Disease relevance of ODC1

• Infection with Rous sarcoma virus resulted in increased ornithine decarboxylase activity which preceded morphological alterations by at least 24 hr [1].
• The observation that a noise field inhibits ODC activity changes is consistent with our speculation that MF-induced ODC activity changes during early development may be related to MF-induced neural tube defects at slightly later stages (which are also inhibited by the superposition of a noise field) [2].

High impact information on ODC1

• Administering either alpha-difluoromethylornithine, a specific inhibitor of ornithine decarboxylase, or N1,N4-bis(2,3-butadienyl)-1,4-butanediamine, a specific inhibitor of polyamine oxidase, to newborn chicks significantly decreased the duodenal content of putrescine and calcium transport activity [3].
• In this paper we report a comparative study on the parameters affecting turnover of nuclear oncoproteins c-myc, c-myb, and the rapidly metabolized cytoplasmic enzyme ornithine decarboxylase [4].
• Infection with a temperature-sensitive mutant of Rous sarcoma virus, T5, stimulated ornithine decarboxylase activity of chick embryo fibroblasts at the permissive (37 degrees) but not at the nonpermissive (42 degrees) temperature [1].
• These unexpected results clearly indicate that spermidine N1-acetyltransferase has a larger role than ornithine decarboxylase in the increase of duodenal putrescine synthesis induced by 1 alpha,25(OH)2D3 [5].
• 1,25(OH)2D3 but not 24R,25(OH)2D3 enhanced the activity of ODC in duodenum and bone [6].

Biological context of ODC1

• The DNA sequence shows 78% identity with the human ODC cDNA sequence and the deduced amino acid sequence is almost 90% homologous to mouse and human [7].
• A chicken embryo cDNA library was screened with a mouse probe for ornithine decarboxylase (ODC) and 14 positively hybridizing clones isolated [7].
• Since ODC activity has been associated with mesenchymal cell proliferation, this suggested that dexamethasone stimulated the proliferation of similar cells in the cultured periostea [8].
• Two rate-limiting enzymes in the biosynthetic pathway of polyamines, ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase, showed their highest activities at the end of spermiogenesis and were not detectable in vas-deferens spermatozoa [9].
• Ornithine decarboxylase (ODC) activity and content of the natural polyamines spermine (Spm), spermidine (Spd), and putrescine (Put) differed during cell cycle [10].

Anatomical context of ODC1

• When T5-transformed fibroblasts were shifted to the nonpermissive temperature, ornithine decarboxylase activity decreased fivefold within 4 hr and paralleled the levels of normal controls in 11 hr [1].
• In the early chick embryo, inhibition of polyamine synthesis by alpha-difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ornithine decarboxylase, blocks development at gastrulation [11].
• The activity of ornithine decarboxylase in the differentiating left and right Müllerian ducts was assayed and compared with that in other embryonic organs, i.e. the liver and the brain throughout the stages of development [12].
• Distribution of ornithine decarboxylase activity induced by 1 alpha,25-dihydroxyvitamin D3 in chick duodenal villus mucosa [13].
• An in situ assay system to measure ornithine decarboxylase activity in primary cultures of chicken osteoblasts: effects of bone-seeking hormones [14].

Associations of ODC1 with chemical compounds

• In this work, the conversion of [3H]ornithine into [3H]putrescine catalyzed by ornithine decarboxylase was compared with the conversion of [14C]spermidine into [14C]putrescine catalyzed by spermidine N1-acetyltransferase and polyamine oxidase [5].
• Activity of ornithine decarboxylase and creatine kinase in soft and hard tissue of vitamin D-deficient chicks following parenteral application of 1,25-dihydroxyvitamin D3 or 24R,25-dihydroxyvitamin D3 [6].
• Inhibition of ODC resulted in levels of Put and Spd comparable to that of quiescent fibroblasts, whereas Spm concentration remained higher [10].
• In addition to AP stimulation, dexamethasone also stimulated ODC activity [8].
• The duodenal ornithine decarboxylase activity decreased in animals fed a vitamin D-deficient diet and its retarded activity was increased dose-dependently by a single injection of cholecalciferol [15].

Other interactions of ODC1

• An increased bioavailability of IGF-1 observed by day 8 may represent a rebound effect and is associated with increases in ornithine decarboxylase activity, a marker of increased growth [16].
• Induction of ornithine decarboxylase activity in isolated chicken osteoblasts by parathyroid hormone: the role of cAMP and calcium [17].
• Diaminopropane inhibits brain ornithine decarboxylase, but does not induce an ornithine decarboxylase-antizyme [18].

Analytical, diagnostic and therapeutic context of ODC1

• Molecular cloning and sequence analysis of a chicken ornithine decarboxylase cDNA [7].
• Cellular proliferation was assessed by measuring ornithine decarboxylase (ODC) activity, [3H]thymidine uptake, and radioautography of cultures that had incorporated [3H]thymidine [8].
• Ornithine decarboxylase activity in granulosa tissue from the largest preovulatory follicle increased significantly 3 h after treatment with LH and PMSG in vivo; no effect was observed with FSH [19].
• ODC protein was identified by indirect immunofluorescence with a monospecific ODC antibody, and catalytically active ODC was identified by autoradiography with alpha-(5-3H) difluoromethylornithine [20].
• Sequence analysis of 4,230 bp of the 3' end of the ornithine decarboxylase gene of 20 chickens from a noninbred White Leghorn strain revealed a total of 62 polymorphisms [21].

References