet oscillatory behavior using adenovirally-delivered mutants of the glycolytic regulatory enzyme PFK2/FBPase2 (6-phosphofructo-2-kinase/fructose-2,6bisphosphatase) (Fig.…”

mentioning

confidence: 99%

“…Based on this hypothesis we have developed a computational model of the beta-cell, termed ( Fig. 1), in which slow oscillations in insulin secretion reflect slow oscillations in glycolytic PFK1 activity, which then interact with fast oscillations arising from membrane electrical activity and Ca 2+ [2]. Here, we have compared specific glycolytic behaviors in the DOM with timelapse imaging of islet oscillatory behavior using adenovirally-delivered mutants of the glycolytic regulatory enzyme PFK2/FBPase2 (6-phosphofructo-2-kinase/fructose-2,6bisphosphatase) (Fig.…”

mentioning

confidence: 99%

Testing a Computational Model of Pancreatic Beta-Cell Oscillations Using Live-Cell Imaging of Islet Oscillatory Behavior

Merrins

Bertram²,

Sherman

et al. 2011

Microsc Microanal

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Befitting their role as a metabolic sensor for the organism, pancreatic beta-cells adjust their metabolic output in accordance with plasma glucose concentrations, and not just their own energy requirements, in order to secrete insulin appropriately on a minute to minute basis. Glucose sensing lies in the commitment to early glycolysis, at the level of glucokinase, which is rate-limiting until phosphofructokinase-1 (PFK1) in turn fully commits substrate to allow glycolysis to proceed. As the archetypical metabolic pathway of mammalian cells, these initial steps of glycolysis have been well-characterized biochemically, which has lead to the proposal that PFK1 activity is oscillatory in beta-cells, and governs downstream oscillations in metabolism (mitochondrial NADH and O 2 , ATP/ADP), electrical activity (K ATP and Ca 2+ channel activity), and finally, pulsatile insulin releaseBased on this hypothesis we have developed a computational model of the beta-cell, termed ( Fig. 1), in which slow oscillations in insulin secretion reflect slow oscillations in glycolytic PFK1 activity, which then interact with fast oscillations arising from membrane electrical activity and Ca 2+ [2]. Here, we have compared specific glycolytic behaviors in the DOM with timelapse imaging of islet oscillatory behavior using adenovirally-delivered mutants of the glycolytic regulatory enzyme PFK2/FBPase2 (6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase) (Fig. 2). This bifunctional enzyme is uniquely positioned to alter flux through PFK1 in two complementary ways. First, PFK2/FBPase2 is the sole catalyst for the production and degradation of Fru2,6-BP, which allosterically activates PFK1 to a greater extent than its own product, Fru1,6-BP. Second, PFK2/FBPase2 has been proposed to bind and directly activate glucokinase, which is rate-limiting for glycolysis and which controls the flux of Fru6-P substrate to PFK1. Thus, in addition to studying the role of this glycolytic modulator as it affects the dynamic oscillatory process in living islets, our interest in the manipulation of PFK2/FBPase2 activity was to test whether the interplay between glucokinase and PFK1, the rate-limiting steps in glycolysis, affect beta-cell oscillations.Islet Ca 2+ oscillations induced by 11.1 mM glucose had reduced period and amplitude after PFK2 overexpression compared to controls, and increased period and amplitude after FBPase2 expression was selectively increased (Fig. 2). Measurements of islet NAD(P)H oscillations were confirmatory. These effects are consistent with our central hypothesis that slow [Ca 2+ ] oscillations are driven by PFK1-mediated oscillations in glycolysis, as shown using an appropriately modified version of the DOM. Additionally, we confirmed that PFK2/FBPase2 physically interacts with glucokinase using a live-cell FRET assay, although the level of FRET observed indicates this interaction is weak or transient. Accordingly, knockdown of endogenous PFK-2/FBPase-2 increased the oscillatory period, consistent with a reduction in Fru2,6-BP l...

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Ueber Isofenchylalkohol

Cited by 22 publications

References 3 publications

Molecular rearrangements. XXX. Applications of an algebraic-graphical model for analyzing rearrangements of bicyclo[2.2.1]heptyl cations

Molecular rearrangements. XXX. Applications of an algebraic-graphical model for analyzing rearrangements of bicyclo[2.2.1]heptyl cations

Synthèses et relations entre constitution chimique et odeur dans la série des terpényl‐3‐cyclohexanols

Testing a Computational Model of Pancreatic Beta-Cell Oscillations Using Live-Cell Imaging of Islet Oscillatory Behavior

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