1.5.3.16: spermine oxidase
This is an abbreviated version!
For detailed information about spermine oxidase, go to the full flat file.
Word Map on EC 1.5.3.16
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1.5.3.16
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polyamine
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putrescine
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acetylpolyamine
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back-conversion
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n1-acetylspermine
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n1-acetylpolyamine
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3-aminopropanal
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acrolein
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benspm
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medicine
- 1.5.3.16
- polyamine
- putrescine
-
acetylpolyamine
-
back-conversion
- n1-acetylspermine
-
n1-acetylpolyamine
- 3-aminopropanal
- acrolein
-
benspm
- medicine
Reaction
Synonyms
AtPAO1, AtPAO4, AtPAO5, EC 1.5.3.11, Fms1 protein, GhPAO, hSMO, MmSMO, mSMO, mSMOalpha, mSMOmu, PAO, PAO1, PAO4, PAO5, PAO6, PAO7, PAOh1, PAOh1/SMO, SelPAO5, SMO, SMO(PAOh1), SMO/PAOh1, SMO5, SMOX, spermine oxidase, Spm oxidase, thermospermine oxidase
ECTree
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medicine
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the inhibitor MDL 72145 might be a chemical lead compound for the design of new chemotherapeutic agents against nematode infections
medicine
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alterations in the levels of spermine synthase SMS and spermine oxidase SMOX have previously been observed in brains of suicide completers. SMS and SMOX display several promoter haplotypes, without consistent effects of haplotype on expression levels in either the brain or in reporter gene assays performed in three different cell lines. There are no overall effects of epigenetic factors in determining expression, with the exception of a relationship between CpG methylation at one site in the promoter of SMOX and its expression in Brodmann area 8/9. The genetic and epigenetic factors examined in this study show little influence on the expression levels of SMS and SMOX
medicine
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both the expression level of SMO mRNA and SMO enzyme activity are significantly lower in breast cancer samples compared to nontumor samples
medicine
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treatment of human C-28/I2 chondrocytes with polyamine analogue N1,N11-diethylnorspermine rapidly induces spermidine/spermine N1-acetyltransferase and spermine oxidase activities, and down-regulates ornithine decarboxylase. The treatment does not provoke cell death and caspase activation when given alone for 24 h, but causes a caspase-3 and -9 dependent apoptosis in chondrocytes further exposed to cycloheximide. The simultaneous addition of N1,N11-diethylnorspermine and cycloheximide rapidly increases caspase activity in C-28/I2 cells in the absence of spermidine/spermineN1-acetyltransferase and spermine oxidase induction or significant reduction of polyamine levels
medicine
spermine oxidase is an important positive regulator of muscle fiber size whose expression is strongly downregulated by conditions that cause muscle atrophy. This reduction in spermine oxidase enables the atrophy process and represents a potential target for therapeutic intervention
medicine
the selective inhibitors of spermine oxidase represent an important tool for the development of novel anti-neoplastic drugs
medicine
spermine oxidase, as a hydrogen peroxide producer, may be involved in the oxidative stress during epilepsy. In a mouse model overexpressing SMOX specifically in the brain cortex, transgenic mice compared to controls showed a higher susceptibility towards pentylentetrazole and display an altered polyamine content with rise of 8-oxo-7,8-dihydro-2'-deoxyguanosine level, and an augmentation of system xc as a defence mechanism
medicine
during C2-C12 myotube differentiation, linear and circular RNA derived from SMOX gene show the same trend of expression. In atrophy, circSMOX levels significantly increase compared to the physiological state, in both in vitro and in vivo models. In both amyotrophic lateral sclerosis mouse models studied, an increased expression of circSMOX and a decreased expression of the linear SMOX mRNA are observed
medicine
SMOX is overexpressed in hepatocellular carcinoma cell lines and clinical hepatocellular carcinoma tissues. SMOX expression levels are gradually increased in normal liver, chronic hepatitis, and hepatocellular carcinoma tissues. Increased SMOX expression is correlated with poor clinical features of hepatocellular carcinoma. Positive SMOX expression in tumor tissues indicate worse overall survival of patients and shorter relapse-free survival. Knockdown of SMOX inhibits hepatocellular carcinoma cell proliferation, arrested cell cycle at S phase, and results in an increase of apoptosis