Disease relevance of Azi1

• Besides, the treatment of Fc gamma RII(-) thymoma cells BW5147 with 5-azacytidine induced a hypomethylation of the beta Fc gamma R gene concomitantly with the transcription of that gene as seen by Northern blotting and the expression of functional Fc gamma RII [1].
• Interleukin-3 increases the incidence of 5-azacytidine-induced thymic lymphomas in pBOR-Il-3 mice [2].
• Comparison of the incidence of 5-azacytidine-induced exencephaly between MT/HokIdr and Slc:ICR mice [3].
• Opposite effects of the maternal immune system activated by interleukin-1beta vs. PSK and OK432 on 5-azacytidine-induced birth defects [4].

High impact information on Azi1

• 5-Azacytidine-induced uncoupling of differentiation and tumorigenicity in a murine cell line [5].
• Inhibitors of tumor promotion, dexamethasone, fluocinolone acetonide, retinoic acid, and antipain, also inhibited the 5-azacytidine-induced differentiation [6].
• Both IFN gamma- and 5-azacytidine-induced placental class II expression have been reported in mice by other scientists, however, which made it important to further clarify this issue [7].
• 5-Azacytidine induced Bxv-1-dependent virus production without inhibiting terminal B-cell differentiation [8].
• Incubation of mouse thymocytes with arabinosylcytosine or 5-azacytidine induced dose-dependent internucleosomal DNA cleavage followed by cell death [9].

Chemical compound and disease context of Azi1

• The primary cause of 5-azacytidine-induced exencephaly is considered to be attributable to a powerful cell-killing action of 5-azacytidine and the subsequent loss of germinal cells in the neurectoderm of the head folds [10].

Biological context of Azi1

• 5-azacytidine-induced re-expression of alleles on the inactive X chromosome in a hybrid mouse cell line [11].
• 5-Azacytidine induced myogenesis in a differentiation defective cell line [12].
• Possible involvement of DNA methylation in 5-azacytidine-induced neuronal cell apoptosis [13].

References