EC Number   |
General Information |
Reference |
|---|
    2.3.1.57 | evolution |
phylogenetic analysis of ssat-like genes dividing the genes into 3 clusters, comparison of zebrafish and human gene sequences and regulation, overview |
737100 |
| 2.3.1.57 | evolution |
phylogenetic analysis of ssat-like genes dividing the genes into 3 clusters, comparison of zebrafish and human gene sequences and regulation, overview. Zebrafish ssat1 homologues are paralogous genes which experience subfunctionalization in their function and regulation |
737100 |
| 2.3.1.57 | evolution |
the enzyme is a member of the Gcn5-related N-acetyltransferase superfamily |
-, 736639 |
| 2.3.1.57 | evolution |
the enzyme is a member of the Gcn5-related N-acetyltransferase superfamily. The open and intermediate states of ligand-free enzyme have a unique open dodecameric ring. The SpeG dodecamer is asymmetric except for the one 2fold axis and is unlike any known dodecameric structure. The SpeG dodecamer is conserved in different bacterial species, structure analysis and comparisons, overview |
-, 736641 |
| 2.3.1.57 | malfunction |
acetylation of triethylenetetramine is increased in SSAT1-overexpressing mice compared with wild-type mice, but SSAT1-deficient mice metabolize TETA at the same rate as the wild-type mice, due to the activity of thialysine acetyltransferase (SSAT2) |
736007 |
| 2.3.1.57 | malfunction |
altered expression of SAT1 in the polyamine stress response, across multiple brain regions between control individuals and depressed individuals who have died by suicide, overview |
701611 |
| 2.3.1.57 | malfunction |
body weights, femur and tibia lengths and diameters, and ash weights of tibia of wild-type, SSAT overexpressing, and SSAT deficient female mice, overview. Enzyme overexpressing SSAT mice have an altered skeletal appearance with increased collagen cleavage and reduced bone strength compared to the wild-type. Engineered mice also show altered differentiation of mesenchymal stromal cells to osteoblasts. Polyamine metabolism of SSAT osteoblasts is disturbed. Osteoblasts of SSAT overexpressing mice show significantly increased SSAT enzyme activity |
-, 737285 |
| 2.3.1.57 | malfunction |
enzyme inhibition also inhibits ongoing joint destruction. Enzyme inhibition or gene silencing by transfection of siRNA targeting SSAT-1 increases 5-methylcytosine levels/PMF-1 promoter methylation within 21 days |
735576 |
| 2.3.1.57 | malfunction |
enzyme knockout mice develop late-onset obesity on a high-fat diet with impaired cold-induced beige adipocyte biogenesis and energy expenditure |
757571 |
| 2.3.1.57 | malfunction |
key polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase1 overexpression in HEK293T cells via adenoviral vector leads to a rapid depletion of spermidine and spermine, arrest in cell growth and a decline in cell viability. AdSAT1-transduced cells reveal morphological changes commonly associated with apoptosis, including cell shrinkage, nuclear fragmentation, mitochondrial alteration, vacuolization and membrane blebbing. As polyamine analogues, alpha-methylspermidine and N1,N12-dimethylspermine that are not substrates for SAT1 partially restore growth and prevent apoptosis of AdSAT1-transduced cells. Inhibition of polyamine oxidases does not restore the growth of AdSAT1-transduced cells or block apoptosis. AdSAT1-transduction causes apoptosis by an intrinsic mitochondrial pathway, release of cytochrome c from mitochondria to cytoplasm concomitant with a decrease in the mitochondrial fraction in AdSAT1-transduced cells |
735640 |
