Sentence examples for cause of uncoupling from inspiring English sources

In recent years, evidence has been mounting for NOS uncoupling as an important factor in a range of pathologies, and BH4 deficiency or its oxidation to BH2 is assumed to be a leading cause of uncoupling.

Fourth, our results on muscle mitochondrial respiration are fully concordant with the long-known effects of methylmercury on mitochondria of human and rat liver, i.e. state 3 respiration was inhibited by 10 to 50 nmol of methylmercury per mg of mitochondrial protein, and the resulting loss in membrane potential was the major cause of uncoupling [ 28].

The most prominent cause of NOS uncoupling is the loss of the critical NOS cofactor BH4[ 34].

Using aortic endothelial cells in an adherent cell model of H/R, we observed that these two mechanisms act together to cause eNOS uncoupling.

These include causes of the uncoupling of morphological and genetic evolution and the role of climatic change, hydrology and regressive evolution as processes shaping and determining subterranean biodiversity.

It is also possible that HDACIs, drugs known to increase reactive oxygen species levels and the basal level of ERK1/2 activity, may have also caused some form of uncoupling of the CXCR4 receptor from some of its downstream signaling intermediates.

Many of these types of replication arrest cause functional uncoupling of the MCM helicase and replicative DNA polymerase activities at replication forks, resulting in production of long stretches of RPA-coated single-stranded DNA (ssDNA) (Byun et al, 2005; Cortez, 2005).

On the other hand, the increase in the V4 (mitochondrial respiration state 4) values suggests that the excess of dietary fat most probably is the cause of a partial uncoupling between respiration and phosphorylation in mitochondria.

The uncoupling proteins (UCPs) are a family of mitochondrial proteins whose best-characterised function (in the presence of suitable activators) is to cause partial uncoupling of oxidative phosphorylation by dissipating the protonmotive force generated by the electron transport chain.

Disruption of the dynein-dynactin pathway through prevention of BICD2 uncoupling causes motor neurone degeneration in mice [ 42].

By blocking those receptors, A1R antagonists cause an uncoupling of the tubuloglomerular feedback which may at least partly explain the elevated concentrations of adenosine measured in the urine of animals treated with SLV329 [16], [16].