both cold and beta3-adrenergic receptor agonist CL-316,243 increase the expression of the enzyme in inguinal white adipose tissue and brown adipose tissue
high levels of enzyme expression are measured in tumor human cell lines, and in breast, prostate and lung tumor tissue. Increases in enzyme protein contents and gene expression in primary tumors is linked to a concomitant higher level of N1-acetylamantadine in urine of cancer patients upon ingestion of amantadine
induction of SSAT gene expression by combined quinoxalines and spermidine analogue treatment, overview. The cDDP-resistant human ovarian cell line, A2780/CP, shows defective expression and inducibility of SSAT by Spm analogues, when compared to the sensitive counterpart A2780
lithium induces enzyme expression in low and high risk groups for suicide commitment as well as in controls, but it has no effect in suicide completers. Differences in lithium-induced increase in SAT1 mRNA levels, overview
N',N''-diethylnorspermine, N'-ethyl-N''-[(cyclopropyl)-methy]-4,8-diazaundecane, and N'-ethyl-N''-[(cycloheptyl)methy]-4,8-diazaundecane treatments lead to high, moderate, or low induction of SSAT activity, respectively
spermidine/spermine N1-acetyltransferase SSAT, has an alternative mRNA splice variant SSATX which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants
SSAT mRNA expression peaks at threefold 24 h following lipopolysaccharide injection and returns to background levels by 48 h. The activity of SSAT correlates with its mRNA levels
the enzyme is upregulated by type I interferon beta stimulation (10000 units/ml for 16 h) or treatment with N1,N11-diethylnorspermine (0.01 mM for 16 h)
treatment of some human cancer cells, such as NCI H157 human lung carcinoma cells, with polyamine analogues N1,N12-bis(ethyl)spermine or N1,N11-bis-(ethyl)norspermine leads to a very high induction of SSAT. SSAT activity is induced via a variety of other stimuli, including toxins, hormones, cytokines, nonsteroidal anti-inflammatory agents, natural products, and stress pathways, and by ischemia-reperfusion injury. Effects of increased SSAT activity include death of pancreatic cells, blockage of regenerative tissue growth, behavioral changes, keratosis follicularis spinulosa decalvans, and hair loss. Polyamine analogs such as BE-3-3-3 or BE-3-4-3 cause a huge increase in Sat1 gene expression in certain tumor cells