更新于：2024-11-01

SMOX

更新于：2024-11-01

基本信息

别名

C20orf16、dJ779E11.1、FLJ20746

+ [8]

简介

Flavoenzyme which catalyzes the oxidation of spermine to spermidine. Can also use N(1)-acetylspermine and spermidine as substrates, with different affinity depending on the isoform (isozyme) and on the experimental conditions. Plays an important role in the regulation of polyamine intracellular concentration and has the potential to act as a determinant of cellular sensitivity to the antitumor polyamine analogs. May contribute to beta-alanine production via aldehyde dehydrogenase conversion of 3-amino-propanal.

关联

项与 SMOX 相关的药物

MDL-72527

靶点

PAOX x SMOX

作用机制

PAOX inhibitors [+2]

在研机构

Veterans Administration Outpatient Clinic [+3]

原研机构

Aventis SA

在研适应症

糖尿病性视网膜病变 [+1]

非在研适应症

肿瘤

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

C9-4

靶点

SMOX

作用机制

SMOX抑制剂

在研机构

Nihon University

原研机构

Nihon University

在研适应症

脑缺血

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SMOX 相关的临床结果

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100 项与 SMOX 相关的转化医学

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0 项与 SMOX 相关的专利（医药）

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469

项与 SMOX 相关的文献（医药）

2024-11-01·Indian Journal of Medical Microbiology

Effect of electric current in viability, biofilm formation and antibiotic resistance of Pseudomonas aeruginosa: A systematic review

Review

作者: Chavez-Manini, Corinna Aimee ; Favila-Pérez, María Alejandra ; Arzate-Quintana, Carlos ; Quiñonez-Flores, Celia María ; Reza-López, Sandra Alicia ; Castillo-González, Alva Rocío ; Camarillo-Cisneros, Javier

BACKGROUNDThe bactericidal effect of electric current has been studied in various microorganisms such as Pseudomonas aeruginosa. The objective of this review is to identify the experimental parameters with the greatest antibacterial effect in the shortest time.METHODSLiterature search was conducted in the databases PubMed, Science Direct, and Google Scholar. Only original articles published between 2014-2023 were included, where the effect of electric current on viability, biofilm formation, and/or antibiotic resistance in P. aeruginosa was analyzed. Quality control criteria considered included specifying control and experimental groups, replicates performed, experimental parameters, and study limitations.RESULTSTen studies were included, which involved the strains Xen5, Xen41, PAO1 persistent cells, and PA14. An average reduction of 3.5 log in biofilm formation was observed in the included studies. The electric current parameters that achieved the greatest effect were 500 μA DC with platinum electrodes for 4 days [5.2-5.5 log], 200 μA intermittent with titanium electrodes for 4 days [4.99 log], and 150 ± 60 μA with silver electrodes for 24 hours [4 log]. Complete eradication of PAO1 persistent cells was achieved in 1 hour with a treatment of 70 μA/cm2 DC followed by 1.5 μg/mL tobramycin for 1 hour each.CONCLUSIONSThe bactericidal effect of electric current is proportional to the exposure time and current intensity. The electrode material influences the effectiveness of the treatment, possibly because of redox reactions, while differences are observed in the effect on the cell membrane and gene expression when using metallic or carbon electrodes, suggesting differences in the mechanism of action.

2024-10-24·Journal of Bacteriology

The relationship between pqs gene expression and acylhomoserine lactone signaling in Pseudomonas aeruginosa

Article

作者: Greenberg, E. Peter ; Smalley, Nicole E. ; Schaefer, Amy L. ; Soto-Aceves, Martín P.

ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa has complex quorum sensing (QS) circuitry, which involves two acylhomoserine lactone (AHL) systems, the LasI AHL synthase and LasR AHL-dependent transcriptional activator system and the RhlI AHL synthase-RhlR AHL-responsive transcriptional activator. There is also a quinoline signaling system [the Pseudomonas quinolone signal (PQS) system]. Although there is a core set of genes regulated by the AHL circuits, there is strain-to-strain variation in the non-core QS regulon. A size reduction of the QS regulon occurs in laboratory evolution experiments with the model strain PAO1. We used transcriptomics to test the hypothesis that reductive evolution in the PAO1 QS regulon can in large part be explained by a null mutation in pqsR , the gene encoding the transcriptional activator of the pqs operon. We found that PqsR had very little influence on the AHL QS regulon. This was a surprising finding because the last gene in the PqsR-dependent pqs operon, pqsE , codes for a protein, which physically interacts with RhlR, and this interaction is required for RhlR-dependent activation of some genes. We used comparative transcriptomics to examine the influence of a pqsE mutation on the QS regulon and identified only three transcripts, which were strictly dependent on PqsE. By using reporter constructs, we showed that the PqsE influence on other genes was dependent on experimental conditions and we have gained some insight about those conditions. This work adds to our understanding of the plasticity of the P. aeruginosa QS regulon and to the role PqsE plays in RhlR-dependent gene activation. IMPORTANCE Over many generations of growth in certain conditions, Pseudomonas aeruginosa undergoes a large reductive evolution in the number of genes activated by quorum sensing. Here, we rule out one plausible route of the reductive evolution: that a mutation in a transcriptional activator PqsR or the PqsR activation of pqsE , which codes for a chaperone for the quorum sensing signal-responsive transcription factor RhlR, explains the finding. We further provide information about the influence of PqsR and PqsE on quorum sensing in P. aeruginosa .

2024-10-01·Clinics and Research in Hepatology and Gastroenterology

Targeting SMOX for the treatment of hepatocellular carcinoma?

Article

作者: Cheng, Chunming ; Tao, Yulei

Dysregulation of the polyamine metabolism is common in different cancer types. SMOX is upregulated in hepatocellular carcinoma (HCC) but the relationship between SMOX and liver inflammation and fibrosis, remains unclear. In this issue of Clin Res Hepatol Gastroenterol, Hu and colleagues find targeting SMOX can alleviate liver cancer progression.