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Data show the the interplay between the enzyme ornithine decarboxylase (ODC) and two regulatory proteins: antizyme (Az) and inhibitor (AzIN).
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the effects of AZ on cell growth are independent of polyamines.
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Results show that ornithine decarboxylase antizyme 1 (OAZ1) simultaneously inhibits the proliferation and induces the differentiation of oral cancer cells.
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To further understand its functions in CML pathogenesis, OAZ1 was overexpressed, and PCR array analysis was used to monitor the expression of key genes commonly involved in leukemia development.
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Gene expression studies have identified altered expression of ornithine decarboxylase antizyme 1 in suicide completers with a history of mood disorders.
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This study demomistrated that H3K4me3 modification plays an important role in up regulation of AOAZ1 in prefrontal cortex.
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In the absence of amino acids, mTORC1 is inhibited, whereas mTORC2 is activated, leading to the inhibition of global protein synthesis and increased AZ1 synthesis via a cap-independent mechanism.
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AZ_95-176 is the minimal AZ peptide that is fully functioning in the binding of ODC and AZI and inhibition of their function.
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the differences in residues 125 and 140 in ODC and AZI are responsible for the differential antizyme-binding affinities
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Data show that OAZ promotes the removal of Mps1 from centrosomes, and centrosome overproduction caused by reducing OAZ activity requires Mps1.
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These data together demonstrate the existence of a c-Jun-dependent mechanism regulating the abundance of the antiapoptotic DNp73 in response to genotoxic stress.
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Human AZI is capable of acting as a general inhibitor for all members of the antizyme family.
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Special polymorphism haplotype of OAZ gene is associated with Chinese systemic lupus erythematosus. OAZ may suggest a new pathway for lupus.
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This study also suggests that highly expressed AZI may be partly responsible for increased ODC activity and cellular transformation.
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OAZ can alter the intensity and duration of the BMP4 stimulus through Smad6
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Ornithine decarboxylase antizyme 1 enhances the ability of UM1 human oral squamous cancer cells to repair DNA double-strand breaks by the nonhomologous end-joining pathway.
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Identified the OAZ1+2222A/G polymorphism as a potential genetic marker of vascular events.
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Yeast antizyme mediates degradation of yeast ornithine decarboxylase by yeast but not by mammalian proteasome: new insights on yeast antizyme
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Data suggest that residue 331 may play a major role in the dimerization of AZI, and the mutating Ser-331 to Tyr in AZI (AZI-S331Y) caused a shift from a monomer configuration to a dimer.
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antizyme expression requires programmed, ribosomal frameshifting
