Disease relevance of AZI1

• Treatment of KM20 cells with demethylating agent 5-azacytidine induced NT/N expression, suggesting a role for DNA methylation in silencing of NT/N in colon cancers [1].
• Strain AZ1 is much more versatile than most other Chromatiaceae with respect to electron donor and organic substrates [2].
• 5-Azacytidine induced few favorable responses; those that did occur usually were of poor quality and short duration and were associated with significant toxicity [3].

High impact information on AZI1

• Furthermore, in each case, treatment with the demethylating agent 5-azacytidine induced expression of the absent hMLH1 protein [4].
• BACKGROUND: Monoclonal anti-rabbit platelet glycoprotein (GP) IIb/IIIa antibody (AZ1) was adsorbed onto cellulose polymer-coated intracoronary stents to enhance their thromboresistance [5].
• Treatment of cancer cells with butyrate or 5-azacytidine induced strongly disialyl Lewis(a) expression, suggesting that histone deacetylation and/or DNA methylation may be involved in the silencing of the gene in cancers [6].
• Furthermore, 5-azacytidine induced the demethylation and the expression of the alpha Fc gamma R gene in the Fc gamma R(-) thymoma BW5147 [7].
• In RA-responsive and RA-resistant APL blasts, TSA and 5-azacytidine induced specific changes on the chromatin state at RA-target sites, increased the RA effect on promoter activity, endogenous RA-target gene expression and differentiation [8].

Biological context of AZI1

• To extend our cDNA project for accumulating basic information on unidentified human genes, we newly determined the sequences of 100 cDNA clones from a set of size-fractionated human adult and fetal brain cDNA libraries, and predicted the coding sequences of the corresponding genes, named KIAA1019 to KIAA1118 [9].
• AZ1 cDNA was encoded by 25 exons distributed within 25 kb of genomic DNA [10].
• Effects of complex extracellular matrices on 5-azacytidine-induced myogenesis [11].
• 5-Azacytidine-induced undercondensations in human chromosomes [12].
• Histological analysis showed that 5-azacytidine induced strong apoptosis of neural cells [13].

Anatomical context of AZI1

• Previous developmental studies suggested that AZ1 gene transcription begins in pachytene spermatocytes and that expression of the gene is induced in cultivated fibroblasts on treatment with 5-azacytidine, which is known to lead to the demethylation of genomic DNA [10].
• The AZ1 protein is localized to the preacrosome region of spermatids [10].
• Specific antibodies raised against the fusion protein including glutathione S-transferase revealed an approximately 130-kDa band of a translation product in testis and in cultured cells transfected with AZ1 cDNA in the expression vector on Western-blot analysis [14].
• Treatment of three of these cell lines with the methylation-interfering agent 5-azacytidine induced ZAC re-expression [15].
• Therefore, cytoskeleton seems to be an important cellular target for AZ-1 effect [16].

Associations of AZI1 with chemical compounds

• Spontaneous and 5-azacytidine-induced revertants of methionine-dependent tumor-derived and H-ras-1-transformed cells [17].
• This paper reports on potential cellular targets of azaspiracid-1 (AZ-1), a new phycotoxin that causes diarrhoeic and neurotoxic symptoms and whose mechanism of action is unknown [16].
• The effect of AZ-1 in cAMP is not extracellularly Ca(2+) dependent and insensitive to okadaic acid (OA) [16].
• 5-Azacytidine-induced 6-thioguanine resistance at the gpt locus in AS52 cells: cellular response [18].
• Inhibitory effects of cobalt chloride and cinnamaldehyde on 5-azacytidine-induced digital malformations in rats [19].

Other interactions of AZI1

• Treatment of GEO cells with the DNA methyltransferase inhibitor, 5 azacytidine induced RI expression and restored TGF-beta response [20].
• Assignment of the germ cell cyritestin gene 2 (CYRN2) to human chromosome 16q12.1 by fluorescence in situ hybridization to 5-azacytidine induced, partially decondensed chromosomes [21].
• Methylation of NT/N promoter constructs in vitro resulted in a 67-fold reduction in promoter activity, whereas treatment with the demethylating agent 5-azacytidine induced NT/N expression in Hep G2 cells, thus suggesting that DNA methylation plays a role in the expression of the gut endocrine gene NT/N [22].
• 5-Azacytidine induced promoter hypomethylation and resulted in SPAN-Xb expression, at both the transcript and protein levels [23].
• 5-azacytidine-induced increase in plasma prolactin levels of immature turkeys [24].

Analytical, diagnostic and therapeutic context of AZI1

• There was a significant improvement in the patency rate of AZ1-eluting stents compared with controls at both 2 hours (92% versus 46%, P = .034) and 28 days (100% versus 40%, P = .015) [5].

References