Words similar to ornithine
Example sentences for: ornithine
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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.
They are: two ubiquitin precursors UBA80 (clone 1) and UBA52 (clone 21), the ornithine decarboxylase antizyme (Az) (clone 15) and the proteasome β subunit HsN3 (clone 18).
The best-characterized example of ubiquitin-independent degradation is the degradation of ornithine decarboxylase (ODC), which is dependent upon ODC interaction with the targeting protein antizyme (Az) [ 18 ] . How ubiquitinated substrates or Az-bound ODC is recognized by the 26S proteasome is not well understood.
When Jesse Gelsinger, a relatively healthy young adult, died in Philadelphia during a clinical trial of a novel adenovirus-based genetic therapy for ornithine transcarbamylase deficiency, it was a tragedy [1].
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.