Example sentences for: ornithine

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

  • 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.

  • The transcript encoding ornithine decar-boxylase (ODC), a known androgen target that catalyzes the rate-limiting step in polyamine biosynthesis [ 26], was induced coordinately with enzymes that catalyze downstream steps in polyamine synthetic pathway (spermine synthase, spermidine/spermine N 1-acetyltransferase, and S-adenosylmethionine decarboxylase) (Figure 5c).

  • Az was previously identified as a polyamine-inducible factor that binds and targets the ornithine decarboxylase (ODC) to proteasome for degradation [ 18 45 ] . Until now, ODC is the only protein known to be targeted by Az to proteasome, although the existence of additional proteins targeted by Az to proteasome has been suspected [ 20 ] . We now find two new Az interactors: Smad1, the key signal transducer of BMPs, as well as SNIP1, the nuclear repressor of CBP/p300.

  • Cells formed NSs during stages 1 and 2. After 2 wk, we transferred 40–80 NSs containing a total of approximately 2–4 × 10 5 cells to single wells in plates coated with 0.005% poly-L-ornithine (Sigma) and 3 μg/ml fibronectin (Invitrogen).

  • 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.

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