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Example sentences for: ornithine
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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).
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.
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).
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 ] .
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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