Example sentences for: decarboxylase

How can you use “decarboxylase” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Many studies have shown that chronic intravenous infusion of norepinephrine is sufficient to cause hypertrophy, and that various forms of hypertrophy are linked to a decrease in either beta-adrenergic receptor density or a decreased responsiveness to beta-adrenergic stimulation [ 46 48 49 56 57 58 59 60 61 62 63 ] . Barth, for example, showed that norepinephrine infusion induced left ventricular hypertrophy that could be prevented by an adrenergic-receptor blocker [ 58 ] . It has been suggested that ornithine decarboxylase is a link between beta-adrenoreceptors and stimulation of tissue growth factor, which results in hypertrophy [ 64 ] . However, recent studies have focused on alpha-adrenergic reception as a mediator of cardiac hypertrophy [ 35 ] , although some question the role of the alpha-adrenergic receptor as a hypertrophic mediator in vivo [ 34 ] . To date, no published studies of which we are aware have examined alpha-adrenergic reception and the development of cardiac hypertrophy with iron deficiency.

  • The 26S proteasome is responsible for the bulk turnover of cytoplasmic and nuclear proteins in eukaryotic cells and also plays a key role in the regulation of cell cycle, signal transduction, transcription as well as antigen presentation [ 17 18 19 20 21 ] . Most of the known proteasomal substrates are marked and targeted to proteasome by ubiquitination [ 17 19 20 ] . Ubiquitination, however, is not an obligatory step for substrate targeting to proteasome [ 17 18 20 ] . The degradation of the ornithine decarboxylase (ODC), the rate-limiting enzyme for polyamine synthesis, involves a protein named antizyme (Az), which binds and targets ODC to 26S proteasome for degradation [ 18 ] . However, ODC has remained an "orphan" in Az-dependent proteasomal degradation.

  • GABA is a well-documented neurotrophic agent involved in brain development [ 27 28 29 30 ] . Most of the work done on the effects of GABA and neural development has been done on embryos and embryonic tissue well past the neural tube stage [ 27 31 32 ] . However, there is evidence of glutamic acid decarboxylase (GAD) and GABA receptor expression about the time of neural tube formation [ 27 ] . Given that GABA is important to neural development, and the early developmental time frame of the GABA system, it is logical that agents active at the GABA receptor (ethanol, BDZs) can have adverse consequences on CNS development.

  • Many genes that are known to amplify in response to selection, primarily during anticancer drug treatments, were found to be present in multiple copies in mammalian genomes as well, in particular, aminoacyl-tRNA synthetases, glutamine synthetase and other anabolic enzymes, adenosine deaminase, ornithine decarboxylase, AMP deaminase, and N -acetyl glucosaminyltransferase [ 34, 46].

  • For example, the complementary sequence shared between Dopa decarboxylase and CG10561 is thought to be involved in regulating the levels of these transcripts [ 45].

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