Several other genes that may play a role in cell death and repair were regulated. SAT was up-regulated, and TXN and PRR13 were down-regulated. For this later protein, reduced expression in cells was correlated with increased sensitivity to taxane-induced cell death, a caspase-independent process characterized by the polymerization of tubulins to extraordinarily stable microtubules [27, 30] . TXN is the major carrier of redox potential in cells, and it is crucial for the defence of cells against oxidative-stressmediated apoptosis. TXN also regulates gene expression by increasing binding of redox-sensitive transcription factors like p53 [44] , NF-jB [25] , and the Nrf-2/polyamine- Table 2 . Information about the Paneth cell marker THOC4 is provided in reference [24] Transcriptional response to rotavirus 1319 inhibited SAT expression [23] . Therefore, up-regulation of SAT gene expression at 18 hpi may be directly related to down-regulation of TXN at 12 hpi. SAT is a rate-limiting enzyme in spermine/spermidine metabolism. Acetylation of these polyamines by SAT promoted their degradation and excretion [46] . Recently, it was reported that depletion of polyamines suppresses apoptosis in normal intestinal epithelial cells by AKT-kinase-mediated inhibition of CASP3 activity [50] . NB analysis showed that the increase in SAT mRNA expression coincided with the goblet cell marker KRT20. Therefore, it would be interesting to determine whether SAT expression in goblet cells can be stimulated by rotavirus infection and whether it plays a role in protecting these cells from apoptosis [8] . Interestingly, it was recently demonstrated that RNA viruses can directly modulate polyamine metabolism by regulation of SAT transcription and splicing [36] .