Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ornithine decarboxylase (ODC) activity increased in goldfish retina, brain, and kidney several days following unilateral intraorbital optic nerve crush. Activity in both retinas followed a similar time course, an elevation being first detectable 3 days following crush, maximal on day 5 and returning to control levels by day 7. Increases were significantly higher in the retina on the lesioned side than in control retina. If one eye was surgically removed, a more prolonged elevation of ODC activity was seen in the remaining eye than was observed in control retinas following contralateral nerve crush. Sham operation or behavioral stress secondary to aversive electrical shock did not lead to significant increases in ODC activity in brain or retina. Explants of retinas whose optic nerve had been crushed 10--14 days prior to explantation, as well as those derived from the unlesioned side, showed increases in ODC activity following addition of beta-NGF to the medium. The response was greater in post-crush retinas than in control retinas. These results taken together suggest an increased responsiveness of the regenerating retina to stimuli that lead to increased ODC activity. While the nature of the in vivo signal(s) may be complex, it is inferred that degenerative changes in the distal stump play a significant role.
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PMID:Increased activity of ornithine decarboxylase in goldfish following optic nerve crush. 726 Jun 45

Sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, causes increased levels of tyrosine phosphorylation and blocks, at noncytotoxic concentrations, the differentiative response of rat pheochromocytoma (PC12) cells to beta-nerve growth factor (beta NGF) and basic fibroblast growth factor (bFGF) in a reversible manner. It also prevents growth factor-induced neurite proliferation in primed cells and causes the retraction of previously formed neurites, even in the presence of beta NGF or bFGF. It is equally effective in blocking neurite proliferation by 8-Br-cAMP. Zinc chloride and ammonium molybdate, two other inhibitors of tyrosine phosphatases, also cause parallel decreases in neurite proliferation. Orthovanadate generally reduces the transcription of immediate early response genes (TIS 8 and c-fos) and secondary response genes (ornithine decarboxylase (ODC), acetyl-cholinesterase (AChE) and SCG 10) induced by beta NGF, bFGF, EGF, and PMA, albeit in a variable fashion. There was no observed effect on the kinetics of expression as judged by TIS 8 induction by beta NGF and protein kinase C (PKC) downregulation did not change the levels of inhibition by orthovanadate seen in control cells. Orthovanadate does not affect the production of diacylglycerol induced by beta NGF or bFGF. These observations are consistent with the view that growth factor stimulation of differentiation in PC12 cells involves at least one other PKC independent pathway, and that cAMP and PMA (and their active analogs) activate tyrosine kinases (albeit probably secondarily), which are at least partially responsible for their actions. Although the exact site(s) of action of orthovanadate that lead to the inhibition of growth factor-induced neurite proliferation are unknown, the results presented suggest that it prolongs tyrosine phosphorylations by nonreceptor tyrosine kinases that act downstream from the receptor kinases.
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PMID:Effect of nerve growth factor and fibroblast growth factor on PC12 cells: inhibition by orthovanadate. 846 55