Killing of oncogenically transformed cells by natural killer cells. However mutations in the gene GMDS 964-52-3 manufacturer coding for a key enzyme involved in the synthesis of GDP-fucose, a donor substrate for fucosyltransferases, further enhance tumor growth due to developed resistance to NK cells. Therefore, zebularine treatments of various cancer cell lines with relatively low fucosylation levels were performed in order to induce up-regulation of fucosylationrelated genes and consequently restore global fucosylation level. Interestingly, we observed in HeLa cells that the 364071-16-9 expression of fucosylated glycans was not altered following the 100 mM zebularine treatment. This finding could imply either the existence of an alternative fucosylation-independent immune-protective mechanism related to cervical carcinoma or that the fucosylation level itself in HeLa cells is not significantly lowered as a result of malignant transformation, thus abrogating the need for its restoration to normal levels. Further insight into the matter could potentially be gained by investigating mutations and expression levels of fucosylation-related genes followed by comparison of obtained results between cancerous and healthy tissue on one hand and cancer cells in culture on the other. In contrast to mostly unaffected fucosylated glycans, the simplest biantennary glycans were strongly up-regulated following zebularine treatment. However, the 72h-recovery in a drug-free medium resulted in almost complete restoration of normal values, arguing in favor of reversible covalent association between the DNMTs and the zebularine-containing DNA. Very importantly, there seemed to be a negative interplay between HATs and Hdac1/HDACs: the newly synthesized HAT, such as Cdyl, might be one direct regulator of HDAC degradation, so that the latter would provide a necessary HDACfree environment for histone hyperacetylation. Anyhow, the HAT in charge of histone hyperacetylation still requires inspection. Taken together, we put forward a working hypothesis of reprogramming in spermiogenesis as follows : After meiosis, transcription restarted in round spermatids, during this period, some essential and special HATs were generated. Next, HDACs catalyzed the deacetylation of histones, which in turn gave rise to the extensive dis
