OAZ1

Last update 08 May 2025

Basic Info

Synonyms

AZ1, AZI, MGC138338

+ [4]

Introduction

Ornithine decarboxylase (ODC) antizyme protein that negatively regulates ODC activity and intracellular polyamine biosynthesis and uptake in response to increased intracellular polyamine levels. Binds to ODC monomers, inhibiting the assembly of the functional ODC homodimer, and targets the monomers for ubiquitin-independent proteolytic destruction by the 26S proteasome (PubMed:17900240, PubMed:26305948, PubMed:26443277). Triggers ODC degradation by inducing the exposure of a cryptic proteasome-interacting surface of ODC (PubMed:26305948). Stabilizes AZIN2 by interfering with its ubiquitination (PubMed:17900240). Also inhibits cellular uptake of polyamines by inactivating the polyamine uptake transporter. SMAD1/OAZ1/PSMB4 complex mediates the degradation of the CREBBP/EP300 repressor SNIP1. Involved in the translocation of AZIN2 from ER-Golgi intermediate compartment (ERGIC) to the cytosol (PubMed:12097147).

100 Clinical Results associated with OAZ1

100 Translational Medicine associated with OAZ1

0 Patents (Medical) associated with OAZ1

Literatures (Medical) associated with OAZ1

01 Aug 2024·Insect Molecular Biology

Ame‐miR‐1‐3p of bee venom reduced cell viability through the AZIN1/OAZ1‐ODC1‐polyamines pathway and enhanced the defense ability of honeybee (Apis mellifera L.)

Article

Author: Liu, Haifeng ; Jiang, Anan ; Huo, Yunfei ; Tian, Xue ; Liu, Jie ; Yang, Mingxian ; Wen, Jie ; Jiang, Jun ; Cao, Quanquan ; Guo, Jiazhong ; Yuan, Kangqi ; Wang, Xun

AbstractBee venom serves as an essential defensive weapon for bees and also finds application as a medicinal drug. MicroRNAs (miRNAs) serve as critical regulators and have been demonstrated to perform a variety of biological functions. However, the presence of miRNAs in bee venom needs to be confirmed. Therefore, we conducted small RNA sequencing and identified 158 known miRNAs, 15 conserved miRNAs and 4 novel miRNAs. It is noteworthy that ame‐miR‐1‐3p, the most abundant among them, accounted for over a quarter of all miRNA reads. To validate the function of ame‐miR‐1‐3p, we screened 28 candidate target genes using transcriptome sequencing and three target gene prediction software (miRanda, PITA and TargetScan) for ame‐miR‐1‐3p. Subsequently, we employed real‐time quantitative reverse transcription PCR (qRT‐PCR), Western blot and other technologies to confirm that ame‐miR‐1‐3p inhibits the relative expression of antizyme inhibitor 1 (AZIN1) by targeting the 3′ untranslated region (UTR) of AZIN1. This, in turn, caused ODC antizyme 1 (OAZ1) to bind to ornithine decarboxylase 1 (ODC1) and mark ODC1 for proteolytic destruction. The reduction in functional ODC1 ultimately resulted in a decrease in polyamine biosynthesis. Furthermore, we determined that ame‐miR‐1‐3p accelerates cell death through the AZIN1/OAZ1‐ODC1‐polyamines pathway. Our studies demonstrate that ame‐miR‐1‐3p diminishes cell viability and it may collaborate with sPLA2 to enhance the defence capabilities of honeybees (Apis mellifera L.). Collectively, these data further elucidate the defence mechanism of bee venom and expand the potential applications of bee venom in medical treatment.

01 Aug 2023·Animal genetics

Integrative genomics analysis highlights functionally relevant genes for equine behaviour.

Article

Author: McGivney, Beatrice A ; Hall, Thomas J ; MacHugh, David E ; Hill, Emmeline W ; Holtby, Amy R ; Han, Haige ; Katz, Lisa M ; Murphy, Keith J

Behavioural plasticity enables horses entering an exercise training programme to adapt with reduced stress. We characterised SNPs associated with behaviour in yearling Thoroughbred horses using genomics analyses for two phenotypes: (1) handler-assessed coping with early training events [coping] (n = 96); and (2) variation in salivary cortisol concentration at the first backing event [cortisol] (n = 34). Using RNA-seq derived gene expression data for amygdala and hippocampus tissues from n = 2 Thoroughbred stallions, we refined the SNPs to those with functional relevance to behaviour by cross-referencing to the 500 most highly expressed genes in each tissue. The SNPs of high significance (q < 0.01) were in proximity to genes (coping - GABARAP, NDM, OAZ1, RPS15A, SPARCL1, VAMP2; cortisol - CEBPA, COA3, DUSP1, HNRNPH1, RACK1) with biological functions in social behaviour, autism spectrum disorder, suicide, stress-induced anxiety and depression, Alzheimer's disease, neurodevelopmental disorders, neuroinflammatory disease, fear-induced behaviours and alcohol and cocaine addiction. The strongest association (q = 0.0002) was with NDN, a gene previously associated with temperament in cattle. This approach highlights functionally relevant genes in the behavioural adaptation of Thoroughbred horses that will contribute to the development of genetic markers to improve racehorse welfare.

15 Jun 2023·Journal of Cell Science

EPLIN-β is a novel substrate of ornithine decarboxylase antizyme 1 and mediates cellular migration

Article

Author: Neo, Suat Peng ; Li, Dan ; Gunaratne, Jayantha ; Sabapathy, Kanaga

ABSTRACTPolyamines promote cellular proliferation. Their levels are controlled by ornithine decarboxylase antizyme 1 (Az1, encoded by OAZ1), through the proteasome-mediated, ubiquitin-independent degradation of ornithine decarboxylase (ODC), the rate-limiting enzyme of polyamine biosynthesis. Az1-mediated degradation of other substrates such as cyclin D1 (CCND1), DNp73 (TP73) or Mps1 regulates cell growth and centrosome amplification, and the currently known six Az1 substrates are all linked with tumorigenesis. To understand whether Az1-mediated protein degradation might play a role in regulating other cellular processes associated with tumorigenesis, we employed quantitative proteomics to identify novel Az1 substrates. Here, we describe the identification of LIM domain and actin-binding protein 1 (LIMA1), also known as epithelial protein lost in neoplasm (EPLIN), as a new Az1 target. Interestingly, between the two EPLIN isoforms (α and β), only EPLIN-β is a substrate of Az1. The interaction between EPLIN-β and Az1 appears to be indirect, and EPLIN-β is degraded by Az1 in a ubiquitination-independent manner. Az1 absence leads to elevated EPLIN-β levels, causing enhanced cellular migration. Consistently, higher LIMA1 levels correlate with poorer overall survival of colorectal cancer patients. Overall, this study identifies EPLIN-β as a novel Az1 substrate regulating cellular migration.

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OAZ1

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