Control of ammoniagenesis by alpha-ketoglutarate in rat kidney mitochondria

Schoolwerth, Anton C.; LaNoue, K. F.

doi:10.1152/ajprenal.1983.244.4.f399

Cited by 8 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One could account for all oxoglutarate formation as a product of aspartate aminotransferase. The data are reminiscent of observations in rat liver mitochondria, where it has been shown that glutamate dehydrogenase is present but inactive until glutamate transamination is inhibited (LaNoue et al,1983; Schoolwerth and LaNoue,1983). This is consistent with the tight regulation of glutamate dehydrogenase in brain.…”

Section: Resultssupporting

confidence: 67%

Mitochondrial transport proteins of the brain

Berkich

Ola

Cole

et al. 2007

J of Neuroscience Research

103

104

View full text Add to dashboard Cite

In this study, cellular distribution and activity of glutamate and gamma-aminobutyric acid (GABA) transport as well as oxoglutarate transport across brain mitochondrial membranes were investigated. A goal was to establish cell-type-specific expression of key transporters and enzymes involved in neurotransmitter metabolism in order to estimate neurotransmitter and metabolite traffic between neurons and astrocytes. Two methods were used to isolate brain mitochondria. One method excludes synaptosomes and the organelles may therefore be enriched in astrocytic mitochondria. The other method isolates mitochondria derived from all regions of the brain. Immunological and enzymatic methods were used to measure enzymes and carriers in the different preparations, in addition to studying transport kinetics. Immunohistochemistry was also employed using brain slices to confirm cell type specificity of enzymes and carriers. The data suggest that the aspartate/glutamate carriers (AGC) are expressed predominantly in neurons, not astrocytes, and that one of two glutamate/hydroxyl carriers is expressed predominantly in astrocytes. The GABA carrier and the oxoglutarate carrier appear to be equally distributed in astrocytes and neurons. As expected, pyruvate carboxylase and branched-chain aminotransferase were predominantly astrocytic. Insofar as the aspartate/glutamate exchange carriers are required for the malate/aspartate shuttle and for reoxidation of cytosolic NADH, the data suggest a compartmentation of glucose metabolism in which astrocytes catalyze glycolytic conversion of glucose to lactate, whereas neurons are capable of oxidizing both lactate and glucose to CO(2) + H(2)O.

show abstract

Section: Resultssupporting

confidence: 67%

Mitochondrial transport proteins of the brain

Berkich

Ola

Cole

et al. 2007

J of Neuroscience Research

103

104

View full text Add to dashboard Cite

show abstract

“…The E1k and E3 subunits are noncovalently bound to a core formed by E2k subunits [82,83]. KGDHC is activated by low concentrations of Ca 2+ (10 −7 −10 −5 M) and ADP (∼10 −4 M for half-maximum activation) [84,85], and it is inhibited by high NADH and its own product, succinyl-CoA [86][87][88].…”

Section: α-Ketoglutarate Dehydrogenase Complexmentioning

confidence: 99%

TCA Cycle Rewiring as Emerging Metabolic Signature of Hepatocellular Carcinoma

Todisco

Convertini

Iacobazzi

et al. 2019

Cancers

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is a common malignancy. Despite progress in treatment, HCC is still one of the most lethal cancers. Therefore, deepening molecular mechanisms underlying HCC pathogenesis and development is required to uncover new therapeutic strategies. Metabolic reprogramming is emerging as a critical player in promoting tumor survival and proliferation to sustain increased metabolic needs of cancer cells. Among the metabolic pathways, the tricarboxylic acid (TCA) cycle is a primary route for bioenergetic, biosynthetic, and redox balance requirements of cells. In recent years, a large amount of evidence has highlighted the relevance of the TCA cycle rewiring in a variety of cancers. Indeed, aberrant gene expression of several key enzymes and changes in levels of critical metabolites have been observed in many solid human tumors. In this review, we summarize the role of the TCA cycle rewiring in HCC by reporting gene expression and activity dysregulation of enzymes relating not only to the TCA cycle but also to glutamine metabolism, malate/aspartate, and citrate/pyruvate shuttles. Regarding the transcriptional regulation, we focus on the link between NF-κB-HIF1 transcriptional factors and TCA cycle reprogramming. Finally, the potential of metabolic targets for new HCC treatments has been explored.

show abstract

“…Liver is not the only organ where Ca 2ϩ activates MAS activity. Evidence for this was obtained in kidney (350) and heart (342). However, the activation by Ca 2ϩ of MAS activity in heart has proven to be elusive.…”

Section: Ca 2ϩ Regulation Of Mas In Heartmentioning

confidence: 99%

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Satrústegui

Pardo²,

Arco³

2007

Physiological Reviews

236

211

View full text Add to dashboard Cite

Ca(2+) signaling in mitochondria is important to tune mitochondrial function to a variety of extracellular stimuli. The main mechanism is Ca(2+) entry in mitochondria via the Ca(2+) uniporter followed by Ca(2+) activation of three dehydrogenases in the mitochondrial matrix. This results in increases in mitochondrial NADH/NAD ratios and ATP levels and increased substrate uptake by mitochondria. We review evidence gathered more than 20 years ago and recent work indicating that substrate uptake, mitochondrial NADH/NAD ratios, and ATP levels may be also activated in response to cytosolic Ca(2+) signals via a mechanism that does not require the entry of Ca(2+) in mitochondria, a mechanism depending on the activity of Ca(2+)-dependent mitochondrial carriers (CaMC). CaMCs fall into two groups, the aspartate-glutamate carriers (AGC) and the ATP-Mg/P(i) carriers, also named SCaMC (for short CaMC). The two mammalian AGCs, aralar and citrin, are members of the malate-aspartate NADH shuttle, and citrin, the liver AGC, is also a member of the urea cycle. Both types of CaMCs are activated by Ca(2+) in the intermembrane space and function together with the Ca(2+) uniporter in decoding the Ca(2+) signal into a mitochondrial response.

show abstract

Control of ammoniagenesis by alpha-ketoglutarate in rat kidney mitochondria

Cited by 8 publications

References 0 publications

Mitochondrial transport proteins of the brain

Mitochondrial transport proteins of the brain

TCA Cycle Rewiring as Emerging Metabolic Signature of Hepatocellular Carcinoma

Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling

Contact Info

Product

Resources

About