Tricarboxylic acid cycles

Kornberg, H. L.

doi:10.1002/bies.950070511

Cited by 9 publications

(6 citation statements)

References 32 publications

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“…The tricarboxylic acid cycle in the mitochondrial matrix is a prime example of a biochemical pathway where many important metabolic intermediates converge [10,11]. A major portion of the urea cycle is also compartmentalized within the mitochondria where metabolic processing of nitrogen-containing amino acid intermediates occurs [12].…”

Section: Key Aspects Of Mitochondrial Biology and Geneticsmentioning

confidence: 99%

Untitled

2002

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Mitochondria play important roles in cellular energy metabolism, free radical generation, and apoptosis. Defects in mitochondrial function have long been suspected to contribute to the development and progression of cancer. In this review article, we aim to provide a brief summary of our current understanding of mitochondrial genetics and biology, review the mtDNA alterations reported in various types of cancer, and offer some perspective as to the emergence of mtDNA mutations, their functional consequences in cancer development, and therapeutic implications.

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Section: Key Aspects Of Mitochondrial Biology and Geneticsmentioning

confidence: 99%

Untitled

2002

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“…[11][12][13] The most wellknown and best-characterized function of mitochondria is the production of adenosine triphosphate (ATP) through oxidative phosphorylation. 14 Glycolysis can also generate ATP and provides a compensatory mechanism when phosphorylation becomes inefficient as a consequence of defects in the respiratory chain. 15 Reactive oxygen species (ROS) are generated during mitochondrial respiration when electrons are transported through respiratory chain leak and react with molecular oxygen.…”

Section: Mitochondria and Antiviral Treatmentmentioning

confidence: 99%

Does mitochondrial dysfunction during antiretroviral therapy in human immunodeficiency virus infection suggest antioxidant supplementation as a beneficial option?

et al. 2005

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Over the last few years, a relative decline of the morbidity and mortality of human immunodeficiency virus (HIV) infection in industrialised countries has been observed due to the use of a potent combined therapy known as high active antiretroviral therapies (HAARTs). It has led to a decrease of viral load and a quantitative and qualitative improvement of immune function in patients, especially CD4+ T-lymphocyte count, having as a consequence a decrease of infectious complications and a global clinical improvement. Besides the positive effects of HAARTs on immune and metabolic alterations during HIV infection, it has been reported that the commonly used drugs AZT, ddI, and ddC are toxic to hepatocytes. Recent reports continue to point to the mitochondria as targets for toxicity. The prevalence of these symptoms is continued during acquired immunodeficiency syndrome (AIDS). The effects of oxidative stress occurring as a consequence of mitochondrial toxicity may amplify some of the pathophysiological and phenotypic events during infection. Mitochondrial stabilisation and antioxidative strategies are possible new therapeutic aims since the antiretroviral treatment is prolonged with increased longevity from AIDS, which has become a more manageable chronic illness. The aim of the present review article is to summarize the current knowledge about mitochondrial dysfunction during HAART and its consequence for patients with chronic treatment. Oxidative stress may serve as one pathway for cellular damage in AIDS and its treatment. One important future goal is to prevent or attenuate the side effects of HAART so that improved disease management can be achieved.

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“…Most of these studies suggest that the establishment of biological signaling profiles in development is a result of complex physical-chemical processes that include the localized production of morphogens that can later diffuse and be removed from the cellular medium by various types of biochemical transitions [7][8][9][10]12]. Based on some experimental observations [64,65,67,68,70,71,74], the possibility of alternative mechanisms of the direct delivery of morphogens to the target cells utilizing dynamic cellular extensions called cytonemes was predicted [11,64,77]. It has been argued that the complex environment of the embryo systems might prevent the free diffusion from establishing the distinguishable morphogen gradients at different regions, implying a different mechanism of the biological signal transduction [11,64].…”

Section: Introductionmentioning

confidence: 99%

“…Based on some experimental observations [64,65,67,68,70,71,74], the possibility of alternative mechanisms of the direct delivery of morphogens to the target cells utilizing dynamic cellular extensions called cytonemes was predicted [11,64,77]. It has been argued that the complex environment of the embryo systems might prevent the free diffusion from establishing the distinguishable morphogen gradients at different regions, implying a different mechanism of the biological signal transduction [11,64].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of the formation of biological signaling profiles

Teimouri¹,

Kolomeisky²

2016

J. Phys. A: Math. Theor.

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Formation and growth of multi-cellular organisms and tissues from several genetically identical embryo cells is one of the most fundamental natural phenomena. These processes are stimulated and governed by multiple biological signaling molecules, which are also called morphogens. Embryo cells are able to read and pass the genetic information by measuring the non-uniform concentration profiles of signaling molecules. It is widely believed that the establishment of concentration profiles of morphogens, commonly referred to as morphogen gradients, is a result of complex biophysical and biochemical processes that might involve diffusion and degradation of locally produced signaling molecules. In this review we discuss various theoretical aspects of the mechanisms for morphogen gradients formation, including stationary and transient dynamics, the effect of source delocalization, diffusion, different degradation mechanisms, and the role of spatial dimensions. Theoretical predictions are compared with experimental observations. In addition, we analyze potential alternative mechanisms of delivery of biological signals in embryo cells and tissues. Current challenges in understanding the mechanisms of morphogen gradients and future directions are also discussed.

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Tricarboxylic acid cycles

Cited by 9 publications

References 32 publications

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Does mitochondrial dysfunction during antiretroviral therapy in human immunodeficiency virus infection suggest antioxidant supplementation as a beneficial option?

Mechanisms of the formation of biological signaling profiles

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