4.1.1.17: ornithine decarboxylase
This is an abbreviated version!
For detailed information about ornithine decarboxylase, go to the full flat file.
Word Map on EC 4.1.1.17
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4.1.1.17
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polyamine
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spermidine
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alpha-difluoromethylornithine
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carcinogenesis
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antizyme
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chemopreventive
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12-o-tetradecanoylphorbol-13-acetate
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phorbol
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mucosa
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difluoromethylornithine
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diamine
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decarboxylases
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n1-acetyltransferase
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hyperplasia
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arginase
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c-myc
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antiproliferative
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tpa-induced
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prostaglandin
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testosterone
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3hthymidine
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tumorigenesis
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mitogen
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cycloheximide
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c-fos
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methylglyoxal
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tpa-treated
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1,2-dimethylhydrazine
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isoproterenol
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hairless
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degrons
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12-o-tetradecanoyl
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hepatectomy
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cadaverine
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s-adenosyl-l-methionine
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drug development
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azoxymethane
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protooncogene
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papilloma
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7,12-dimethylbenzaanthracene
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agmatine
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phorbol-13-acetate
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medicine
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tumor-promoting
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food industry
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diagnostics
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nitrilotriacetate
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pharmacology
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prolactin
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crypt
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trypanothione
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12-o-tetradecanoylphorbol
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ester-induced
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actinomycin
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mezerein
- 4.1.1.17
- polyamine
- spermidine
- alpha-difluoromethylornithine
- carcinogenesis
- antizyme
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chemopreventive
- 12-o-tetradecanoylphorbol-13-acetate
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phorbol
- mucosa
- difluoromethylornithine
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diamine
- decarboxylases
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n1-acetyltransferase
- hyperplasia
- arginase
- c-myc
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antiproliferative
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tpa-induced
- prostaglandin
- testosterone
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3hthymidine
- tumorigenesis
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mitogen
- cycloheximide
- c-fos
- methylglyoxal
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tpa-treated
- 1,2-dimethylhydrazine
- isoproterenol
- hairless
- degrons
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12-o-tetradecanoyl
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hepatectomy
- cadaverine
- s-adenosyl-l-methionine
- drug development
- azoxymethane
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protooncogene
- papilloma
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7,12-dimethylbenzaanthracene
- agmatine
- phorbol-13-acetate
- medicine
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tumor-promoting
- food industry
- diagnostics
- nitrilotriacetate
- pharmacology
- prolactin
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crypt
- trypanothione
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12-o-tetradecanoylphorbol
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ester-induced
- actinomycin
- mezerein
Reaction
Synonyms
AdoMetDC/ODC, BN36_1212510, bODC, DDB_G0281109, DdODC, Decarboxylase, ornithine, dODC, LDC/ODC, LdODC, lysine/ornithine decarboxylase, ODC, ODC-paralogue, ODC1, ornithine decarboxylase, PfAdoMetDC-ODC, PfODC/AdoMetDC, S-adenosylmethionine decarboxylase/ornithine decarboxylase, SpeC, XODC1, XODC2, YODC
ECTree
4.1.1.17 ornithine decarboxylaseAdvanced search results
results (
results (Engineering
Engineering on EC 4.1.1.17 - ornithine decarboxylase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
C334A
mutation of a putative active site at the dimer interface, completely abolishes enzyme activity. Partial restoration of the enzyme activity is observed when inactive K57A and C334A mutants are mixed, confirming that the dimer is the active form
G361Y
mutation at dimer interface, abolishes enzyme activity and destabilizes the dimer
K157A
mutation at dimer interface, abolishes enzyme activity and destabilizes the dimer
K57A
mutation of a putative active site at the dimer interface, completely abolishes enzyme activity. Partial restoration of the enzyme activity is observed when inactive K57A and C334A mutants are mixed, confirming that the dimer is the active form
A124R/N125D/Q129D/E136V/V137D/M140E
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mutant shows very little resistance to antizyme inhibition
G316A
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the naturally occuring ODC G316A genotype is prognostic for colorectal adenoma recurrence and predicts efficacy of aspirin chemoprevention, genotyping, overview
Q119H/A124R/N125D/E136V/V137D/M140E
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mutant is moderately resistant to antizyme inhibition
Q119H/A124R/N125D/Q129D/E136V/M140E
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mutant shows very little resistance to antizyme inhibition
Q119H/A124R/N125D/Q129D/E136V/V137D
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mutant shows very little resistance to antizyme inhibition
Q119H/A124R/N125D/Q129D/E136V/V137D/M140E
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mutations introduced to match the Trypanosoma brucei onithine decarboxylase protein sequence. Mutant is less sensitive to antizyme inhibition
Q119H/A124R/N125D/Q129D/V137D/M140E
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mutant shows a pattern of inhibition similar to mutant Q119H/A124R/N125D/Q129D/E136V/V137D/M140E
Q119H/A124R/Q129D/E136V/V137D/M140E
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mutant is moderately resistant to antizyme inhibition
Q119H/N125D/Q129D/E136V/V137D/M140E
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mutant shows a pattern of inhibition similar to mutant Q119H/A124R/N125D/Q129D/E136V/V137D/M140E
Q119H/V137D
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mutant is much less sensitive to antizyme inhibition than wild-type, pattern similar to mutant Q119H/A124R/N125D/Q129D/E136V/V137D/M140E
Q119H/V137D/M140E
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mutant is much less sensitive to antizyme inhibition than wild-type, pattern similar to mutant Q119H/A124R/N125D/Q129D/E136V/V137D/M140E
G121Y
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Gly121 is buried in the dimer-dimer interface, mutation of Gly121 into Tyr prevents association of dimers into dodecamers, G121Y shows similar activity as native ODC
A123S
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mutation in a conserved residue of the antizyme-binding region, mutant is somehow more resistant to degradation than wild-type. About 130% of wild-type activity
A457W
C360A
C441A
C441A/A442C
site-directed mutagenesis, swapping the cysteine residue with either of the two adjacent residues stabilizes ODC, reducing degradation from 25% to less than 5% in each case
C441S
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the isosteric alteration of the enzyme completely stabilizes ODC even in the presence of excess antizyme
E138A
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mutation in a conserved residue of the antizyme-binding region, mutant is degraded as efficientlyas wild-type. Almost complete loss of activity. Mutation diminishes the formation of enzyme dimers
E138A/L139S
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mutation prevents the degradation by the proteasome, complete loss of activity. Mutation diminishes the formation of enzyme dimers
K115A
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mutation in a conserved residue of the antizyme-binding region. About 30 of wild-type activity. Mutation diminishes the formation of enzyme dimers
K115A/K141A
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degradation by the proteasome occurs with similar efficiency as for wild-type. About 10% of wild-type activity. Mutation diminishes the formation of enzyme dimers
K141A
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mutation in a conserved residue of the antizyme-binding region. About 25% of wild-type activity
K69A
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mutant enzyme K69A shows a changed spectrum and a 550fold decrease in the turnover/Km value
L139A
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mutation in a conserved residue of the antizyme-binding region, mutant is resistant to degradation. About 15% of wild-type activity. Mutation diminishes the formation of enzyme dimers
L139S
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mutation in a conserved residue of the antizyme-binding region, mutant is resistant to degradation. Almost complete loss of activity
S440C/C441S
site-directed mutagenesis, swapping the cysteine residue with either of the two adjacent residues stabilizes ODC, reducing degradation from 25% to less than 5% in each case. The stabilization of ODC by the C441S mutation implies that the hydroxy group cannot replicate the functional properties of the thiol of Cys441
S456A
S73A
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no AdometDC, i.e. ec4.1.1.50, activity, 90% of wild-type ODC activity
C360A
D364E
the mutant shows almost no activity compared to the wild type enzyme
F397A
K294A
K69A
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ODC copurifies with amines, e.g. putrescine, similar affinity for pyridoxal 5'-phosphate as wild-type
K69R
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0.02% of wild-type activity, binds diamines and amino acids with higher affinity than wild-type ODC
S396A
the mutant shows about 2fold increased activity compared to the wild type enzyme
additional information
A457W
site-directed mutagenesis, the mutation does not stabilize the enzyme
C360A
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mutation C360A 26fold reduces the specificity constant and 2fold decreases the Km
C360A
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mutant enzyme C360A is completely resistant to inactivation by (R,R)-delta-methyl-alpha-acetylenicputrescine and is much less sensitive than the wild type enzyme to alpha-monofluoromethyldehydromethylornithine
C441A
construction of a duplicated cODC, from fusing ODC to a tandem cODC-cODCC441A at its C-terminus, with the first ODC copy being wild-type including a wild-type Cys441, and the distal C-terminal copy of cODC carrying mutation C441A
C441A
site-directed mutagenesis, the mutation stabilizes the enzyme but also profoundly reduces its activity
S456A
site-directed mutagenesis, the mutation does not stabilize the enzyme
K294A
mutation increases the disorder of residues Leu166 - Ala172 and increases the population of inactive conformations
additional information
construction of chimeric mutant enzymes consisting of sequence from the Crithidia fasciculata and the Leishmania donovani enzymes, e.g. exchanging the C-terminal PEST region, which show altered protein stability compared to the wild-type enzymes, overview
additional information
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construction of chimeric mutant enzymes consisting of sequence from the Crithidia fasciculata and the Leishmania donovani enzymes, e.g. exchanging the C-terminal PEST region, which show altered protein stability compared to the wild-type enzymes, overview
additional information
enzyme overexpression in Dictyostelium discoideum cells inhibits cell proliferation and leads to mild developmental defect, because high putrescine levels are detrimental for cell proliferation, phenotype, overview
additional information
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enzyme overexpression in Dictyostelium discoideum cells inhibits cell proliferation and leads to mild developmental defect, because high putrescine levels are detrimental for cell proliferation, phenotype, overview
additional information
the wild-type enzyme's substrate binding site is mutated at three amino acids D332, D361, and Y323 leading to reduced substrate binding activity, computational modelling, overview
additional information
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the wild-type enzyme's substrate binding site is mutated at three amino acids D332, D361, and Y323 leading to reduced substrate binding activity, computational modelling, overview
additional information
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adenovirus-mediated expression of both antisense ornithine decarboxylase and S-adenosylmethionine decarboxylase in A-549 cells injected into BALB/c nude male mice inhibits lung cancer cell growth in the mouse tumor, overview
additional information
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ODC transgenic rodent models of skin carcinogenesis, phenotypes, overview
additional information
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construction of transgenic mice expressing the human MYCN gene under the control of the rat tyrosine hydroxylase promoter, targeting ornithine decarboxylase impairs development of MYCN-amplified neuroblastoma
additional information
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ornithine decarboxylase overexpression prevents TNF-alpha- and methotrexate-induced apoptosis via reduction of reactive oxygen species, e.g. in curcumin-induced apoptosis, ODC overexpression prevents cytochrome c release and the activation of caspase-9 and caspase-3 following curcumin treatment, overview
additional information
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overexpression of ODC leads to restored MMP-9 secretion involving stimulation by TNF-alpha, and reduced MMP-9 activity and expression during macrophage-like differentiation
additional information
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overexpression of ODC prevents apoptosis induced by tumor necrosis factor-alpha and methotrexate. ODC overexpressing cells seem to overcome the G1 arrest and G2/M arrest, caused by VP-16 and TAX, respectively, and keep on the cell cycle rolling. Overexpression of ODC increases the expression of Cyclin A, D, E and Cdk4 and the enzyme activity of Cdk1 and Cdk2 after the treatment of VP-16 and TAX, respectively
additional information
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positive correlation between the level of ODC mRNA and the staging of tumors in MDA-MB-231 cells expressing an ODC antisense construct. Gene transfection of rAd-ODC/Ex3as markedly down-regulates expression of ODC and cyclin D1, resulting in suppression of proliferation and cell cycle arrest at G0-G1 phase, and the inhibition of colony formation, an anchorage-independent growth pattern, and the migratory ability of MDA-MB-231 cells. rAd-ODC/Ex3as also markedly reduces the concentration of putrescine, but not spermidine or spermine, in MDA-MB-231 cells
additional information
ODC paralogue ODCp-overexpressing cells display elevated ODC and polyamine uptake activity as compared with control cells
additional information
construction of chimeric mutant enzymes consisting of sequence from the Crithidia fasciculata and the Leishmania donovani enzymes, e.g. exchanging the C-terminal PEST region, which show altered protein stability compared to the wild-type enzymes, overview
additional information
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construction of chimeric mutant enzymes consisting of sequence from the Crithidia fasciculata and the Leishmania donovani enzymes, e.g. exchanging the C-terminal PEST region, which show altered protein stability compared to the wild-type enzymes, overview
additional information
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construction of conditionally lethal DELTAodc null mutants by double targeted gene replacement within a virulent strain. Parasitemias of DELTAodc null mutants are reduced by 6 and 3 orders of magnitude, respectively, in livers and spleens of BALB/c mice showing compromised infectivity phenotypes, overview. Nutritional phenotypes and Survival of DELTAodc parasites in peritoneal macrophages, overview
additional information
removal of the N-terminal extended region of LdODC results in improved stability of the protein, but the truncated enzyme LdODC does not show any activity
additional information
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removal of the N-terminal extended region of LdODC results in improved stability of the protein, but the truncated enzyme LdODC does not show any activity
additional information
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construction of conditionally lethal DELTAodc null mutants by double targeted gene replacement within a virulent strain. Parasitemias of DELTAodc null mutants are reduced by 6 and 3 orders of magnitude, respectively, in livers and spleens of BALB/c mice showing compromised infectivity phenotypes, overview. Nutritional phenotypes and Survival of DELTAodc parasites in peritoneal macrophages, overview
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additional information
Leishmania guyanensis odc overexpressor cell lines are generated to investigate the contribution of the gene to the trivalent antimony (SbIII)-resistance phenotype. The ODC-overexpressors parasites present an increase of 2fold in SbIII-resistance index, when compared with the wild-type line. Pharmacological inhibition of ODC with the specific inhibitor alpha-difluoromethylornithine (DFMO) increases the antileishmanial effect of SbIII in all cell lines. Nevertheless the ODC-overexpressor is still more resistant to SbIII than the parental cell line
additional information
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Leishmania guyanensis odc overexpressor cell lines are generated to investigate the contribution of the gene to the trivalent antimony (SbIII)-resistance phenotype. The ODC-overexpressors parasites present an increase of 2fold in SbIII-resistance index, when compared with the wild-type line. Pharmacological inhibition of ODC with the specific inhibitor alpha-difluoromethylornithine (DFMO) increases the antileishmanial effect of SbIII in all cell lines. Nevertheless the ODC-overexpressor is still more resistant to SbIII than the parental cell line
additional information
Leishmania guyanensis BR/1985/M9945
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Leishmania guyanensis odc overexpressor cell lines are generated to investigate the contribution of the gene to the trivalent antimony (SbIII)-resistance phenotype. The ODC-overexpressors parasites present an increase of 2fold in SbIII-resistance index, when compared with the wild-type line. Pharmacological inhibition of ODC with the specific inhibitor alpha-difluoromethylornithine (DFMO) increases the antileishmanial effect of SbIII in all cell lines. Nevertheless the ODC-overexpressor is still more resistant to SbIII than the parental cell line
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additional information
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construction of enzyme overexpressing and enzyme-deficient transgenic mice, deletion of the 5 terminal residues 457-461 also stabilizes ODC but to a lesser extent than removing the terminal 37 residues or mutation of Cys441
additional information
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transgenic mice overexpressing ODC in hair follicle keratinocytes using keratin promotors are much more sensitive than littermate controls to DMBA-induced carcinogenesis, and do not require treatment with a tumor promoter to develop tumors, overview
additional information
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construction of ODC-overexpressing K6/ODC transgenic mice in which a keratin 6 promoter directs the expression of ODC to the outer root sheath cells of hair follicles in the skin. Although elevated levels of ODC and polyamines stimulate proliferation of keratinocytes, mutant Ker/ODC cells undergo apoptotic cell death within days of primary culture unlike wild-type Ker/Norm cells that continue to proliferate. Ker/ODC also displays increased generation of H2O2, acroleinlysine conjugates, and protein oxidation products as well as polyamine-dependent DNA damage, phenotype, overview
additional information
construction of several truncated enzyme mutants, mutant protein stabilities, overview
additional information
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construction of several truncated enzyme mutants, mutant protein stabilities, overview
additional information
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establishment of an embryonic stem cell clone with disrupted Azin1 gene by the gene trap technique, construction of a mutant mouse line using these trapped embryonic stem cells. Homozygous mutant mice die at P0 with abnormal liver morphology, deletion of Azin1 in homozygous mice results in the degradation of ODC, and reduced the biosynthesis of putrescine and spermidine, genotype and phenotype, overview
additional information
construction of myeloid-specific Odc deletion mutant mice (OdcDELTAmye). Increased mRNA expression of Nos2, Tnfa, Il1b, Il12a, Ccl5 and Cxcl10 is demonstrated in dextran sulfate sodium-treated OdcDELTAmye versus Odcfl/fl mice, while expression levels of the M2 markers, Arg1 and Chil3, are comparable in colonic tissues of dextran sulfate sodium-treated Odcfl/fl and OdcDELTAmye mice. OdcDELTAmye mice are protected from colitis-associated carcinogenesis
additional information
in ODC-ER transgenic mice, in which an involucrin promoter directs the expression of the inducible ODC cDNA fused in frame to a 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor ligand binding domain to the suprabasal epidermis, elevated expression of ornithine decarboxylase (ODC), the regulatory enzyme in polyamine biosynthesis, targeted to the epidermis is sufficient to promote skin tumor development following a single subthreshold dose of dimethylbenz(a)anthracene (DMBA). ODC-ER transgenic mice and their normal littermates have been backcrossed into either the FVB or C57Bl/6 background for at least 10 generations. An inducible Cre-activated bi-transgenic mouse system is used to track hair follicle bulge stem cells and their progeny. K15-CrePR1 transgenic mice, that express CrePR1 under the control of a keratin 15 (K15) promoter, are generated to target expression of genes to the adult epidermal stem cells located in the hair follicle bulge cells. K15-CrePR1 transgenic mice are crossed with Cre-responsive R26R transgenic mice, that express lacZ under the control of a ubiquitous promoter, after Cre-mediated removal of an inactivating sequence. The resulting K15-CrePR1-R26R bitransgenic mice are treated topically with RU486 to induce expression of lacZ in the bulge stem cells of the skin. Polyamine oxidase inhibitor MDL72527 is applied. MDL72527 treatment increases skin tumor growth and conversion to carcinomas in DMBA-initiated ODC-ER mice, overview
additional information
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in ODC-ER transgenic mice, in which an involucrin promoter directs the expression of the inducible ODC cDNA fused in frame to a 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor ligand binding domain to the suprabasal epidermis, elevated expression of ornithine decarboxylase (ODC), the regulatory enzyme in polyamine biosynthesis, targeted to the epidermis is sufficient to promote skin tumor development following a single subthreshold dose of dimethylbenz(a)anthracene (DMBA). ODC-ER transgenic mice and their normal littermates have been backcrossed into either the FVB or C57Bl/6 background for at least 10 generations. An inducible Cre-activated bi-transgenic mouse system is used to track hair follicle bulge stem cells and their progeny. K15-CrePR1 transgenic mice, that express CrePR1 under the control of a keratin 15 (K15) promoter, are generated to target expression of genes to the adult epidermal stem cells located in the hair follicle bulge cells. K15-CrePR1 transgenic mice are crossed with Cre-responsive R26R transgenic mice, that express lacZ under the control of a ubiquitous promoter, after Cre-mediated removal of an inactivating sequence. The resulting K15-CrePR1-R26R bitransgenic mice are treated topically with RU486 to induce expression of lacZ in the bulge stem cells of the skin. Polyamine oxidase inhibitor MDL72527 is applied. MDL72527 treatment increases skin tumor growth and conversion to carcinomas in DMBA-initiated ODC-ER mice, overview
additional information
Odc knockdown in myeloid cells, generation of mutant mice with a myeloid-specific deletion of gene Odc, by crossing C57BL/6 Odcfl/fl mice with myeloid-specific LysMcre/cre driver mice, yielding the OdcDELTAmye mice
additional information
purified [35S]methionine-labeled recombinant His6-TEV (tobacco etch virus)-FLAG-ODC is generated and degraded in vitro
additional information
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in ODC-ER transgenic mice, in which an involucrin promoter directs the expression of the inducible ODC cDNA fused in frame to a 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor ligand binding domain to the suprabasal epidermis, elevated expression of ornithine decarboxylase (ODC), the regulatory enzyme in polyamine biosynthesis, targeted to the epidermis is sufficient to promote skin tumor development following a single subthreshold dose of dimethylbenz(a)anthracene (DMBA). ODC-ER transgenic mice and their normal littermates have been backcrossed into either the FVB or C57Bl/6 background for at least 10 generations. An inducible Cre-activated bi-transgenic mouse system is used to track hair follicle bulge stem cells and their progeny. K15-CrePR1 transgenic mice, that express CrePR1 under the control of a keratin 15 (K15) promoter, are generated to target expression of genes to the adult epidermal stem cells located in the hair follicle bulge cells. K15-CrePR1 transgenic mice are crossed with Cre-responsive R26R transgenic mice, that express lacZ under the control of a ubiquitous promoter, after Cre-mediated removal of an inactivating sequence. The resulting K15-CrePR1-R26R bitransgenic mice are treated topically with RU486 to induce expression of lacZ in the bulge stem cells of the skin. Polyamine oxidase inhibitor MDL72527 is applied. MDL72527 treatment increases skin tumor growth and conversion to carcinomas in DMBA-initiated ODC-ER mice, overview
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additional information
in vivo knockdown of translation of ODC1 and ADC (EC 4.1.1.19) mRNAs individually and in combination. Double knockdown of ODC1 and ADC (MAO-ODC1:ADC) results in two phenotypes (a or b) of conceptuses: 33% of conceptuses appear to be morphologically and functionally normal (phenotype a) and 67% of the conceptuses present an abnormal morphology and functionality (phenotype b). Furthermore, MAO-ODC1:ADC (a) conceptuses have greater tissue concentrations of agmatine, putrescine, and spermidine than MAO control conceptuses, while AO-ODC1:ADC (b) conceptuses only have greater tissue concentrations of agmatine. Uterine flushes from ewes with MAO-ODC1:ADC (a) have greater amounts of arginine, aspartate, tyrosine, citrulline, lysine, phenylalanine, isoleucine, leucine, and glutamine, while uterine flushes of ewes with MAO-ODC1:ADC (b) conceptuses have lower amount of putrescine, spermidine, spermine, alanine, aspartate, glutamine, tyrosine, phenylalanine, isoleucine, leucine, and lysine. Phenotypes, overview
additional information
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in vivo knockdown of translation of ODC1 and ADC (EC 4.1.1.19) mRNAs individually and in combination. Double knockdown of ODC1 and ADC (MAO-ODC1:ADC) results in two phenotypes (a or b) of conceptuses: 33% of conceptuses appear to be morphologically and functionally normal (phenotype a) and 67% of the conceptuses present an abnormal morphology and functionality (phenotype b). Furthermore, MAO-ODC1:ADC (a) conceptuses have greater tissue concentrations of agmatine, putrescine, and spermidine than MAO control conceptuses, while AO-ODC1:ADC (b) conceptuses only have greater tissue concentrations of agmatine. Uterine flushes from ewes with MAO-ODC1:ADC (a) have greater amounts of arginine, aspartate, tyrosine, citrulline, lysine, phenylalanine, isoleucine, leucine, and glutamine, while uterine flushes of ewes with MAO-ODC1:ADC (b) conceptuses have lower amount of putrescine, spermidine, spermine, alanine, aspartate, glutamine, tyrosine, phenylalanine, isoleucine, leucine, and lysine. Phenotypes, overview
additional information
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in vivo knockdown of translation of ODC1 and ADC (EC 4.1.1.19) mRNAs individually and in combination. Double knockdown of ODC1 and ADC (MAO-ODC1:ADC) results in two phenotypes (a or b) of conceptuses: 33% of conceptuses appear to be morphologically and functionally normal (phenotype a) and 67% of the conceptuses present an abnormal morphology and functionality (phenotype b). Furthermore, MAO-ODC1:ADC (a) conceptuses have greater tissue concentrations of agmatine, putrescine, and spermidine than MAO control conceptuses, while AO-ODC1:ADC (b) conceptuses only have greater tissue concentrations of agmatine. Uterine flushes from ewes with MAO-ODC1:ADC (a) have greater amounts of arginine, aspartate, tyrosine, citrulline, lysine, phenylalanine, isoleucine, leucine, and glutamine, while uterine flushes of ewes with MAO-ODC1:ADC (b) conceptuses have lower amount of putrescine, spermidine, spermine, alanine, aspartate, glutamine, tyrosine, phenylalanine, isoleucine, leucine, and lysine. Phenotypes, overview
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additional information
enzyme activity is reduced up to 95% when the deletion of a parasite-specific insert occurs within the respective domain. Inserts mediate specific physical interactions between the two domains of the bifunctional enzyme that are essential for both S-adenosylmethionine decarboxylase and ornithine decarboxylase activities
additional information
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enzyme activity is reduced up to 95% when the deletion of a parasite-specific insert occurs within the respective domain. Inserts mediate specific physical interactions between the two domains of the bifunctional enzyme that are essential for both S-adenosylmethionine decarboxylase and ornithine decarboxylase activities
additional information
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development of the bla gene-based organism identification, confirmed by 16S rDNA and rpoB sequencing, ODC detection provides a reliable Raoultella identification method widely available as not requiring sequencing equipment, overview
additional information
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overexpression of yeast antizyme in Saccharomyces cerevisiae results in polyamine depletion and growth inhibition of yeast cells mainly through inhibiting ODC. Overexpression of mammalian antizyme in mammalian cells leads to growth arrest due to polyamine depletion, being an outcome of reduced ODC activity and polyamine uptake. Construction of an ODC mutant lacking the first 47 amino acids and fusion to the C-terminus of mammalian ODC
additional information
the stability of yODC in mammalian cells is not a result of the absence of a compatible antizyme Az or lack of a C-terminal-destabilizing signal found on the mammalian enzyme, but is rather a result of the inability of the mammalian proteasome to degrade yeast ODC
additional information
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the stability of yODC in mammalian cells is not a result of the absence of a compatible antizyme Az or lack of a C-terminal-destabilizing signal found on the mammalian enzyme, but is rather a result of the inability of the mammalian proteasome to degrade yeast ODC
additional information
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the stability of yODC in mammalian cells is not a result of the absence of a compatible antizyme Az or lack of a C-terminal-destabilizing signal found on the mammalian enzyme, but is rather a result of the inability of the mammalian proteasome to degrade yeast ODC
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additional information
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inhibition of ODC translation by antisense morpholino oligos, xODC mo, abolishes ODC activity increase during oocyte maturation
