Example sentences for: ornithine

How can you use “ornithine” 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 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.

  • 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 cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .

  • 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].


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