PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11485561-1 2001 Spermidine/spermine N(1)-acetyltransferase (SSAT), a key enzyme in mammalian polyamine catabolism, undergoes rapid turnover (half-life approx. Polyamines 77-86 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 11485561-7 2001 These results indicate that conformational changes brought about by the binding of polyamine analogues prevent the efficient polyubiquitination of SSAT, leading to a major increase in the amount of SSAT protein, and that alteration of the C-terminal end of the protein has a similar effect in preventing the productive interaction with an E2 or E3 component of the ubiquitin pathway. Polyamines 83-92 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 198-202 11485561-1 2001 Spermidine/spermine N(1)-acetyltransferase (SSAT), a key enzyme in mammalian polyamine catabolism, undergoes rapid turnover (half-life approx. Polyamines 77-86 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 11485561-7 2001 These results indicate that conformational changes brought about by the binding of polyamine analogues prevent the efficient polyubiquitination of SSAT, leading to a major increase in the amount of SSAT protein, and that alteration of the C-terminal end of the protein has a similar effect in preventing the productive interaction with an E2 or E3 component of the ubiquitin pathway. Polyamines 83-92 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 147-151 10978316-6 2000 Growth inhibition could not be prevented with exogenous polyamines due to a previously unrecognized ability of SSAT to rapidly acetylate influxing polyamines and thereby prevent restoration of the endogenous pools. Polyamines 56-66 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 111-115 11256947-0 2001 Characterization of the interaction between the transcription factors human polyamine modulated factor (PMF-1) and NF-E2-related factor 2 (Nrf-2) in the transcriptional regulation of the spermidine/spermine N1-acetyltransferase (SSAT) gene. Polyamines 76-85 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 229-233 11171097-4 2001 Spermidine/spermine N1-acetyltransferase (SSAT) regulates the polyamine degradation/excretion pathway. Polyamines 62-71 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 11171097-4 2001 Spermidine/spermine N1-acetyltransferase (SSAT) regulates the polyamine degradation/excretion pathway. Polyamines 62-71 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 11166157-1 2001 The growth inhibition that occurs in cisplatin-sensitive 2008 human ovarian cancer cells in response to the spermine analogue, N1,N12-bis(ethyl)spermine (BESpm), is associated with a potent induction of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in polyamine catabolism. Polyamines 280-289 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 203-243 10978316-1 2000 Acetylation of polyamines by spermidine/spermine N(1)-acetyltransferase (SSAT) has been implicated in their degradation and/or export out of the cell. Polyamines 15-25 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 29-71 10978316-1 2000 Acetylation of polyamines by spermidine/spermine N(1)-acetyltransferase (SSAT) has been implicated in their degradation and/or export out of the cell. Polyamines 15-25 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 73-77 10978316-2 2000 The relationship of SSAT to polyamine pool dynamics and cell growth is not yet clearly understood. Polyamines 28-37 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 20-24 10978316-6 2000 Growth inhibition could not be prevented with exogenous polyamines due to a previously unrecognized ability of SSAT to rapidly acetylate influxing polyamines and thereby prevent restoration of the endogenous pools. Polyamines 147-157 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 111-115 10978316-9 2000 Overall, the findings demonstrate that conditional overexpression of SSAT lowers polyamine pools, inhibits cell growth, and markedly enhances growth sensitivity to certain analogs. Polyamines 81-90 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 69-73 9717831-0 1998 Two active copies of the X-linked gene spermidine/spermine N1-acetyltransferase (SSAT) in a female lung cancer cell line are associated with an increase in sensitivity to an antitumor polyamine analogue. Polyamines 184-193 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 39-79 10212127-2 1999 Some of these polyamine analogues appear to produce their cell-type-specific cytotoxic activity through the superinduction of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 126-166 10212127-2 1999 Some of these polyamine analogues appear to produce their cell-type-specific cytotoxic activity through the superinduction of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 168-172 9852135-0 1998 The identification of a cis-element and a trans-acting factor involved in the response to polyamines and polyamine analogues in the regulation of the human spermidine/spermine N1-acetyltransferase gene transcription. Polyamines 90-100 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 156-196 9852135-0 1998 The identification of a cis-element and a trans-acting factor involved in the response to polyamines and polyamine analogues in the regulation of the human spermidine/spermine N1-acetyltransferase gene transcription. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 156-196 9852135-1 1998 The superinduction of spermidine/spermine N1-acetyltransferase (SSAT) gene has been associated with a cytotoxic response to a new class of antineoplastic polyamine analogues. Polyamines 154-163 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 22-62 9852135-1 1998 The superinduction of spermidine/spermine N1-acetyltransferase (SSAT) gene has been associated with a cytotoxic response to a new class of antineoplastic polyamine analogues. Polyamines 154-163 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 64-68 10419538-1 1999 The increased transcription and ultimate superinduction of the spermidine/spermine N(1)-acetyltransferase (SSAT) gene has been associated with the antineoplastic activity of several new antitumor polyamine analogues. Polyamines 196-205 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 63-105 10419538-1 1999 The increased transcription and ultimate superinduction of the spermidine/spermine N(1)-acetyltransferase (SSAT) gene has been associated with the antineoplastic activity of several new antitumor polyamine analogues. Polyamines 196-205 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 107-111 10419538-3 1999 Using the yeast two-hybrid system, a new transcriptional cofactor, polyamine-modulated factor-1 (PMF-1), has been identified as a partner protein of Nrf-2 that, in combination with Nrf-2, regulates the polyamine analogue-induced transcription of SSAT. Polyamines 67-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 246-250 10419538-6 1999 In addition to the transcriptional regulation of SSAT, PMF-1 or similar factors should be considered in the regulation of other polyamine-dependent genes. Polyamines 128-137 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 49-53 10430062-0 1999 The induction of spermidine/spermine N1-acetyltransferase (SSAT) is a common event in the response of human primary non-small cell lung carcinomas to exposure to the new antitumor polyamine analogue N1,N11-bis(ethyl)norspermine. Polyamines 180-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 17-57 10430062-0 1999 The induction of spermidine/spermine N1-acetyltransferase (SSAT) is a common event in the response of human primary non-small cell lung carcinomas to exposure to the new antitumor polyamine analogue N1,N11-bis(ethyl)norspermine. Polyamines 180-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 59-63 10430062-2 1999 The phenotype-specific activity of some of these analogues has been associated with the superinduction of the rate-limiting enzyme in polyamine catabolism spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 134-143 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 155-195 10430062-2 1999 The phenotype-specific activity of some of these analogues has been associated with the superinduction of the rate-limiting enzyme in polyamine catabolism spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 134-143 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 197-201 9724091-6 1998 The lower polyamine content of 2008 cells could be related to a higher degree of induction of spermidine/ spermine N1-acetyltransferase (SSAT) activity by BESPM in sensitive cells than in their resistant counterpart. Polyamines 10-19 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-135 9724091-6 1998 The lower polyamine content of 2008 cells could be related to a higher degree of induction of spermidine/ spermine N1-acetyltransferase (SSAT) activity by BESPM in sensitive cells than in their resistant counterpart. Polyamines 10-19 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 137-141 9717831-0 1998 Two active copies of the X-linked gene spermidine/spermine N1-acetyltransferase (SSAT) in a female lung cancer cell line are associated with an increase in sensitivity to an antitumor polyamine analogue. Polyamines 184-193 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-85 9717831-1 1998 The expression of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), has been associated with tumor sensitivity to antitumor polyamine analogues. Polyamines 22-31 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-90 9717831-1 1998 The expression of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), has been associated with tumor sensitivity to antitumor polyamine analogues. Polyamines 22-31 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 92-96 9717831-1 1998 The expression of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), has been associated with tumor sensitivity to antitumor polyamine analogues. Polyamines 155-164 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-90 9717831-1 1998 The expression of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), has been associated with tumor sensitivity to antitumor polyamine analogues. Polyamines 155-164 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 92-96 9717831-8 1998 Most importantly, the H727 line expressed high amounts of SSAT mRNA and protein in response to treatment with the polyamine analogue, N1,N12-bis(ethyl)spermine, a compound known to increase SSAT transcription in sensitive cell types. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 58-62 9717831-8 1998 Most importantly, the H727 line expressed high amounts of SSAT mRNA and protein in response to treatment with the polyamine analogue, N1,N12-bis(ethyl)spermine, a compound known to increase SSAT transcription in sensitive cell types. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 190-194 9717831-10 1998 These data suggest that both copies of the SSAT allele may be expressed and that the inappropriate expression of the second copy can lead to an increase in tumor sensitivity to polyamine analogues that induce SSAT. Polyamines 177-186 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 43-47 9717831-10 1998 These data suggest that both copies of the SSAT allele may be expressed and that the inappropriate expression of the second copy can lead to an increase in tumor sensitivity to polyamine analogues that induce SSAT. Polyamines 177-186 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 209-213 8706937-1 1996 Ornithine decarboxylase (ODC) and spermidine/ spermine N1-acetyltransferase (SSAT) are short-lived polyamine enzymes with rate-limiting roles in controlling polyamine biosynthesis and catabolism, respectively. Polyamines 99-108 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 34-75 9605436-6 1998 These results suggest that induction of SSAT may be a protective response to oxidative stress in mammalian cells facilitating removal of polyamines from the cell to prevent their toxic accumulation. Polyamines 137-147 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 40-44 9462700-4 1998 Specificity of the downregulation of MYC expression by BESpm treatment was demonstrated by comparison to effects on the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) and the polyamine biosynthetic enzyme ornithine decarboxylase (ODC). Polyamines 120-129 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 189-193 9480841-3 1998 In addition to polyamine degradation, spermidine/spermine acetyltransferase (SSAT) regulates interconversion pathway of spermine and spermidine to putrescine. Polyamines 15-24 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 77-81 8917345-1 1996 Induction of the polyamine acetylating enzyme, spermidine/spermine N1-acetyltransferase (SSAT), is one of several biochemical effects associated with the antiproliferative action of polyamine analogs such as N1, N11 diethylnorspermine (DENSPM). Polyamines 17-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-87 8917345-1 1996 Induction of the polyamine acetylating enzyme, spermidine/spermine N1-acetyltransferase (SSAT), is one of several biochemical effects associated with the antiproliferative action of polyamine analogs such as N1, N11 diethylnorspermine (DENSPM). Polyamines 17-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 8917345-1 1996 Induction of the polyamine acetylating enzyme, spermidine/spermine N1-acetyltransferase (SSAT), is one of several biochemical effects associated with the antiproliferative action of polyamine analogs such as N1, N11 diethylnorspermine (DENSPM). Polyamines 182-191 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-87 8917345-1 1996 Induction of the polyamine acetylating enzyme, spermidine/spermine N1-acetyltransferase (SSAT), is one of several biochemical effects associated with the antiproliferative action of polyamine analogs such as N1, N11 diethylnorspermine (DENSPM). Polyamines 182-191 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 8702554-1 1996 Polyamine catabolism is rate limited by spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 40-80 8702554-1 1996 Polyamine catabolism is rate limited by spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 82-86 9326648-3 1997 CPENSpm treatment results in the superinduction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) in sensitive cell types and has been demonstrated to induce programmed cell death (PCD). Polyamines 55-64 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 124-128 9326648-4 1997 The catalysis of polyamines by the SSAT/polyamine oxidase (PAO) pathway produces H2O2 as one product, suggesting that PCD produced by CPENSpm may be, in part, due to oxidative stress as a result of H2O2 production. Polyamines 17-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 35-39 9224814-1 1997 The spermine analog N1,N11-diethylnorspermine (DE-333, also known as DENSPM or BENSPM) is regarded as the most potent known inducer of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), increasing activity by more than 200- to 1000-fold in certain cell types. Polyamines 139-148 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 167-207 9224814-1 1997 The spermine analog N1,N11-diethylnorspermine (DE-333, also known as DENSPM or BENSPM) is regarded as the most potent known inducer of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT), increasing activity by more than 200- to 1000-fold in certain cell types. Polyamines 139-148 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 209-213 9115288-1 1997 The rapid turnover of spermidine/spermine N1-acetyltransferase (SSAT), a key enzyme in the regulation of polyamine levels, was found to be mediated via ubiquitination and the proteasomal system. Polyamines 105-114 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 22-62 9115288-1 1997 The rapid turnover of spermidine/spermine N1-acetyltransferase (SSAT), a key enzyme in the regulation of polyamine levels, was found to be mediated via ubiquitination and the proteasomal system. Polyamines 105-114 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 64-68 9115288-2 1997 SSAT degradation was blocked by the binding of polyamines or of the polyamine analog, N1,N12-bis(ethyl)spermine (BE-3-4-3), to the protein, providing a mechanism for the increase of SSAT activity in response to these agents. Polyamines 47-57 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 9115288-2 1997 SSAT degradation was blocked by the binding of polyamines or of the polyamine analog, N1,N12-bis(ethyl)spermine (BE-3-4-3), to the protein, providing a mechanism for the increase of SSAT activity in response to these agents. Polyamines 47-57 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 182-186 9115288-2 1997 SSAT degradation was blocked by the binding of polyamines or of the polyamine analog, N1,N12-bis(ethyl)spermine (BE-3-4-3), to the protein, providing a mechanism for the increase of SSAT activity in response to these agents. Polyamines 47-56 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 9115288-2 1997 SSAT degradation was blocked by the binding of polyamines or of the polyamine analog, N1,N12-bis(ethyl)spermine (BE-3-4-3), to the protein, providing a mechanism for the increase of SSAT activity in response to these agents. Polyamines 47-56 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 182-186 9115288-4 1997 These residues have previously been shown to reduce the affinity for the binding of polyamines to the SSAT protein, and these results indicate that the change in protein configuration brought about by this binding renders the protein resistant to proteasomal degradation. Polyamines 84-94 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 102-106 9115288-11 1997 The binding of BE-3-4-3 or polyamines is therefore likely to change the configuration of the SSAT protein in a way that prevents the exposure of the carboxyl-terminal region of the ubiquitinated protein to the proteasome. Polyamines 27-37 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 93-97 8916930-0 1996 Effects of polyamines, polyamine analogs, and inhibitors of protein synthesis on spermidine-spermine N1-acetyltransferase gene expression. Polyamines 11-21 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-121 8916930-0 1996 Effects of polyamines, polyamine analogs, and inhibitors of protein synthesis on spermidine-spermine N1-acetyltransferase gene expression. Polyamines 11-20 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-121 8916930-1 1996 The key polyamine catabolizing enzyme spermidine-spermine N1-acetyltransferase (SSAT) is among the few genes known to be inducible by the natural polyamines. Polyamines 8-17 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 38-78 8916930-1 1996 The key polyamine catabolizing enzyme spermidine-spermine N1-acetyltransferase (SSAT) is among the few genes known to be inducible by the natural polyamines. Polyamines 8-17 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 80-84 8916930-1 1996 The key polyamine catabolizing enzyme spermidine-spermine N1-acetyltransferase (SSAT) is among the few genes known to be inducible by the natural polyamines. Polyamines 146-156 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 38-78 8916930-1 1996 The key polyamine catabolizing enzyme spermidine-spermine N1-acetyltransferase (SSAT) is among the few genes known to be inducible by the natural polyamines. Polyamines 146-156 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 80-84 8916930-11 1996 Taken together, these findings suggest the involvement of two separate but possibly converging pathways in the regulation of SSAT mRNA, one mediated by polyamines and their analogs and the other mediated by a labile repressor of SSAT gene transcription and/or mRNA stabilization. Polyamines 152-162 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 125-129 8706937-1 1996 Ornithine decarboxylase (ODC) and spermidine/ spermine N1-acetyltransferase (SSAT) are short-lived polyamine enzymes with rate-limiting roles in controlling polyamine biosynthesis and catabolism, respectively. Polyamines 99-108 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 77-81 8706937-1 1996 Ornithine decarboxylase (ODC) and spermidine/ spermine N1-acetyltransferase (SSAT) are short-lived polyamine enzymes with rate-limiting roles in controlling polyamine biosynthesis and catabolism, respectively. Polyamines 157-166 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 34-75 8706937-1 1996 Ornithine decarboxylase (ODC) and spermidine/ spermine N1-acetyltransferase (SSAT) are short-lived polyamine enzymes with rate-limiting roles in controlling polyamine biosynthesis and catabolism, respectively. Polyamines 157-166 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 77-81 8706937-5 1996 This indicates post-transcriptional regulation which, due to the similarity between polyamine-mediated increases in SSAT activity and available mRNA, probably occurs at the level of mRNA translation. Polyamines 84-93 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 116-120 7720179-3 1995 Cytotoxicity is accompanied by a significant increase in expression of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) at the levels of activity and steady-state mRNA. Polyamines 75-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 144-148 8818232-9 1996 The unsymmetrically substituted polyamine analogue CHENSpm (3) and the phosphinate transition state analogue 5 represent the first functional, nonsuperinducing inhibitors of human SSAT. Polyamines 32-41 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 180-184 7577929-0 1995 Role of the carboxyl terminal MATEE sequence of spermidine/spermine N1-acetyltransferase in the activity and stabilization by the polyamine analog N1,N12-bis(ethyl)spermine. Polyamines 130-139 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-88 7577929-1 1995 Purified recombinant spermidine/spermine N1-acetyltransferase (SSAT) was found to be unstable in the absence of polyamines, but the loss of activity could be prevented or reversed by the addition of the polyamine analog and potential antitumor agent N1,N12-bis(ethyl)spermine (BE-3-4-3), which is known to be a potent inducer of SSAT in mammalian cells. Polyamines 112-122 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 21-61 7577929-1 1995 Purified recombinant spermidine/spermine N1-acetyltransferase (SSAT) was found to be unstable in the absence of polyamines, but the loss of activity could be prevented or reversed by the addition of the polyamine analog and potential antitumor agent N1,N12-bis(ethyl)spermine (BE-3-4-3), which is known to be a potent inducer of SSAT in mammalian cells. Polyamines 112-122 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 63-67 7577929-1 1995 Purified recombinant spermidine/spermine N1-acetyltransferase (SSAT) was found to be unstable in the absence of polyamines, but the loss of activity could be prevented or reversed by the addition of the polyamine analog and potential antitumor agent N1,N12-bis(ethyl)spermine (BE-3-4-3), which is known to be a potent inducer of SSAT in mammalian cells. Polyamines 112-121 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 21-61 7577929-1 1995 Purified recombinant spermidine/spermine N1-acetyltransferase (SSAT) was found to be unstable in the absence of polyamines, but the loss of activity could be prevented or reversed by the addition of the polyamine analog and potential antitumor agent N1,N12-bis(ethyl)spermine (BE-3-4-3), which is known to be a potent inducer of SSAT in mammalian cells. Polyamines 112-121 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 63-67 7577929-5 1995 These results indicate that the structure of SSAT contains a region that binds to the polyamine analog, BE-3-4-3, and that binding alters the configuration of the protein to prevent protease access to the region from amino acid residue 141 to the carboxyl terminal end (residue 171) of the SSAT. Polyamines 86-95 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 45-49 7559809-0 1995 Significant induction of spermidine/spermine N1-acetyltransferase without cytotoxicity by the growth-supporting polyamine analogue 1,12-dimethylspermine. Polyamines 112-121 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 25-65 7559809-1 1995 The superinduction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) has been implicated in the cell type-specific cytotoxic activity of some polyamine analogues. Polyamines 26-35 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-93 7559809-1 1995 The superinduction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) has been implicated in the cell type-specific cytotoxic activity of some polyamine analogues. Polyamines 26-35 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 95-99 7559809-1 1995 The superinduction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) has been implicated in the cell type-specific cytotoxic activity of some polyamine analogues. Polyamines 174-183 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-93 7559809-1 1995 The superinduction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) has been implicated in the cell type-specific cytotoxic activity of some polyamine analogues. Polyamines 174-183 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 95-99 7559809-2 1995 We now report that one polyamine analogue, 1,12-dimethylspermine (DMSpm), produces a large induction of SSAT with no significant effects on growth in the human large cell lung carcinoma line, NCl H157. Polyamines 23-32 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 104-108 7559809-6 1995 The current results suggest that significant induction of SSAT can occur in the absence of cytotoxicity when the inducing polyamine analogue can support growth and that increased SSAT activity alone is not sufficient for cytotoxicity to occur. Polyamines 122-131 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 58-62 8818232-1 1996 Polyamine analogues such as bis(ethyl)norspermine and N1-ethyl-N11-[(cyclopropyl)methyl]-4,8-diazaundecane (CPENSpm) act as inhibitors of the enzyme spermidine/spermine-N1-acetyltransferase (SSAT) in vitro and possess impressive antitumor activity against a number of cell lines. Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 149-189 8818232-1 1996 Polyamine analogues such as bis(ethyl)norspermine and N1-ethyl-N11-[(cyclopropyl)methyl]-4,8-diazaundecane (CPENSpm) act as inhibitors of the enzyme spermidine/spermine-N1-acetyltransferase (SSAT) in vitro and possess impressive antitumor activity against a number of cell lines. Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 191-195 8573111-1 1996 The expression of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in the catabolism of polyamines, is highly regulated by a number of factors including the natural polyamines and their analogues. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 18-58 8573111-1 1996 The expression of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in the catabolism of polyamines, is highly regulated by a number of factors including the natural polyamines and their analogues. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 60-64 8573111-1 1996 The expression of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in the catabolism of polyamines, is highly regulated by a number of factors including the natural polyamines and their analogues. Polyamines 190-200 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 18-58 8573111-1 1996 The expression of spermidine/spermine N1-acetyltransferase (SSAT), the rate-limiting enzyme in the catabolism of polyamines, is highly regulated by a number of factors including the natural polyamines and their analogues. Polyamines 190-200 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 60-64 8573111-2 1996 The phenotype-specific cytotoxicity that occurs in response to a class of polyamine analogues, the diethylpolyamines, is associated with a phenotype-specific superinduction of SSAT in human non-small-cell lung carcinomas, whereas in non-responding cell types, including the small-cell lung carcinomas, the superinduction of SSAT does not occur. Polyamines 74-83 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 176-180 8573111-2 1996 The phenotype-specific cytotoxicity that occurs in response to a class of polyamine analogues, the diethylpolyamines, is associated with a phenotype-specific superinduction of SSAT in human non-small-cell lung carcinomas, whereas in non-responding cell types, including the small-cell lung carcinomas, the superinduction of SSAT does not occur. Polyamines 74-83 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 324-328 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 212-222 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 212-222 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 113-122 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 7832759-1 1995 Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. Polyamines 113-122 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 7832759-11 1995 These results show that the increased transcription of the SSAT gene that occurs in the presence of polyamine analogues such as BESM is not sufficient for SSAT expression and that post-transcriptional regulation is critical for the control of SSAT content. Polyamines 100-109 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 59-63 8033120-0 1994 Immunohistochemical staining of human spermidine/spermine N1-acetyltransferase superinduced in response to treatment with antitumor polyamine analogues. Polyamines 132-141 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 38-78 8033120-1 1994 A superinduction of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT) accompanies the phenotype-specific cytotoxic response to a class of antitumor polyamine analogues in several important human solid tumor models. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 52-92 8033120-1 1994 A superinduction of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT) accompanies the phenotype-specific cytotoxic response to a class of antitumor polyamine analogues in several important human solid tumor models. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-98 8033120-1 1994 A superinduction of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT) accompanies the phenotype-specific cytotoxic response to a class of antitumor polyamine analogues in several important human solid tumor models. Polyamines 178-187 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 52-92 8033120-1 1994 A superinduction of the polyamine catabolic enzyme, spermidine/spermine N1-acetyltransferase (SSAT) accompanies the phenotype-specific cytotoxic response to a class of antitumor polyamine analogues in several important human solid tumor models. Polyamines 178-187 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-98 8033120-3 1994 Using this antiserum we demonstrate that polyamine analogue treatment in vitro or in vivo results in an induction of SSAT protein which is uniformly distributed throughout the cytoplasm of treated tumor cells. Polyamines 41-50 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-121 8033120-5 1994 Additionally, since clinical trials have begun on one of the SSAT-inducing polyamine analogues, this antiserum may be useful as a diagnostic tool in differentiating responsive and nonresponsive tumor cell populations in treated patients. Polyamines 75-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 61-65 7982492-5 1994 The SSAT-induced changes in cellular polyamine content resulted in a compensatory increase in the activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, i.e. the enzymes catalyzing the rate-limiting steps in polyamine biosynthesis. Polyamines 37-46 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 4-8 7982492-5 1994 The SSAT-induced changes in cellular polyamine content resulted in a compensatory increase in the activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, i.e. the enzymes catalyzing the rate-limiting steps in polyamine biosynthesis. Polyamines 231-240 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 4-8 7982492-6 1994 This is the first demonstration that a primary increase in SSAT activity will induce an interconversion-like change in the polyamine levels and the physiological role of SSAT is most likely to protect cells against too high concentrations of spermidine and spermine. Polyamines 123-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 59-63 8241266-2 1993 SSAT has recently been shown to be positively regulated in human cell lines by polyamines and their analogs at the level of mRNA accumulation. Polyamines 79-89 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 8411017-0 1993 Synthesis and evaluation of unsymmetrically substituted polyamine analogues as modulators of human spermidine/spermine-N1-acetyltransferase (SSAT) and as potential antitumor agents. Polyamines 56-65 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 99-139 8411017-0 1993 Synthesis and evaluation of unsymmetrically substituted polyamine analogues as modulators of human spermidine/spermine-N1-acetyltransferase (SSAT) and as potential antitumor agents. Polyamines 56-65 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 141-145 8411017-1 1993 Spermidine/spermine-N1-acetyltransferase (SSAT), the rate-limiting step in polyamine catabolism, is critical for the interconversion and modulation of cellular polyamines. Polyamines 75-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 8411017-1 1993 Spermidine/spermine-N1-acetyltransferase (SSAT), the rate-limiting step in polyamine catabolism, is critical for the interconversion and modulation of cellular polyamines. Polyamines 75-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 8411017-1 1993 Spermidine/spermine-N1-acetyltransferase (SSAT), the rate-limiting step in polyamine catabolism, is critical for the interconversion and modulation of cellular polyamines. Polyamines 160-170 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 8411017-1 1993 Spermidine/spermine-N1-acetyltransferase (SSAT), the rate-limiting step in polyamine catabolism, is critical for the interconversion and modulation of cellular polyamines. Polyamines 160-170 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 8411017-3 1993 Thus, terminally alkylated polyamines which modulate the cellular level of SSAT could be of great value for understanding the role of this enzyme both in analogue-mediated cytotoxicity and in overall cellular polyamine metabolism. Polyamines 27-37 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 75-79 8411017-3 1993 Thus, terminally alkylated polyamines which modulate the cellular level of SSAT could be of great value for understanding the role of this enzyme both in analogue-mediated cytotoxicity and in overall cellular polyamine metabolism. Polyamines 27-36 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 75-79 8500690-0 1993 Spermidine/spermine N1-acetyltransferase--the turning point in polyamine metabolism. Polyamines 63-72 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 8360194-1 1993 In MALME-3M human melanoma cells the polyamine analog N1,N12-bis(ethyl)spermine (BESPM) suppresses the key polyamine biosynthetic enzymes, ornithine and S-adenosylmethionine decarboxylase, and increases the polyamine catabolizing enzyme, spermidine/spermine N1-acetyl-transferase (SSAT) by more than 200-fold. Polyamines 37-46 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 238-279 8360194-1 1993 In MALME-3M human melanoma cells the polyamine analog N1,N12-bis(ethyl)spermine (BESPM) suppresses the key polyamine biosynthetic enzymes, ornithine and S-adenosylmethionine decarboxylase, and increases the polyamine catabolizing enzyme, spermidine/spermine N1-acetyl-transferase (SSAT) by more than 200-fold. Polyamines 37-46 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 281-285 8360194-9 1993 As indicated by actinomycin D studies, the SSAT mRNA half-life increased with BESPM treatment from 17 to 64 h. The natural polyamine, spermine, also increased SSAT mRNA (5.5-fold at 24 h) and behaved similarly to BESPM in inducing the appearance of the same three transcript forms. Polyamines 123-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 43-47 8360194-9 1993 As indicated by actinomycin D studies, the SSAT mRNA half-life increased with BESPM treatment from 17 to 64 h. The natural polyamine, spermine, also increased SSAT mRNA (5.5-fold at 24 h) and behaved similarly to BESPM in inducing the appearance of the same three transcript forms. Polyamines 123-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 159-163 8360194-11 1993 Lowering intracellular polyamine pools with inhibitors of biosynthesis decreased basal SSAT mRNA levels by at least 70% indicating, that the gene can be down-regulated as well as up-regulated by polyamines. Polyamines 23-32 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 87-91 8360194-11 1993 Lowering intracellular polyamine pools with inhibitors of biosynthesis decreased basal SSAT mRNA levels by at least 70% indicating, that the gene can be down-regulated as well as up-regulated by polyamines. Polyamines 195-205 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 87-91 8360194-12 1993 These findings indicate that SSAT represents a unique example of gene expression being positively influenced at the RNA level by polyamines and their analogs. Polyamines 129-139 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 29-33 8396915-1 1993 Heat shock and diethyldithiocarbamate stimulate polyamine catabolism in animal cells by a mechanism involving the induction of spermidine/spermine N1-acetyltransferase (N1-SSAT) activity. Polyamines 48-57 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 169-176 8343127-7 1993 These results indicate that the expression of SAT was growth-controlled and that SAT mRNA level was regulated by polyamines. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 46-49 8343127-7 1993 These results indicate that the expression of SAT was growth-controlled and that SAT mRNA level was regulated by polyamines. Polyamines 113-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-84 8477847-0 1993 Regulation of spermidine/spermine N1-acetyltransferase by intracellular polyamine pools. Polyamines 72-81 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 14-54 8477847-2 1993 Through its role in polyamine acetylation and the back-conversion pathway, spermidine/spermine N1-acetyltransferase (SSAT) has the potential to control intracellular polyamine pools by facilitating their catabolism and/or excretion. Polyamines 20-29 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 75-115 8477847-2 1993 Through its role in polyamine acetylation and the back-conversion pathway, spermidine/spermine N1-acetyltransferase (SSAT) has the potential to control intracellular polyamine pools by facilitating their catabolism and/or excretion. Polyamines 20-29 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-121 8477847-2 1993 Through its role in polyamine acetylation and the back-conversion pathway, spermidine/spermine N1-acetyltransferase (SSAT) has the potential to control intracellular polyamine pools by facilitating their catabolism and/or excretion. Polyamines 166-175 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 75-115 8477847-2 1993 Through its role in polyamine acetylation and the back-conversion pathway, spermidine/spermine N1-acetyltransferase (SSAT) has the potential to control intracellular polyamine pools by facilitating their catabolism and/or excretion. Polyamines 166-175 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-121 8477847-4 1993 Increases in intracellular polyamine pools by treatment with 3 microM exogenous spermidine or spermine for 48 h caused SSAT activity to increase 111% and 226%, respectively, and SSAT-specific mRNA to rise 19% and 66%, respectively. Polyamines 27-36 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 119-123 8477847-4 1993 Increases in intracellular polyamine pools by treatment with 3 microM exogenous spermidine or spermine for 48 h caused SSAT activity to increase 111% and 226%, respectively, and SSAT-specific mRNA to rise 19% and 66%, respectively. Polyamines 27-36 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 178-182 8477847-5 1993 Decreases in polyamine pools by treatment with inhibitors of polyamine biosynthesis caused SSAT activity to decrease by 46% and mRNA to fall by 89%. Polyamines 13-22 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 91-95 8477847-5 1993 Decreases in polyamine pools by treatment with inhibitors of polyamine biosynthesis caused SSAT activity to decrease by 46% and mRNA to fall by 89%. Polyamines 61-70 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 91-95 8477847-7 1993 The identification of a positive regulatory relationship between SSAT and intracellular polyamine pools further implicates this enzyme in a proposed model for polyamine pool homeostasis. Polyamines 88-97 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-69 8477847-7 1993 The identification of a positive regulatory relationship between SSAT and intracellular polyamine pools further implicates this enzyme in a proposed model for polyamine pool homeostasis. Polyamines 159-168 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-69 1503400-1 1992 We have previously found that in one of two human melanoma cell lines, potent increase in the polyamine catabolizing enzyme, spermidine/spermine N1-acetyltransferase (SSAT), correlate with growth sensitivity to the spermine analog, N1, N12-bis(ethyl) spermine (BESPM). Polyamines 94-103 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 125-165 8425191-14 1993 Overall, the findings reveal meaningful antitumor activity by BENSPM against 2 human melanoma xenografts and provide in vivo evidence consistent with SSAT-induced polyamine depletion playing a determining role in at least the initial phase of the antitumor response. Polyamines 163-172 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 150-154 1327507-4 1992 Further, there appears to be a positive association between the level of induction of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT) in response to the analogue and the kinetic response of cells. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 159-163 1503400-1 1992 We have previously found that in one of two human melanoma cell lines, potent increase in the polyamine catabolizing enzyme, spermidine/spermine N1-acetyltransferase (SSAT), correlate with growth sensitivity to the spermine analog, N1, N12-bis(ethyl) spermine (BESPM). Polyamines 94-103 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 167-171 1503400-8 1992 Polyamine pool reduction occurred to a greater extent than predicted in cell lines where SSAT was increased to greater than 2500 pmol/min/mg suggesting a possible role for the enzyme in enhancing polyamine excretion and/or catabolism. Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 1503400-8 1992 Polyamine pool reduction occurred to a greater extent than predicted in cell lines where SSAT was increased to greater than 2500 pmol/min/mg suggesting a possible role for the enzyme in enhancing polyamine excretion and/or catabolism. Polyamines 196-205 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 2065327-0 1991 Correlations between polyamine analogue-induced increases in spermidine/spermine N1-acetyltransferase activity, polyamine pool depletion, and growth inhibition in human melanoma cell lines. Polyamines 21-30 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 61-101 2065327-4 1991 In MALME-3 cells, SSAT accumulation was found to be differentially modulated by the BESPM homologues, N1,N11-bis-(ethyl)norspermine and N1,N14-bis-(ethyl)homospermine, which were 5-fold more and 9-fold less effective, respectively, than BESPM in increasing SSAT but similar in analogue uptake and effects on polyamine biosynthesis and cell growth inhibition. Polyamines 308-317 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 18-22 2065327-6 1991 The relationship between SSAT induction and growth sensitivity was deduced to be a possible function of increased excretion of acetylated polyamines leading to enhanced polyamine pool depletion. Polyamines 138-148 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 25-29 2065327-6 1991 The relationship between SSAT induction and growth sensitivity was deduced to be a possible function of increased excretion of acetylated polyamines leading to enhanced polyamine pool depletion. Polyamines 138-147 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 25-29 33973637-7 2021 In contrast, specific depletion of natural polyamines mediated by spermidine/spermine N1-acetyltransferase (SSAT; also known as SAT1) activation did not reduce translation but enhanced stemness. Polyamines 43-53 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 66-106 2241897-1 1990 The cytotoxic response of the human large cell lung carcinoma line NCI H157 to exposure to the polyamine analogue N1 N12-bis(ethyl)spermine (BESpm) is preceded by an extremely high induction of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 194-234 2241897-1 1990 The cytotoxic response of the human large cell lung carcinoma line NCI H157 to exposure to the polyamine analogue N1 N12-bis(ethyl)spermine (BESpm) is preceded by an extremely high induction of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 236-240 2241897-3 1990 Although other acetylases are capable of acetylating polyamines using acetyl-CoA as the acetyl donor, the greater than 600-fold induction within 24 h was found to be specifically SSAT, since essentially all activity was precipitable by the specific antisera. Polyamines 53-63 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 179-183 2241897-7 1990 The large cell lung carcinoma line NCI H157 represents a useful system to produce large amounts of the SSAT protein and to study the molecular events responsible for the induction and control of this important polyamine-metabolic enzyme. Polyamines 210-219 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 103-107 33973637-7 2021 In contrast, specific depletion of natural polyamines mediated by spermidine/spermine N1-acetyltransferase (SSAT; also known as SAT1) activation did not reduce translation but enhanced stemness. Polyamines 43-53 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 108-112 33973637-7 2021 In contrast, specific depletion of natural polyamines mediated by spermidine/spermine N1-acetyltransferase (SSAT; also known as SAT1) activation did not reduce translation but enhanced stemness. Polyamines 43-53 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 128-132 3084209-2 1986 In this study of the mechanism involved, the activities of ornithine decarboxylase and spermidine/spermine-N1-acetyltransferase (SAT), the rate-limiting enzymes of polyamine metabolism, as well as the cellular levels of polyamine were measured. Polyamines 164-173 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 129-132 34871830-2 2022 It is catalysed by GCN5-related N-acetyltransferases, which transfer acetyl groups from acetyl-coenzyme A to the primary amino groups of spermidine, spermine (Spm), or other polyamines and diamines, as was shown for the human Spermidine/Spermine N1-acetyltransferase 1 (HsSSAT1). Polyamines 174-184 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 226-268 35151773-6 2022 Through intervening SAT1 level in PEDV-infected Vero cells, it is identified that overexpression of SAT1 inhibited PEDV replication by reducing polyamine levels. Polyamines 144-153 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 20-24 3084209-2 1986 In this study of the mechanism involved, the activities of ornithine decarboxylase and spermidine/spermine-N1-acetyltransferase (SAT), the rate-limiting enzymes of polyamine metabolism, as well as the cellular levels of polyamine were measured. Polyamines 220-229 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 129-132 32493979-2 2020 Spermidine/spermine acetyltransferase (SAT1) is the rate-limiting enzyme in polyamine catabolism and a primary genetic risk factor for suicidality. Polyamines 76-85 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 39-43 33965862-7 2021 At last, 13b down-regulated the concentrations of Put, Spd and Spm by modulating polyamine metabolism key enzymes SSAT and PAO, which favored the suppression of fast growing tumor cells. Polyamines 81-90 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 114-118 32432721-3 2020 SAT1 is a spermidine/spermine acetyl-transferase enzyme that decreases the reservoir of cellular polyamines, limiting viral replication. Polyamines 97-107 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 31911608-2 2020 Enhanced flux is driven by spermidine/spermine N1-acetyltransferase (SSAT) activity, which acetylates polyamines leading to their secretion and drives biosynthetic demand. Polyamines 102-112 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 27-67 31629858-13 2020 The mechanism underlying the role of acrolein in stroke-related neuronal damage occurs through SSAT-induced polyamine oxidation by NF-kB pathway activation. Polyamines 108-117 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 95-99 31911608-2 2020 Enhanced flux is driven by spermidine/spermine N1-acetyltransferase (SSAT) activity, which acetylates polyamines leading to their secretion and drives biosynthetic demand. Polyamines 102-112 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 69-73 28157137-0 2017 Extracellular polyamines-induced proliferation and migration of cancer cells by ODC, SSAT, and Akt1-mediated pathway. Polyamines 14-24 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 85-89 31399646-1 2019 Spermidine/spermine N1-acetyltransferase 1 (SAT1), the rate-limiting enzyme in polyamine catabolism, has broad regulatory roles due to near ubiquitous polyamine binding. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 31399646-1 2019 Spermidine/spermine N1-acetyltransferase 1 (SAT1), the rate-limiting enzyme in polyamine catabolism, has broad regulatory roles due to near ubiquitous polyamine binding. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 31399646-1 2019 Spermidine/spermine N1-acetyltransferase 1 (SAT1), the rate-limiting enzyme in polyamine catabolism, has broad regulatory roles due to near ubiquitous polyamine binding. Polyamines 151-160 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 31399646-1 2019 Spermidine/spermine N1-acetyltransferase 1 (SAT1), the rate-limiting enzyme in polyamine catabolism, has broad regulatory roles due to near ubiquitous polyamine binding. Polyamines 151-160 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 31399646-2 2019 We describe a novel function of SAT1 as a gene-specific transcriptional regulator through local polyamine acetylation. Polyamines 96-105 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 32-36 31362354-6 2019 The intent of our study was to explore metabolomic effects and profiles of lung cancer patients to determine if metabolic perturbations in the SSAT-1/polyamine pathway can distinguish between healthy participants and lung cancer patients as a diagnostic and treatment monitoring tool. Polyamines 150-159 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 143-149 29729200-7 2018 RESULTS: We found loss of the polyamine catabolic enzymes spermidine/spermine-N (1)-acetyltransferase-1 (SAT1) and spermine oxidase (SMOX) predominantly in bronchial epithelial cells (BECs) of human asthmatic lung samples and mice with AAI. Polyamines 30-39 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 105-109 29777905-9 2018 Regarding mechanism, the "reprogramming" of polyamine metabolism by iron-depletion is consistent with the down-regulation of ADI1 and MAT2alpha, and the up-regulation of SAT1. Polyamines 44-53 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 170-174 30214636-7 2018 Results:ASS1 and SAT1, genes for amino acid and polyamine metabolism catalysts, respectively, were found to be vastly hypermethylated, resulting in greatly downregulated expression. Polyamines 48-57 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 17-21 29554129-12 2018 Based on its substrate profile and transcriptional levels after blood feeding, together with previous reports for polyamines required in arboviruses replication, SAT might be potentially used as a target to control arboviruses with human interference. Polyamines 114-124 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 162-165 29533973-8 2018 Recent studies indicate that induction of polyamine catabolic enzymes SSAT and spermine oxidase (SMO) play key roles in the anti-proliferative and apoptotic effects of polyamine analogues and their combinations with chemotherapeutic agents such as 5-fluorouracil (5-FU) and paclitaxel. Polyamines 42-51 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 70-74 29533973-8 2018 Recent studies indicate that induction of polyamine catabolic enzymes SSAT and spermine oxidase (SMO) play key roles in the anti-proliferative and apoptotic effects of polyamine analogues and their combinations with chemotherapeutic agents such as 5-fluorouracil (5-FU) and paclitaxel. Polyamines 168-177 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 70-74 31352009-2 2019 The human SAT1 gene produces two transcript variants: one translates spermidine/spermine N-1 acetyltransferase (SSAT1), the rate-limiting enzyme in the catabolism of polyamines, and the other generates SSATX, which has largely unknown biological functions. Polyamines 166-176 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 10-14 31352009-2 2019 The human SAT1 gene produces two transcript variants: one translates spermidine/spermine N-1 acetyltransferase (SSAT1), the rate-limiting enzyme in the catabolism of polyamines, and the other generates SSATX, which has largely unknown biological functions. Polyamines 166-176 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 112-117 31484073-7 2019 SAT1 transcripts, protein, and activity are induced in a dose-dependent manner, which depletes polyamine levels and reduces viral titers. Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 30138353-6 2018 Simultaneously, curcumin down regulated spermidine/spermine N1-acetyltransferase (SSAT) activity and the biosynthetic enzymes ODC and S-adenosylmethionine decarboxylase (SAMDC), thereby diminishing intracellular polyamine pools. Polyamines 212-221 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 40-80 28423064-9 2017 The release of PG-11047 highly induced the polyamine catabolic enzyme activities of spermidine/spermine N1-acetyltransferase (SSAT) and spermine oxidase (SMOX). Polyamines 43-52 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 84-124 28423064-9 2017 The release of PG-11047 highly induced the polyamine catabolic enzyme activities of spermidine/spermine N1-acetyltransferase (SSAT) and spermine oxidase (SMOX). Polyamines 43-52 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 126-130 28157137-9 2017 Polyamines upregulated the expression of ornithine decarboxylase (ODC), SSAT, Akt1, Akt, hypoxia-inducible factors-1alpha, vascular endothelial growth factor, and matrix metalloproteinases, and downregulated p27 expression. Polyamines 0-10 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 72-76 28157137-11 2017 In Akt1-overexpression cells, polyamines also upregulated the expression of ODC, SSAT, hypoxia-inducible factors-1alpha, vascular endothelial growth factor, and matrix metalloproteinases and downregulated p27 expression. Polyamines 30-40 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-85 28157137-12 2017 In conclusion, extracellular polyamines induced proliferation and cancer cell migration by inducing ODC and SSAT expression, and the Akt1-mediated pathway. Polyamines 29-39 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 108-112 28017891-8 2017 Intracellular BENSpm generated from the degraded nanoparticles induced the expression of rate-limiting enzymes in polyamine catabolism (SMOX, SSAT) and depleted cellular natural polyamines. Polyamines 178-188 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 142-146 28082202-4 2017 Here we show that in cell lines expressing two viral proteins, capsid and the non-structural protein 5A, expression of the two key enzymes of polyamine biosynthesis and degradation, respectively, ornithine decarboxylase (ODC) and spermidine/spermine-N1-acetyl transferase (SSAT), increases transiently. Polyamines 142-151 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 230-271 28082202-4 2017 Here we show that in cell lines expressing two viral proteins, capsid and the non-structural protein 5A, expression of the two key enzymes of polyamine biosynthesis and degradation, respectively, ornithine decarboxylase (ODC) and spermidine/spermine-N1-acetyl transferase (SSAT), increases transiently. Polyamines 142-151 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 273-277 28017891-8 2017 Intracellular BENSpm generated from the degraded nanoparticles induced the expression of rate-limiting enzymes in polyamine catabolism (SMOX, SSAT) and depleted cellular natural polyamines. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 142-146 27427208-4 2016 Depletion of spermidine and spermine via type I interferon signaling-mediated induction of spermidine/spermine N1-acetyltransferase (SAT1), a key catabolic enzyme in the polyamine pathway, restricts CHIKV and ZIKV replication. Polyamines 170-179 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 133-137 27901475-3 2017 Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Polyamines 101-111 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 27901475-3 2017 Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Polyamines 101-111 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 27901475-3 2017 Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Polyamines 177-187 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 27901475-3 2017 Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Polyamines 177-187 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 27901475-6 2017 In this study, depletion of polyamines mediated by SSAT not only attenuated the tumor cell proliferation but also dramatically inhibited cell migration and invasion in hepatocellular and colorectal carcinoma cells. Polyamines 28-38 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 51-55 27901475-7 2017 Subsequent investigations revealed introduction of SSAT into HepG2, SMMC7721 hepatocellular carcinoma cells and HCT116 colorectal carcinoma cells significantly suppressed p-AKT, p-GSK3beta expression as well as beta-catenin nuclear translocation, while inhibition of GSK3beta activity or exogenous polyamines could restore SSAT-induced decreases in the protein expression of p-AKT, p-GSK3beta and beta-catenin. Polyamines 298-308 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 51-55 27901475-9 2017 Taken together, our results indicated depletion of polyamines by SSAT significantly inhibited cell proliferation, migration and invasion through AKT/GSK3beta/beta-catenin signaling pathway in hepatocellular carcinoma and colorectal cancer cells. Polyamines 51-61 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-69 27698118-0 2016 Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses. Polyamines 27-36 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 14-18 27698118-4 2016 SAT1 is a rate-limiting enzyme in polyamine catabolism critically involved in the conversion of spermidine and spermine back to putrescine. Polyamines 34-43 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 27535047-6 2016 Here, we describe the antiviral effects of two molecules that alter polyamine levels: difluoromethylornithine (DFMO; also called eflornithine), which is a suicide inhibitor of ornithine decarboxylase 1 (ODC1), and diethylnorspermine (DENSpm), an activator of spermidine/spermine N1-acetyltransferase (SAT1). Polyamines 68-77 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 301-305 27283903-13 2016 SAT1 encodes spermidine/spermine N1-acetyltransferase, which maintains intracellular polyamine levels. Polyamines 85-94 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 27283903-14 2016 Abnormal polyamine metabolism as a result of altered SAT1 activity has an adverse effect on cells through the induction of PCD. Polyamines 9-18 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-57 28572828-4 2017 Ornithine decarboxylase (ODC) is the rate-limiting enzyme in the metabolism, and spermidine/spermine-N1-Acetyl transferase (SSAT) is the rate-limiting enzyme in the catabolism of polyamines. Polyamines 179-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-122 28572828-4 2017 Ornithine decarboxylase (ODC) is the rate-limiting enzyme in the metabolism, and spermidine/spermine-N1-Acetyl transferase (SSAT) is the rate-limiting enzyme in the catabolism of polyamines. Polyamines 179-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 124-128 28572828-8 2017 Apigenin appears to decrease the proliferation rate of human SW620 cells by facilitating SSAT expression to induce polyamine catabolism and increasing ROS levels to induce cell apoptosis. Polyamines 115-124 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 25277523-0 2014 The polyamine catabolic enzyme SAT1 modulates tumorigenesis and radiation response in GBM. Polyamines 4-13 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 31-35 25893668-5 2015 We have shown that in cultured human PCa cells, an activation of spermidine/spermine N(1) -acetyl transferase (SSAT; EC 2.3.1.57) enzyme initiates a polyamine oxidation pathway and generates copious amounts of reactive oxygen species in polyamine-rich PCa cells. Polyamines 149-158 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-109 25893668-5 2015 We have shown that in cultured human PCa cells, an activation of spermidine/spermine N(1) -acetyl transferase (SSAT; EC 2.3.1.57) enzyme initiates a polyamine oxidation pathway and generates copious amounts of reactive oxygen species in polyamine-rich PCa cells. Polyamines 149-158 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 111-115 25893668-5 2015 We have shown that in cultured human PCa cells, an activation of spermidine/spermine N(1) -acetyl transferase (SSAT; EC 2.3.1.57) enzyme initiates a polyamine oxidation pathway and generates copious amounts of reactive oxygen species in polyamine-rich PCa cells. Polyamines 237-246 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-109 25893668-5 2015 We have shown that in cultured human PCa cells, an activation of spermidine/spermine N(1) -acetyl transferase (SSAT; EC 2.3.1.57) enzyme initiates a polyamine oxidation pathway and generates copious amounts of reactive oxygen species in polyamine-rich PCa cells. Polyamines 237-246 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 111-115 25959060-1 2015 Low brain expression of the spermidine/spermine N-1 acetyltransferase (SAT1) gene, the rate-limiting enzyme involved in catabolism of polyamines that mediate the polyamine stress response (PSR), has been reported in depressed suicides. Polyamines 134-144 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 71-75 25959060-1 2015 Low brain expression of the spermidine/spermine N-1 acetyltransferase (SAT1) gene, the rate-limiting enzyme involved in catabolism of polyamines that mediate the polyamine stress response (PSR), has been reported in depressed suicides. Polyamines 134-143 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 71-75 25849284-0 2015 Depletion of the polyamines spermidine and spermine by overexpression of spermidine/spermine N1-acetyltransferase 1 (SAT1) leads to mitochondria-mediated apoptosis in mammalian cells. Polyamines 17-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 73-115 25849284-0 2015 Depletion of the polyamines spermidine and spermine by overexpression of spermidine/spermine N1-acetyltransferase 1 (SAT1) leads to mitochondria-mediated apoptosis in mammalian cells. Polyamines 17-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-121 25849284-2 2015 Transduction of human embryonic kidney (HEK) 293T cells with an adenovirus encoding a key polyamine catabolic enzyme, spermidine N1-acetyltransferase 1 (SSAT1)/SAT1 (AdSAT1), leads to a rapid depletion of spermidine and spermine, arrest in cell growth and a decline in cell viability. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 153-158 25849284-2 2015 Transduction of human embryonic kidney (HEK) 293T cells with an adenovirus encoding a key polyamine catabolic enzyme, spermidine N1-acetyltransferase 1 (SSAT1)/SAT1 (AdSAT1), leads to a rapid depletion of spermidine and spermine, arrest in cell growth and a decline in cell viability. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 154-158 25153488-6 2015 The released BENSpm depletes cellular levels of spermidine and spermine and upregulates polyamine catabolic enzymes spermine/spermidine N(1)-acetyltransferase (SSAT) and spermine oxidase (SMO). Polyamines 88-97 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 160-164 26704566-4 2016 In order to investigate the link between polyamine catabolism and the effects of aspirin we used a "Tet off" system that induced the activity of spermidine/spermine N (1)-acetyltransferase (SSAT) in human prostate cancer cells (LNCap). Polyamines 41-50 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 190-194 26704566-6 2016 A negative correlation was observed between increased polyamine catabolism via increased SSAT activity and the sensitivity to aspirin. Polyamines 54-63 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 26704566-9 2016 The results indicate that SSAT and its related polyamine metabolism may play a key role in sensitivity of cancer cells to aspirin and possibly other NSAIDs and this may have implications for the development of novel chemopreventative agents. Polyamines 47-56 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 26-30 26572277-6 2016 Cell cycle progression was determined by flow cytometry, and the protein expression levels of spermidine/spermine N1-acetyltransferase (SSAT; the key enzyme in the terminal degradation of polyamine), ornithine decarboxylase (ODC; the key enzyme of polyamine biosynthesis), cyclin D1 and p27 were measured by western blot analysis. Polyamines 188-197 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-134 26572277-6 2016 Cell cycle progression was determined by flow cytometry, and the protein expression levels of spermidine/spermine N1-acetyltransferase (SSAT; the key enzyme in the terminal degradation of polyamine), ornithine decarboxylase (ODC; the key enzyme of polyamine biosynthesis), cyclin D1 and p27 were measured by western blot analysis. Polyamines 188-197 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 136-140 25277523-5 2014 Spermidine/spermine-N1-acetyltransferase 1 (SAT1), an enzyme involved in polyamine catabolism, was identified as a gene that promotes resistance to ionizing radiation (IR), is overexpressed in brain tumors, and correlates with poor outcomes. Polyamines 73-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 25277523-5 2014 Spermidine/spermine-N1-acetyltransferase 1 (SAT1), an enzyme involved in polyamine catabolism, was identified as a gene that promotes resistance to ionizing radiation (IR), is overexpressed in brain tumors, and correlates with poor outcomes. Polyamines 73-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 25214240-10 2014 However, the silencing of spermidine-spermineacetyltransferase (SSAT), a key enzyme at polyamine catabolic machinery prevented the EBR-induced apoptosis. Polyamines 87-96 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 64-68 24607957-3 2014 In this study, the polyamine metabolism and function of SSAT were characterized in acute myeloid leukemia (AML), chronic myeloid leukemia (CML), and acute lymphoid leukemia patient samples. Polyamines 19-28 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 56-60 24649071-4 2014 Putrescine, spermidine and spermine are natural polyamines that are catabolized by a specific enzyme, spermidine/spermine acetyltransferase (SSAT). Polyamines 48-58 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 102-139 24735382-8 2014 DISCUSSION AND CONCLUSION: Gender differences in the regulation of SSAT1 gene expression may possibly be due to gender-specific effects of stress, ethanol toxicity, and/or polyamines levels. Polyamines 172-182 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 67-72 23771789-8 2014 Consequently, the polyamine catabolic pathway in general and specifically SMO and SSAT provide exciting new targets for chemoprevention and/or chemotherapy. Polyamines 18-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 82-86 24649071-4 2014 Putrescine, spermidine and spermine are natural polyamines that are catabolized by a specific enzyme, spermidine/spermine acetyltransferase (SSAT). Polyamines 48-58 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 141-145 24649071-5 2014 The single-nucleotide polymorphisms (SNPs) in the intron region of ODC (+316 G>A) and promoter region of SSAT (-1415 T>C) genes have been found to be associated with the polyamines expression levels. Polyamines 176-186 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 108-112 25893137-1 2014 OBJECTIVES: Spermidine/spermine-N1-acetytransferase (SSAT) is the key enzyme in the catabolism of polyamines that are involved in regulating NMDA functioning. Polyamines 98-108 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 12-51 23794266-7 2013 Exogenous polyamines increased the mRNA expression of polyamine-modulated factor 1 (PMF-1) and its downstream effector, spermidine/spermine N(1)-acetyltransferase (SSAT), while that of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, was suppressed. Polyamines 10-19 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 120-162 23794266-7 2013 Exogenous polyamines increased the mRNA expression of polyamine-modulated factor 1 (PMF-1) and its downstream effector, spermidine/spermine N(1)-acetyltransferase (SSAT), while that of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, was suppressed. Polyamines 10-19 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 164-168 23701543-13 2014 Similarly to classical chemotherapeutic agents, both drugs could up-regulate polyamine catabolic enzymes (SSAT, SMO and PAO) in cell type dependent manner. Polyamines 77-86 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 106-110 23701549-1 2014 Spermidine/spermine-N1-acetyltransferase (SSAT) is a mitochondrial-localized enzyme that is highly inducible and tightly controlled and is the rate-limiting enzyme in polyamine catabolism. Polyamines 167-176 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 23701549-1 2014 Spermidine/spermine-N1-acetyltransferase (SSAT) is a mitochondrial-localized enzyme that is highly inducible and tightly controlled and is the rate-limiting enzyme in polyamine catabolism. Polyamines 167-176 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 23701549-2 2014 It is known that SSAT is induced when polyamine level increases. Polyamines 38-47 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 17-21 23701549-5 2014 Besides polyamines and their analogs, certain stimuli can increase SSAT levels, suggesting that the development of reporters for high throughput screening can lead to the identification of novel pharmacophores that can modulate SSAT translation. Polyamines 8-18 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 228-232 24190492-5 2014 Especially induction of polyamine catabolic enzymes spermidine/spermine N1-acetyltransferase (SSAT), polyamine oxidase (PAO) and spermine oxidase (SMO) induced toxic by-products in correlation with the induction of apoptosis in cancer cells. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 52-92 23794266-7 2013 Exogenous polyamines increased the mRNA expression of polyamine-modulated factor 1 (PMF-1) and its downstream effector, spermidine/spermine N(1)-acetyltransferase (SSAT), while that of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, was suppressed. Polyamines 10-20 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 120-162 23794266-7 2013 Exogenous polyamines increased the mRNA expression of polyamine-modulated factor 1 (PMF-1) and its downstream effector, spermidine/spermine N(1)-acetyltransferase (SSAT), while that of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, was suppressed. Polyamines 10-20 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 164-168 23768751-2 2013 Recent post-mortem studies have shown that spermidine/spermine N1-acetyltransferase (SAT1), the key regulator of cellular polyamine content, is under-expressed in brains from suicide victims compared to controls. Polyamines 122-131 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 85-89 23768751-7 2013 Our findings suggest that SAT1 transcription is influenced by lithium and that this effect is altered in BD patients who completed suicide, further supporting a role for polyamines in suicide. Polyamines 170-180 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 26-30 25893137-1 2014 OBJECTIVES: Spermidine/spermine-N1-acetytransferase (SSAT) is the key enzyme in the catabolism of polyamines that are involved in regulating NMDA functioning. Polyamines 98-108 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-57 25893137-8 2014 RESULTS: Activation of the polyamine catabolic enzyme, SSAT increases polyamine flux in brain and CSF of HIV infected individuals with HIV-associated neurocognitive disorders. Polyamines 27-36 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 55-59 25893137-8 2014 RESULTS: Activation of the polyamine catabolic enzyme, SSAT increases polyamine flux in brain and CSF of HIV infected individuals with HIV-associated neurocognitive disorders. Polyamines 70-79 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 55-59 23891576-2 2013 Examination of global cellular gene expression in Akata subclones that retained or lost EBV identified spermidine/spermine N(1)-acetyltransferase (SAT1), an inducible enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes downregulated by EBV. Polyamines 194-204 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 147-151 23943804-5 2013 Evidence indicates that the mechanism of this synergy includes reactivation of miR-200a, which targets and destabilizes kelch-like ECH-associated protein 1 (KEAP1) mRNA, resulting in the translocation and binding of nuclear factor (erythroid-derived 2)-like 2 (NRF2) to the polyamine-responsive element of the SSAT promoter. Polyamines 274-283 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 310-314 23943804-6 2013 This transcriptional stimulation, combined with positive regulation of SSAT mRNA and protein by the analogs, results in decreased intracellular concentrations of natural polyamines and growth inhibition. Polyamines 170-180 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 71-75 23345430-3 2013 We investigated the cellular function of polyamines by overexpression of a key catabolic enzyme, spermidine/spermine N(1)-acetyltransferase 1 (SAT1) in mammalian cells. Polyamines 41-51 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 97-141 23345430-6 2013 Overexpression of SAT1 using a SAT1 adenovirus led to rapid depletion of cellular spermidine and spermine, total inhibition of protein synthesis, and growth arrest within 24 h. The SAT1 effect is most likely due to depletion of spermidine and spermine, because stable polyamine analogs that are not substrates for SAT1 restored GFP and endogenous protein synthesis. Polyamines 268-277 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 18-22 23345430-6 2013 Overexpression of SAT1 using a SAT1 adenovirus led to rapid depletion of cellular spermidine and spermine, total inhibition of protein synthesis, and growth arrest within 24 h. The SAT1 effect is most likely due to depletion of spermidine and spermine, because stable polyamine analogs that are not substrates for SAT1 restored GFP and endogenous protein synthesis. Polyamines 268-277 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 31-35 23345430-6 2013 Overexpression of SAT1 using a SAT1 adenovirus led to rapid depletion of cellular spermidine and spermine, total inhibition of protein synthesis, and growth arrest within 24 h. The SAT1 effect is most likely due to depletion of spermidine and spermine, because stable polyamine analogs that are not substrates for SAT1 restored GFP and endogenous protein synthesis. Polyamines 268-277 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 31-35 23345430-6 2013 Overexpression of SAT1 using a SAT1 adenovirus led to rapid depletion of cellular spermidine and spermine, total inhibition of protein synthesis, and growth arrest within 24 h. The SAT1 effect is most likely due to depletion of spermidine and spermine, because stable polyamine analogs that are not substrates for SAT1 restored GFP and endogenous protein synthesis. Polyamines 268-277 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 31-35 23345430-3 2013 We investigated the cellular function of polyamines by overexpression of a key catabolic enzyme, spermidine/spermine N(1)-acetyltransferase 1 (SAT1) in mammalian cells. Polyamines 41-51 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 143-147 23024204-2 2013 We recently showed that TETA is metabolized in vitro by polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT1) and by thialysine acetyltransferase (SSAT2) to its monoacetylated derivative (MAT). Polyamines 56-65 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 127-132 22579641-6 2012 The balance in antagonistic activities of ODC and SSAT in the stressed hepatoma cells was shifted towards polyamine biosynthesis, which resulted in increased intracellular levels of putrescine, spermidine, and spermine. Polyamines 106-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-54 23021806-4 2012 The TOF MS method was successfully applied to measure the activity of enzymes involved in polyamine catabolic pathways, namely N(1)-acetylpolyamine oxidase (APAO), spermine oxidase (SMO), and spermidine/spermine N(1)-acetyltransferase (SSAT). Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 236-240 22579641-7 2012 Accumulation of putrescine is indicating for accelerated degradation of polyamines by SSAT - acetylpolyamine oxidase (APAO) pathway generating toxic products that promote carcinogenesis, whereas accelerated polyamine synthesis via activation of ODC is favorable for proliferation of cells including those sub-lethally damaged by oxidative stress. Polyamines 72-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 86-90 22579641-7 2012 Accumulation of putrescine is indicating for accelerated degradation of polyamines by SSAT - acetylpolyamine oxidase (APAO) pathway generating toxic products that promote carcinogenesis, whereas accelerated polyamine synthesis via activation of ODC is favorable for proliferation of cells including those sub-lethally damaged by oxidative stress. Polyamines 72-81 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 86-90 19727732-0 2010 The role of the polyamine catabolic enzymes SSAT and SMO in the synergistic effects of standard chemotherapeutic agents with a polyamine analogue in human breast cancer cell lines. Polyamines 127-136 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 23-32 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-92 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 23-32 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-98 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 125-135 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-92 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 125-135 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-98 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 125-134 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-92 22354986-1 2012 Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Polyamines 125-134 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-98 22354986-5 2012 Nucleolin exists in several isoforms, and we report that the isoform that binds to SSAT mRNA undergoes autocatalysis in the presence of polyamines, a result suggesting that there is a negative feedback system that helps control the cellular content of polyamines. Polyamines 136-146 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 83-87 22354986-5 2012 Nucleolin exists in several isoforms, and we report that the isoform that binds to SSAT mRNA undergoes autocatalysis in the presence of polyamines, a result suggesting that there is a negative feedback system that helps control the cellular content of polyamines. Polyamines 252-262 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 83-87 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 58-67 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 80-122 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 58-67 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 124-128 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 58-67 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 171-175 21818565-6 2012 Moreover, the obtained results clearly show that the increased SSAT expression is associated with accelerated polyamine flux. Polyamines 110-119 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 63-67 20443003-9 2011 CONCLUSIONS: Increased DENSPM levels following co-treatment with Pt agents enhances the translation and stability of SSAT protein leading to polyamine pool depletion, facilitating more Pt-DNA adduct formation in parental cells. Polyamines 141-150 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-121 21318890-3 2011 Recent microarray studies have found that spermidine/spermine-N1-acetyltransferase (SAT1, SSAT), the key enzyme in charge of the polyamine catabolic pathway, is downregulated in brain tissue of individuals who were depressed and died by suicide. Polyamines 129-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 84-88 21318890-3 2011 Recent microarray studies have found that spermidine/spermine-N1-acetyltransferase (SAT1, SSAT), the key enzyme in charge of the polyamine catabolic pathway, is downregulated in brain tissue of individuals who were depressed and died by suicide. Polyamines 129-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 90-94 22170508-10 2012 CONCLUSION: These data clearly show that intrinsic elevations of PMFBP1 and SSAT1 enhance the catabolism and recycling of polyamines in RASFs and suggest that high consumption of SAM via this pathway is an important factor contributing to global DNA hypomethylation in these cells. Polyamines 122-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 76-81 22294330-0 2012 Silencing of the polyamine catabolic key enzyme SSAT prevents CDK inhibitor-induced apoptosis in Caco-2 colon cancer cells. Polyamines 17-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-52 22294330-5 2012 Intracellular polyamine levels are under the control of several catabolic enzymes, such as spermidine/spermine-N-acetyl transferase (SSAT), acetylpolyamine oxidase (APAO) and spermine oxidase (SMO), which could be altered by several therapeutic drugs. Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 91-131 22294330-5 2012 Intracellular polyamine levels are under the control of several catabolic enzymes, such as spermidine/spermine-N-acetyl transferase (SSAT), acetylpolyamine oxidase (APAO) and spermine oxidase (SMO), which could be altered by several therapeutic drugs. Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 133-137 22179681-1 2012 N1,N11-diethylnorspermine (DENSPM), a polyamine analog that induces expression of spermidine/spermine N1-acetyltransferase (SSAT) and reduces polyamine levels in eukaryotic cells, has demonstrated anticancer effects in many cancer cell types. Polyamines 38-47 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 94-134 22179681-1 2012 N1,N11-diethylnorspermine (DENSPM), a polyamine analog that induces expression of spermidine/spermine N1-acetyltransferase (SSAT) and reduces polyamine levels in eukaryotic cells, has demonstrated anticancer effects in many cancer cell types. Polyamines 38-47 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 136-140 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 281-290 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 80-122 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 281-290 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 124-128 21809078-2 2012 We have previously shown that the rate-limiting enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), has an alternative mRNA splice variant (SSATX) which undergoes degradation via nonsense-mediated mRNA decay (NMD) pathway, and that the intracellular polyamine level regulates the ratio of the SSATX and SSAT splice variants. Polyamines 281-290 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 171-175 21809078-9 2012 However, in addition to polyamine level there seems to be additional factors regulating tissue-specific alternative splicing of SSAT. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 128-132 21809081-5 2012 DENSPM depletes cells of polyamines, e.g., by inducing the activity of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT). Polyamines 25-35 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 102-144 21809081-5 2012 DENSPM depletes cells of polyamines, e.g., by inducing the activity of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT). Polyamines 25-35 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 146-150 21809081-5 2012 DENSPM depletes cells of polyamines, e.g., by inducing the activity of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT). Polyamines 25-34 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 102-144 21809081-5 2012 DENSPM depletes cells of polyamines, e.g., by inducing the activity of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT). Polyamines 25-34 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 146-150 20514439-2 2010 Several studies including our own established that platinum drugs combined with polyamine analog DENSPM produces synergistic increase in SSAT activity with polyamine depletion. Polyamines 80-89 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 137-141 20460526-4 2010 We also recently showed that androgen induces the first and regulatory enzyme spermidine/spermine N1-acetyltransferase (SSAT) in a polyamine catabolic pathway that produces copious amounts of metabolic ROS. Polyamines 131-140 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 78-118 20460526-4 2010 We also recently showed that androgen induces the first and regulatory enzyme spermidine/spermine N1-acetyltransferase (SSAT) in a polyamine catabolic pathway that produces copious amounts of metabolic ROS. Polyamines 131-140 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 120-124 20460526-8 2010 The elucidation of JunD-AR complex inducing SSAT expression leading to polyamine oxidation establishes the mechanistic basis of androgen-induced ROS production in CaP cells and opens up a new prostate-specific target for CaP chemopreventive/chemotherapeutic drug development. Polyamines 71-80 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 20212040-1 2010 Spermidine/spermine N(1)-acetyltransferase 1 (SSAT1), which catalyzes the N(1)-acetylation of spermidine and spermine to form acetyl derivatives, is a rate-limiting enzyme in polyamine catabolism. Polyamines 175-184 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-44 20212040-1 2010 Spermidine/spermine N(1)-acetyltransferase 1 (SSAT1), which catalyzes the N(1)-acetylation of spermidine and spermine to form acetyl derivatives, is a rate-limiting enzyme in polyamine catabolism. Polyamines 175-184 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 46-51 20212040-7 2010 SSAT1 may regulate exogenous gene expression by blocking steps involved in transcription/translation from an episomal vector by targeting non-polyamine substrate(s) critical for this pathway. Polyamines 142-151 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-5 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 92-101 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 188-228 20031193-3 2010 Recent studies showed that the thymidylate synthase inhibitor 5-fluorouracil (5-FU) affects polyamine metabolism in colon carcinoma cells through the induction of the key catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 92-101 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 230-234 19956992-1 2010 Transgenic mice with activated polyamine catabolism due to overexpression of spermidine/spermine N(1)-acetyltransferase (SSAT) have significantly reduced plasma total cholesterol levels. Polyamines 31-40 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 77-119 19956992-1 2010 Transgenic mice with activated polyamine catabolism due to overexpression of spermidine/spermine N(1)-acetyltransferase (SSAT) have significantly reduced plasma total cholesterol levels. Polyamines 31-40 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 121-125 19727732-7 2010 Since the cytotoxic effects of many polyamine analogues and cytotoxic agents are believed to act, in part, through induction of the polyamine catabolic enzymes SSAT and SMO, the role of these enzymes on synergistic response was evaluated in MDA-MB-231 and MCF-7 treated with BENSpm and 5-FU or paclitaxel. Polyamines 36-45 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 160-164 19727732-7 2010 Since the cytotoxic effects of many polyamine analogues and cytotoxic agents are believed to act, in part, through induction of the polyamine catabolic enzymes SSAT and SMO, the role of these enzymes on synergistic response was evaluated in MDA-MB-231 and MCF-7 treated with BENSpm and 5-FU or paclitaxel. Polyamines 132-141 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 160-164 20388096-4 2010 Ornithine decarboxylase (ODC) and spermidine/spermine N1-acetyltransferase (SSAT) are the key enzymes involved in polyamine biosynthesis and catabolism, respectively. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 34-74 20388096-4 2010 Ornithine decarboxylase (ODC) and spermidine/spermine N1-acetyltransferase (SSAT) are the key enzymes involved in polyamine biosynthesis and catabolism, respectively. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 76-80 20095967-6 2009 SSAT (spermidine/spermine N1-acetyltransferase), which is a crucial enzyme for degradation and efflux of polyamines, is also highly regulated by polyamines. Polyamines 105-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 19685053-3 2009 A selective polyamine transport system provides access for PG11047 into rapidly dividing cells to inhibit polyamine biosynthetic enzymes, to induce the polyamine catabolic enzymes spermidine/spermine N(1)-acetyltransferase (SSAT) and spermine oxidase (SMO) which could subsequently induce reactive oxygen species that contribute to tumor cell responses to PG11047, and to function as a polyamine with altered function when it binds to natural polyamine binding sites. Polyamines 12-21 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 180-222 19685053-3 2009 A selective polyamine transport system provides access for PG11047 into rapidly dividing cells to inhibit polyamine biosynthetic enzymes, to induce the polyamine catabolic enzymes spermidine/spermine N(1)-acetyltransferase (SSAT) and spermine oxidase (SMO) which could subsequently induce reactive oxygen species that contribute to tumor cell responses to PG11047, and to function as a polyamine with altered function when it binds to natural polyamine binding sites. Polyamines 12-21 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 224-228 19956562-12 2009 SAT1 exerts its effects through control of polyamine levels. Polyamines 43-52 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 20095967-6 2009 SSAT (spermidine/spermine N1-acetyltransferase), which is a crucial enzyme for degradation and efflux of polyamines, is also highly regulated by polyamines. Polyamines 105-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 6-46 20095967-6 2009 SSAT (spermidine/spermine N1-acetyltransferase), which is a crucial enzyme for degradation and efflux of polyamines, is also highly regulated by polyamines. Polyamines 145-155 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-4 20095967-6 2009 SSAT (spermidine/spermine N1-acetyltransferase), which is a crucial enzyme for degradation and efflux of polyamines, is also highly regulated by polyamines. Polyamines 145-155 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 6-46 20095967-7 2009 A cellular excess of polyamines rapidly induces SSAT, resulting in increased degradation/efflux of the polyamines. Polyamines 21-31 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-52 20095967-7 2009 A cellular excess of polyamines rapidly induces SSAT, resulting in increased degradation/efflux of the polyamines. Polyamines 103-113 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-52 20095967-8 2009 The polyamines appear to induce both transcription and translation of the SSAT mRNA. Polyamines 4-14 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 74-78 20095967-9 2009 However, the major part of the polyamine-induced increase in SSAT is caused by a marked stabilization of the enzyme against degradation by the 26S proteasome. Polyamines 31-40 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 61-65 19152344-2 2009 The authors have sought to expand their previous findings implicating altered expression of spermidine/spermine N(1)-acetyltransferase 1 (SAT1), the rate-limiting enzyme involved in catabolism of the polyamines spermidine and spermine in the polyamine stress response (PSR), across multiple brain regions between control individuals and depressed individuals who have died by suicide. Polyamines 200-210 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 92-136 19686286-1 2009 Spermidine/spermine N(1)-acetyltransferase (SSAT) is the rate-limiting step in polyamine catabolism. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 19686286-1 2009 Spermidine/spermine N(1)-acetyltransferase (SSAT) is the rate-limiting step in polyamine catabolism. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 19152344-2 2009 The authors have sought to expand their previous findings implicating altered expression of spermidine/spermine N(1)-acetyltransferase 1 (SAT1), the rate-limiting enzyme involved in catabolism of the polyamines spermidine and spermine in the polyamine stress response (PSR), across multiple brain regions between control individuals and depressed individuals who have died by suicide. Polyamines 200-210 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 138-142 19152344-2 2009 The authors have sought to expand their previous findings implicating altered expression of spermidine/spermine N(1)-acetyltransferase 1 (SAT1), the rate-limiting enzyme involved in catabolism of the polyamines spermidine and spermine in the polyamine stress response (PSR), across multiple brain regions between control individuals and depressed individuals who have died by suicide. Polyamines 200-209 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 92-136 19152344-2 2009 The authors have sought to expand their previous findings implicating altered expression of spermidine/spermine N(1)-acetyltransferase 1 (SAT1), the rate-limiting enzyme involved in catabolism of the polyamines spermidine and spermine in the polyamine stress response (PSR), across multiple brain regions between control individuals and depressed individuals who have died by suicide. Polyamines 200-209 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 138-142 19152344-8 2009 These findings suggest that downregulation of SAT1 expression may play a role in depression and suicidality, possibly by impeding the normal PSR program or through compensation for the increased polyamine metabolism accompanying the psychological distress associated with depressive disorders. Polyamines 195-204 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 46-50 19589128-5 2009 The activity of SSAT provides substrates for APAO or substrates for the polyamine exporter, thus reducing the intracellular polyamine concentration, the net effect of which depends on the magnitude and rate of any increase in SSAT. Polyamines 72-81 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 19589128-5 2009 The activity of SSAT provides substrates for APAO or substrates for the polyamine exporter, thus reducing the intracellular polyamine concentration, the net effect of which depends on the magnitude and rate of any increase in SSAT. Polyamines 72-81 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 226-230 19589128-5 2009 The activity of SSAT provides substrates for APAO or substrates for the polyamine exporter, thus reducing the intracellular polyamine concentration, the net effect of which depends on the magnitude and rate of any increase in SSAT. Polyamines 124-133 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 19589128-5 2009 The activity of SSAT provides substrates for APAO or substrates for the polyamine exporter, thus reducing the intracellular polyamine concentration, the net effect of which depends on the magnitude and rate of any increase in SSAT. Polyamines 124-133 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 226-230 18301893-6 2008 Effects of in vitro treatment with CGC-11047 on cell growth, the activity of the polyamine biosynthetic enzyme ornithine decarboxylase (ODC), and the expression and activity of the polyamine catabolic enzymes spermidine/spermine N(1)-acetyltransferase (SSAT) and spermine oxides (SMO) were measured. Polyamines 181-190 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 209-251 19162121-2 2009 Spermidine/spermine N1-acetyltransferase (SSAT-1) and its coding gene (SAT-1) are the main factors regulating polyamine catabolism. Polyamines 110-119 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-48 19162121-2 2009 Spermidine/spermine N1-acetyltransferase (SSAT-1) and its coding gene (SAT-1) are the main factors regulating polyamine catabolism. Polyamines 110-119 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 43-48 18759322-3 2009 Spermidine/spermine N1-acetyltransferase (SSAT-1) is the main enzyme regulating polyamine catabolism. Polyamines 80-89 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-48 19036131-7 2008 We also found up-regulation of spermidine/spermine N1-acetyltransferase (SSAT), a polyamine metabolic enzyme. Polyamines 82-91 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 73-77 19036131-7 2008 We also found up-regulation of spermidine/spermine N1-acetyltransferase (SSAT), a polyamine metabolic enzyme. Polyamines 82-91 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 31-71 18949426-1 2008 Spermidine/spermine N1-acetyltransferase (SSAT) is a key enzyme of polyamine catabolism. Polyamines 67-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 18949426-1 2008 Spermidine/spermine N1-acetyltransferase (SSAT) is a key enzyme of polyamine catabolism. Polyamines 67-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 18660501-11 2008 The interaction between SLC3A2 and SAT1 suggests that these proteins may facilitate excretion of acetylated polyamines. Polyamines 108-118 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 35-39 17920945-1 2008 The subcellular distribution of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) was studied in L56Br-C1 cells treated with 10 microM N(1),N(11)-diethylnorspermine (DENSPM) for 24 h. Cells were fractioned into three subcellular fractions. Polyamines 36-45 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 63-105 18089555-1 2008 Recent studies suggest that overexpression of the polyamine-acetylating enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) significantly increases metabolic flux through the polyamine pathway. Polyamines 50-59 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 79-121 18089555-1 2008 Recent studies suggest that overexpression of the polyamine-acetylating enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) significantly increases metabolic flux through the polyamine pathway. Polyamines 50-59 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 123-127 18089555-1 2008 Recent studies suggest that overexpression of the polyamine-acetylating enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) significantly increases metabolic flux through the polyamine pathway. Polyamines 180-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 79-121 18089555-1 2008 Recent studies suggest that overexpression of the polyamine-acetylating enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) significantly increases metabolic flux through the polyamine pathway. Polyamines 180-189 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 123-127 18089555-2 2008 The concept derives from the observation that SSAT-induced acetylation of polyamines gives rise to a compensatory increase in biosynthesis and presumably to increased flow through the pathway. Polyamines 74-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 46-50 18089555-12 2008 The latter sustains the flux cycle by providing a constant supply of polyamines for subsequent acetylation by SSAT. Polyamines 69-79 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 110-114 18690703-1 2008 The enzyme spermidine/spermine N (1)-acetyltransferase (SSAT) catalyzes the transfer of acetyl groups from acetylcoenzyme A to spermidine and spermine, as part of a polyamine degradation pathway. Polyamines 165-174 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 56-60 18571584-9 2008 The activity of SSAT increased significantly together with an increase in the ratios of pancreatic putrescine/spermidine and putrescine/spermine at 24 h, which indicates SSAT-induced polyamine catabolism. Polyamines 183-192 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 18571584-9 2008 The activity of SSAT increased significantly together with an increase in the ratios of pancreatic putrescine/spermidine and putrescine/spermine at 24 h, which indicates SSAT-induced polyamine catabolism. Polyamines 183-192 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 170-174 18349109-1 2008 Spermidine/spermine-N(1)-acetyltransferase (SSAT) regulates cellular polyamine content. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 18349109-1 2008 Spermidine/spermine-N(1)-acetyltransferase (SSAT) regulates cellular polyamine content. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 18349109-3 2008 Since polyamines play critical roles in normal and neoplastic growth and in ion channel regulation, SSAT is a key enzyme in these processes. Polyamines 6-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 100-104 18349109-6 2008 Certain polyamine analogs can mimic the induction of SSAT and cause a loss of normal polyamines. Polyamines 8-17 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-57 18349109-10 2008 Transgenic manipulation of SSAT activity has revealed that SSAT activity links polyamine metabolism to lipid and carbohydrate metabolism by means of alterations in the content of acetyl-CoA and ATP. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 27-31 18349109-10 2008 Transgenic manipulation of SSAT activity has revealed that SSAT activity links polyamine metabolism to lipid and carbohydrate metabolism by means of alterations in the content of acetyl-CoA and ATP. Polyamines 79-88 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 59-63 18349109-11 2008 A high level of SSAT stimulates flux through the polyamine biosynthetic pathway, since biosynthetic enzymes are induced in response to the fall in polyamines. Polyamines 49-58 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 18349109-11 2008 A high level of SSAT stimulates flux through the polyamine biosynthetic pathway, since biosynthetic enzymes are induced in response to the fall in polyamines. Polyamines 147-157 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 18430370-13 2008 CONCLUSION: The successfully constructed recombinant adenovirus Ad-hTERT-SSAT could accelerate polyamine catabolism and inhibit the colorectal cell growth in vitro. Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 73-77 17920945-1 2008 The subcellular distribution of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) was studied in L56Br-C1 cells treated with 10 microM N(1),N(11)-diethylnorspermine (DENSPM) for 24 h. Cells were fractioned into three subcellular fractions. Polyamines 36-45 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 107-111 17237273-2 2007 We identified the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) as being one of the most highly inducible genes in two DNA microarray screens to identify novel determinants of response to chemotherapeutic agents in colorectal cancer. Polyamines 18-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 45-87 17516632-1 2007 The N1-acetylation of spermidine and spermine by spermidine/spermine acetyltransferase (SSAT) is a crucial step in the regulation of the cellular polyamine levels in eukaryotic cells. Polyamines 146-155 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 49-86 17516632-1 2007 The N1-acetylation of spermidine and spermine by spermidine/spermine acetyltransferase (SSAT) is a crucial step in the regulation of the cellular polyamine levels in eukaryotic cells. Polyamines 146-155 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 88-92 17516632-2 2007 Altered polyamine levels are associated with a variety of cancers as well as other diseases, and key enzymes in the polyamine pathway, including SSAT, are being explored as potential therapeutic drug targets. Polyamines 8-17 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 145-149 17516632-2 2007 Altered polyamine levels are associated with a variety of cancers as well as other diseases, and key enzymes in the polyamine pathway, including SSAT, are being explored as potential therapeutic drug targets. Polyamines 116-125 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 145-149 17382924-10 2007 These results suggest that acute heart ischemia activates myocardial polyamine stress response characterized by increased ODC and SSAT activities and accumulation of putrescine. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 130-134 17021820-6 2007 Mathematical/Statistical modeling of the data from time-course and concentration-effect experiments of gene expression from nine polyamine pathway genes represented on the HGU95Av2 chip, indicates that three biosynthetic pathway genes (SAMDC, ODC1 and SRM) are down-regulated and one catabolic pathway gene (SSAT) is up-regulated. Polyamines 129-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 308-312 17021820-11 2007 CONCLUSION: The data indicate a concerted effect of platinum drugs on the polyamine metabolic pathway with down-regulation in the expression of several enzyme genes involved in biosynthesis and many-fold up-regulation in expression of SSAT, an acetylating enzyme gene that is critically involved in polyamine catabolism and export. Polyamines 74-83 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 235-239 17021820-11 2007 CONCLUSION: The data indicate a concerted effect of platinum drugs on the polyamine metabolic pathway with down-regulation in the expression of several enzyme genes involved in biosynthesis and many-fold up-regulation in expression of SSAT, an acetylating enzyme gene that is critically involved in polyamine catabolism and export. Polyamines 299-308 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 235-239 17690107-1 2007 Spermidine-spermine N(1)-acetyltransferase (SSAT) is induced in response to an elevation in intracellular polyamine pools. Polyamines 106-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 17690107-1 2007 Spermidine-spermine N(1)-acetyltransferase (SSAT) is induced in response to an elevation in intracellular polyamine pools. Polyamines 106-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 17690107-3 2007 Induction of SSAT by polyamine analogues can lead to intracellular polyamine depletion and apoptosis. Polyamines 21-30 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-17 17690107-3 2007 Induction of SSAT by polyamine analogues can lead to intracellular polyamine depletion and apoptosis. Polyamines 67-76 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-17 17690107-4 2007 The mechanism by which polyamines alter the translational efficiency of SSAT mRNA is not well understood. Polyamines 23-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 72-76 17690107-5 2007 In this study, we investigated the regulation of SSAT translation by the polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM). Polyamines 73-82 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 49-53 17690107-10 2007 Deletion constructs identified two regions of the SSAT protein-coding RNA sequence that conferred polyamine responsiveness. Polyamines 98-107 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 50-54 17690107-13 2007 These results suggest that polyamines regulate SSAT mRNA translational efficiency by inhibiting a repressor protein from binding to regions of the coding sequence of the SSAT transcript. Polyamines 27-37 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-51 17690107-13 2007 These results suggest that polyamines regulate SSAT mRNA translational efficiency by inhibiting a repressor protein from binding to regions of the coding sequence of the SSAT transcript. Polyamines 27-37 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 170-174 17637456-1 2007 Polyamine-modulated factor 1 (PMF-1) has been reported to interact with NF-E2 related factor 2 (Nrf-2) and activate the polyamine-induced transcription of spermidine/spermine N(1)-acetyltransferase (SSAT) gene. Polyamines 120-129 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 155-197 17637456-1 2007 Polyamine-modulated factor 1 (PMF-1) has been reported to interact with NF-E2 related factor 2 (Nrf-2) and activate the polyamine-induced transcription of spermidine/spermine N(1)-acetyltransferase (SSAT) gene. Polyamines 120-129 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 199-203 17371265-2 2007 The relatively recent finding of an inducible mammalian spermine oxidase (SMO/PAOh1), in addition to the two-step spermidine/spermine N(1)-acetyltransferanse (SSAT)/N(1)-acetylpolyamine oxidase (APAO) catabolic pathway, underscores the complexities of the regulation of polyamine catabolism by various stimuli. Polyamines 176-185 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 159-163 17371265-4 2007 Induction of SSAT by these agents can reduce intracellular polyamine concentrations and cell growth rate, thus providing a beneficial mechanism by which cells may adapt to inflammatory stress. Polyamines 59-68 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-17 17065202-2 2007 Increased expression of SSAT in vitro leads to alterations in cellular polyamine content, depletion of cofactors and precursors of polyamine synthesis, and reduced cell proliferation. Polyamines 71-80 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 24-28 17065202-2 2007 Increased expression of SSAT in vitro leads to alterations in cellular polyamine content, depletion of cofactors and precursors of polyamine synthesis, and reduced cell proliferation. Polyamines 131-140 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 24-28 17065202-3 2007 In our model system, a >28-fold increase in SSAT levels in HEK-293 cells leads to depletion of polyamines and elevation in the enzymatic activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, suggestive of a compensatory reaction to increased polyamine catabolism. Polyamines 98-108 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-51 17065202-3 2007 In our model system, a >28-fold increase in SSAT levels in HEK-293 cells leads to depletion of polyamines and elevation in the enzymatic activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, suggestive of a compensatory reaction to increased polyamine catabolism. Polyamines 98-107 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-51 17065202-9 2007 These results indicate that the disruption of polyamine homeostasis due to enhanced SSAT activity leads to DNA damage and reduced cell proliferation via activation of DNA repair and cell cycle checkpoint and disruption of Raf --> MEK --> ERK pathways. Polyamines 46-55 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 84-88 17237273-5 2007 The polyamine analogue N(1),N(11)-diethylnorspermine (DENSpm) depletes polyamine pools and potently induces SSAT. Polyamines 4-13 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 108-112 17011643-4 2006 SSAT2 was originally identified based on homology to SSAT1, a protein involved in polyamine catabolism. Polyamines 82-91 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 53-58 16854216-13 2006 CONCLUSION: In conclusion, our data demonstrated a close relationship between PPARgamma and SSAT in human colorectal cancer and this could represent an attempt to decrease polyamine levels and to reduce cell growth and tumour development. Polyamines 172-181 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 92-96 16637064-1 2006 Spermidine/spermine N(1)-acetyltransferase (SSAT) is a key enzyme in polyamine catabolism. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 16637064-1 2006 Spermidine/spermine N(1)-acetyltransferase (SSAT) is a key enzyme in polyamine catabolism. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 16757480-5 2006 Induction of SSAT, a stress-inducible gene that encodes a rate-limiting polyamine catabolic enzyme, leads to lower intracellular polyamine contents and has been associated with decreased cell growth and increased apoptosis. Polyamines 72-81 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-17 16757480-5 2006 Induction of SSAT, a stress-inducible gene that encodes a rate-limiting polyamine catabolic enzyme, leads to lower intracellular polyamine contents and has been associated with decreased cell growth and increased apoptosis. Polyamines 129-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-17 16809818-0 2006 Polyamine-regulated unproductive splicing and translation of spermidine/spermine N1-acetyltransferase. Polyamines 0-9 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 61-101 16809818-1 2006 Spermidine/spermine N1-acetyltransferase (SSAT), the rate-controlling enzyme in the interconversion of spermidine and spermine, is regulated by polyamines and their analogs at many levels of gene expression. Polyamines 144-154 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 16809818-1 2006 Spermidine/spermine N1-acetyltransferase (SSAT), the rate-controlling enzyme in the interconversion of spermidine and spermine, is regulated by polyamines and their analogs at many levels of gene expression. Polyamines 144-154 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 16809818-3 2006 In the present study, we show that alterations in the intracellular polyamine level resulted in a change in the relative abundance of SSAT transcripts. Polyamines 68-77 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 134-138 16809818-7 2006 Our present results suggest that in the case of SSAT, RUST is mediated by polyamines, and this system functions to fine-tune the polyamine metabolism. Polyamines 74-84 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-52 16809818-7 2006 Our present results suggest that in the case of SSAT, RUST is mediated by polyamines, and this system functions to fine-tune the polyamine metabolism. Polyamines 74-83 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 48-52 16854216-2 2006 Spermidine/spermine N1-acetyltransferase (SSAT) and ornithine decarboxylase (ODC) are key enzymes involved in the metabolism of polyamines, compounds that play an important role in cell proliferation. Polyamines 128-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 16854216-2 2006 Spermidine/spermine N1-acetyltransferase (SSAT) and ornithine decarboxylase (ODC) are key enzymes involved in the metabolism of polyamines, compounds that play an important role in cell proliferation. Polyamines 128-138 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 17237273-2 2007 We identified the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) as being one of the most highly inducible genes in two DNA microarray screens to identify novel determinants of response to chemotherapeutic agents in colorectal cancer. Polyamines 18-27 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 89-93 16262603-2 2006 It has been shown that the NSAID sulindac induces apoptosis and suppresses carcinogenesis, in part, by a mechanism leading to the transcriptional activation of the gene encoding SSAT (spermidine/spermine N1-acetyltransferase), a rate-limiting enzyme in polyamine catabolism. Polyamines 253-262 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 178-182 16262603-2 2006 It has been shown that the NSAID sulindac induces apoptosis and suppresses carcinogenesis, in part, by a mechanism leading to the transcriptional activation of the gene encoding SSAT (spermidine/spermine N1-acetyltransferase), a rate-limiting enzyme in polyamine catabolism. Polyamines 253-262 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 184-224 16262603-9 2006 Aspirin-induced SSAT ultimately leads to a decrease in cellular polyamine content, which has been associated with decreased carcinogenesis. Polyamines 64-73 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 16-20 16452302-1 2006 Activation of polyamine catabolism through the overexpression of spermidine/spermine N1-acetyltransferase (SSAT) in transgenic rodents does not only lead to distorted tissue polyamine homeostasis, manifested as striking accumulation of putrescine, appearance N1-acetylspermidine and reduction of tissue spermidine and/or spermine pools, but likewise creates striking phenotypic changes. Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-105 16207710-2 2005 The original hypothesis was that analogue induction of the rate-limiting spermidine/spermine N1-acetyltransferase (SSAT) provided substrate for the peroxisomal acetylpolyamine oxidase (PAO), resulting in a decrease in polyamine pools through catabolism, oxidation, and excretion of acetylated polyamines and the production of toxic aldehydes and H2O2. Polyamines 166-175 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 115-119 16207710-2 2005 The original hypothesis was that analogue induction of the rate-limiting spermidine/spermine N1-acetyltransferase (SSAT) provided substrate for the peroxisomal acetylpolyamine oxidase (PAO), resulting in a decrease in polyamine pools through catabolism, oxidation, and excretion of acetylated polyamines and the production of toxic aldehydes and H2O2. Polyamines 293-303 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 115-119 16455797-1 2006 Spermidine/spermine N1-acetyltransferase (SSAT) is a key enzyme in the control of polyamine levels in human cells, as acetylation of spermidine and spermine triggers export or degradation. Polyamines 82-91 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-40 16455797-1 2006 Spermidine/spermine N1-acetyltransferase (SSAT) is a key enzyme in the control of polyamine levels in human cells, as acetylation of spermidine and spermine triggers export or degradation. Polyamines 82-91 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-46 16455797-2 2006 Increased intracellular polyamine levels accompany several types of cancers as well as other human diseases, and compounds that affect the expression, activity, or stability of SSAT are being explored as potential therapeutic drugs. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 177-181 16455797-7 2006 These unexpected and intriguing complexities seem likely to have some as yet undefined role in regulating SSAT activity or stability as a part of polyamine homeostasis. Polyamines 146-155 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 106-110 16452302-1 2006 Activation of polyamine catabolism through the overexpression of spermidine/spermine N1-acetyltransferase (SSAT) in transgenic rodents does not only lead to distorted tissue polyamine homeostasis, manifested as striking accumulation of putrescine, appearance N1-acetylspermidine and reduction of tissue spermidine and/or spermine pools, but likewise creates striking phenotypic changes. Polyamines 14-23 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 107-111 16452302-1 2006 Activation of polyamine catabolism through the overexpression of spermidine/spermine N1-acetyltransferase (SSAT) in transgenic rodents does not only lead to distorted tissue polyamine homeostasis, manifested as striking accumulation of putrescine, appearance N1-acetylspermidine and reduction of tissue spermidine and/or spermine pools, but likewise creates striking phenotypic changes. Polyamines 174-183 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-105 16452302-1 2006 Activation of polyamine catabolism through the overexpression of spermidine/spermine N1-acetyltransferase (SSAT) in transgenic rodents does not only lead to distorted tissue polyamine homeostasis, manifested as striking accumulation of putrescine, appearance N1-acetylspermidine and reduction of tissue spermidine and/or spermine pools, but likewise creates striking phenotypic changes. Polyamines 174-183 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 107-111 15252047-10 2004 The latter led to heightened metabolic flux through the polyamine pathway and an associated approximately 70% reduction in the SSAT cofactor acetyl-CoA and a approximately 40% reduction in the polyamine aminopropyl donor S-adenosylmethionine in TRAMP/SSAT compared with TRAMP prostatic tissue. Polyamines 56-65 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 251-255 15252047-2 2004 We have previously shown that activation of polyamine catabolism by conditional overexpression of SSAT has antiproliferative consequences in LNCaP prostate carcinoma cells. Polyamines 44-53 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 98-102 15845361-1 2005 Spermidine/spermine N(1)-acetyltransferase (SSAT) is the key enzyme with regard to the maintenance of intracellular polyamine levels. Polyamines 116-125 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 15845361-1 2005 Spermidine/spermine N(1)-acetyltransferase (SSAT) is the key enzyme with regard to the maintenance of intracellular polyamine levels. Polyamines 116-125 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 15283699-1 2004 Spermidine/spermine-N1-acetyltransferase (SSAT1) is a short-lived polyamine catabolic enzyme inducible by polyamines and polyamine analogues. Polyamines 66-75 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-47 15283699-1 2004 Spermidine/spermine-N1-acetyltransferase (SSAT1) is a short-lived polyamine catabolic enzyme inducible by polyamines and polyamine analogues. Polyamines 106-116 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-47 15283699-1 2004 Spermidine/spermine-N1-acetyltransferase (SSAT1) is a short-lived polyamine catabolic enzyme inducible by polyamines and polyamine analogues. Polyamines 106-115 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 42-47 15283699-2 2004 Induction of SSAT1 plays an important role in polyamine homoeostasis, since the N1-acetylated polyamines can be excreted or oxidized by acetylpolyamine oxidase. Polyamines 46-55 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-18 15283699-2 2004 Induction of SSAT1 plays an important role in polyamine homoeostasis, since the N1-acetylated polyamines can be excreted or oxidized by acetylpolyamine oxidase. Polyamines 94-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 13-18 15283699-5 2004 Despite similarity in sequence to SSAT1, polyamines were found to be poor substrates of purified SSAT2, having K(m) values in the low millimolar range and kcat values of <0.01 s(-1). Polyamines 41-51 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 34-39 15492267-3 2004 This negative regulation was established by showing that the PMA-induced macrophage phenotype, but not PMA-associated replication arrest, was abrogated (a) by replenishing the PMA-evoked decrease in cellular spermine levels with this polyamine from an exogenous source and (b) by blocking PMA-induced expression of the polyamine catabolic enzyme N(1)-spermidine/spermine acetyltransferase (SSAT) with antisense oligonucleotides in the presence of low substrate level. Polyamines 234-243 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 346-388 15492267-3 2004 This negative regulation was established by showing that the PMA-induced macrophage phenotype, but not PMA-associated replication arrest, was abrogated (a) by replenishing the PMA-evoked decrease in cellular spermine levels with this polyamine from an exogenous source and (b) by blocking PMA-induced expression of the polyamine catabolic enzyme N(1)-spermidine/spermine acetyltransferase (SSAT) with antisense oligonucleotides in the presence of low substrate level. Polyamines 234-243 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 390-394 15479742-4 2004 Using yeast two-hybrid screening, we identified the polyamine catabolizing enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) as a specific binding partner of the alpha9 cytoplasmic domain. Polyamines 52-61 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 82-124 15479742-4 2004 Using yeast two-hybrid screening, we identified the polyamine catabolizing enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) as a specific binding partner of the alpha9 cytoplasmic domain. Polyamines 52-61 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 126-130 15479742-7 2004 We conclude that SSAT directly binds to the alpha9 cytoplasmic domain and mediates alpha9-dependent enhancement of cell migration, presumably by localized effects on acetylation of polyamines or of unidentified substrates. Polyamines 181-191 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 17-21 15096507-2 2004 Although this is usually accomplished by inhibiting polyamine biosynthesis, we reasoned that this might be more effectively achieved by activation of polyamine catabolism at the level of spermidine/spermine N(1)-acetyltransferase (SSAT); a strategy first validated in MCF-7 breast carcinoma cells. Polyamines 150-159 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 187-229 15138709-2 2004 The response of solid tumors to this drug has been associated with superinduction of the polyamine catabolic enzyme, spermine/spermidine N1-acetyltransferase (SSAT). Polyamines 89-98 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 117-157 15138709-2 2004 The response of solid tumors to this drug has been associated with superinduction of the polyamine catabolic enzyme, spermine/spermidine N1-acetyltransferase (SSAT). Polyamines 89-98 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 159-163 15138709-3 2004 Therefore, to estimate the response of breast cancers to DENSpm, we measured induction of SSAT in breast cancer explants treated in vitro with this polyamine analogue. Polyamines 148-157 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 90-94 15213272-1 2004 To ascertain the role of spermidine/spermine N-1-acetyl-transferase (SSAT; the rate-limiting enzyme in polyamine catabolism) in cell injury, cultured kidney (HEK 293) cells conditionally overexpressing SSAT were generated. Polyamines 103-112 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 25-67 15213272-1 2004 To ascertain the role of spermidine/spermine N-1-acetyl-transferase (SSAT; the rate-limiting enzyme in polyamine catabolism) in cell injury, cultured kidney (HEK 293) cells conditionally overexpressing SSAT were generated. Polyamines 103-112 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 69-73 15096507-2 2004 Although this is usually accomplished by inhibiting polyamine biosynthesis, we reasoned that this might be more effectively achieved by activation of polyamine catabolism at the level of spermidine/spermine N(1)-acetyltransferase (SSAT); a strategy first validated in MCF-7 breast carcinoma cells. Polyamines 150-159 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 231-235 15223770-1 2004 PURPOSE: A key enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), is responsive to antiproliferative agents. Polyamines 25-34 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 47-89 15223770-1 2004 PURPOSE: A key enzyme of polyamine catabolism, spermidine/spermine N(1)-acetyltransferase (SSAT), is responsive to antiproliferative agents. Polyamines 25-34 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 91-95 14573765-1 2003 N1,N11-diethylnorspermine (DENSPM) is a polyamine analog that down-regulates polyamine biosynthesis and potently upregulates the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 40-49 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 198-202 14750214-2 2004 Multiple clones selected for expression of the mutant Ki-ras transgene displayed a suppression of transcription of a key catabolic enzyme in polyamine catabolism spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 141-150 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 162-202 14750214-2 2004 Multiple clones selected for expression of the mutant Ki-ras transgene displayed a suppression of transcription of a key catabolic enzyme in polyamine catabolism spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 141-150 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 204-208 14506281-4 2003 Spermidine/sperm-ine N1-acetyltransferase (SSAT) gene, which encodes a polyamine catabolic enzyme, was induced by clinically relevant sulindac sulfone concentrations. Polyamines 71-80 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-41 14506281-4 2003 Spermidine/sperm-ine N1-acetyltransferase (SSAT) gene, which encodes a polyamine catabolic enzyme, was induced by clinically relevant sulindac sulfone concentrations. Polyamines 71-80 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 43-47 12827295-2 2003 Initially, human polyamine catabolism was assumed to be under the control of a rate-limiting spermidine/spermine N1-acetyltransferase (SSAT) that provides substrate for an acetylpolyamine oxidase (PAO). Polyamines 17-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 93-133 12827295-2 2003 Initially, human polyamine catabolism was assumed to be under the control of a rate-limiting spermidine/spermine N1-acetyltransferase (SSAT) that provides substrate for an acetylpolyamine oxidase (PAO). Polyamines 17-26 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 135-139 14573765-3 2003 In this study, we used small interfering RNA (siRNA) to examine the role of SSAT induction in mediating polyamine pool depletion and apoptosis. Polyamines 104-113 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 76-80 14573765-9 2003 This represents the first use of siRNA technology directed toward a polyamine gene and the first unequivocal demonstration that SSAT induction initiates events leading to polyamine analog-induced apoptosis. Polyamines 171-180 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 128-132 12798351-1 2003 The effect of amino acids on the regulation of the expression of spermidine/spermine N(1)-acetyltransferase (SSAT), the key enzyme of polyamine catabolism, was studied in HeLa cells. Polyamines 134-143 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-107 12798351-1 2003 The effect of amino acids on the regulation of the expression of spermidine/spermine N(1)-acetyltransferase (SSAT), the key enzyme of polyamine catabolism, was studied in HeLa cells. Polyamines 134-143 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 109-113 12798351-3 2003 Experiments utilizing (i) constructs containing fragments of the SSAT promoter linked to a luciferase reporter gene or (ii) actinomycin D (Act-D)-treated cells indicated that the increase in the SSAT mRNA level was due to an augmentation in gene transcription and message stability after omission of one of the polyamine precursor amino acids. Polyamines 311-320 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 65-69 12798351-3 2003 Experiments utilizing (i) constructs containing fragments of the SSAT promoter linked to a luciferase reporter gene or (ii) actinomycin D (Act-D)-treated cells indicated that the increase in the SSAT mRNA level was due to an augmentation in gene transcription and message stability after omission of one of the polyamine precursor amino acids. Polyamines 311-320 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 195-199 12902979-2 2003 Upstream to these events, DENSPM downregulates polyamine biosynthesis and potently upregulates polyamine catabolism at the level of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 132-172 12902979-2 2003 Upstream to these events, DENSPM downregulates polyamine biosynthesis and potently upregulates polyamine catabolism at the level of spermidine/spermine N1-acetyltransferase (SSAT). Polyamines 95-104 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 174-178 12803540-1 2003 In the polyamine back-conversion pathway, spermine and spermidine are first acetylated by spermidine/spermine N(1) -acetyl-transferase (SSAT-1) and then oxidized by polyamine oxidase to produce spermidine and putrescine respectively. Polyamines 7-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 136-142 12803540-10 2003 While SSAT-1 mRNA was inducible by polyamine analogues in a variety of cell lines, SSAT-2 was not. Polyamines 35-44 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 6-12 12804587-1 2003 Spermidine/spermine N(1)-acetyltransferase (SSAT) regulates polyamine catabolism. Polyamines 60-69 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 12697027-1 2003 Spermidine/spermine N (1)-acetyltransferase (SSAT) activity is typically highly inducible in non-small-cell lung carcinomas in response to treatment with anti-tumour polyamine analogues, and this induction is associated with subsequent cell death. Polyamines 166-175 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 45-49 12697027-5 2003 Individual clones were selected based on their ability to show induced SSAT activity in response to exposure to a polyamine analogue, and an increase in the steady-state SSAT mRNA level. Polyamines 114-123 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 71-75 12697027-8 2003 These studies indicate that both the genomic SSAT sequence and polyamine analogue exposure play a role in the transcriptional and post-transcriptional regulation and subsequent induction of SSAT activity in these cells. Polyamines 63-72 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 190-194 12839950-1 2003 The clinically relevant polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) inhibits cell growth by down-regulating polyamine biosynthesis, up-regulating polyamine catabolism at the level of spermidine/spermine N(1)-acetyltransferase (SSAT), and depleting intracellular polyamine pools. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 197-239 12839950-1 2003 The clinically relevant polyamine analogue N(1),N(11)-diethylnorspermine (DENSPM) inhibits cell growth by down-regulating polyamine biosynthesis, up-regulating polyamine catabolism at the level of spermidine/spermine N(1)-acetyltransferase (SSAT), and depleting intracellular polyamine pools. Polyamines 24-33 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 241-245 12804587-1 2003 Spermidine/spermine N(1)-acetyltransferase (SSAT) regulates polyamine catabolism. Polyamines 60-69 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 12427553-1 2002 Spermidine/spermine N(1)-acetyltransferase (SSAT), the key enzyme of polyamine catabolism, is induced by antiproliferative stresses. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 0-42 12653645-5 2003 This PPAR, in turn, activates the expression of the spermidine/spermine-N(1)-acetyltransferase (SSAT), the first enzyme in polyamine catabolism. Polyamines 123-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 52-94 12653645-5 2003 This PPAR, in turn, activates the expression of the spermidine/spermine-N(1)-acetyltransferase (SSAT), the first enzyme in polyamine catabolism. Polyamines 123-132 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 96-100 12477380-13 2003 In Northern blot analysis, PAO mRNA was much less abundant in HEK-293 cells than SMO or SSAT mRNA, and all three were differentially induced in a similar manner by selected polyamine analogues. Polyamines 173-182 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 88-92 12653639-2 2003 Human polyamine catabolism was considered to be a two-step pathway regulated by the rate-limiting enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) that provides substrate for an acetylpolyamine oxidase (APAO). Polyamines 6-15 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 105-147 12653639-2 2003 Human polyamine catabolism was considered to be a two-step pathway regulated by the rate-limiting enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) that provides substrate for an acetylpolyamine oxidase (APAO). Polyamines 6-15 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 149-153 12653639-3 2003 Further, the super-induction of SSAT by several anti-tumour polyamine analogues has been implicated in the cytotoxic response of specific solid-tumour phenotypes to these agents. Polyamines 60-69 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 32-36 12653639-4 2003 This high induction of SSAT has been correlated with cellular response to the anti-tumour polyamine analogues in several systems and considerable progress has been made in understanding the molecular mechanisms that regulate the analogue-induced expression of SSAT. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 23-27 12653639-4 2003 This high induction of SSAT has been correlated with cellular response to the anti-tumour polyamine analogues in several systems and considerable progress has been made in understanding the molecular mechanisms that regulate the analogue-induced expression of SSAT. Polyamines 90-99 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 260-264 12653639-5 2003 A polyamine response element has been identified and the transacting transcription factors that bind and stimulate transcription of SSAT have been cloned and characterized. Polyamines 2-11 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 132-136 12653639-7 2003 The high induction of SSAT and the subsequent activity of APAO are linked to the cytotoxic response of some tumour cell types to specific polyamine analogues. Polyamines 138-147 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 22-26 12477380-1 2003 In the polyamine back-conversion pathway, spermine and spermidine are first acetylated by spermidine/spermine N1 -acetyltransferase (SSAT) and then oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine respectively. Polyamines 7-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 90-131 12477380-1 2003 In the polyamine back-conversion pathway, spermine and spermidine are first acetylated by spermidine/spermine N1 -acetyltransferase (SSAT) and then oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine respectively. Polyamines 7-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 133-137 12427553-1 2002 Spermidine/spermine N(1)-acetyltransferase (SSAT), the key enzyme of polyamine catabolism, is induced by antiproliferative stresses. Polyamines 69-78 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 44-48 11846806-2 2002 In the breast cancer cell line L56Br-C1, treatment with 10 microm DENSPM induced SSAT activity 60 and 240-fold at 24 and 48 h after seeding, respectively, which resulted in polyamine depletion. Polyamines 173-182 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 81-85 12215835-9 2002 Analysis of polyamine metabolism in the cells of the patient indicated that the levels of metabolites such as putrescine, spermidine and spermine were consistent with the overexpression of the SSAT gene as in the murine model. Polyamines 12-21 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 193-197 12141946-1 2002 During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively. Polyamines 7-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 77-119 12141946-1 2002 During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively. Polyamines 7-16 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 121-125 11522638-6 2001 Dose-dependent inhibition of polyamine oxidase, an enzyme that oxidizes acetylated polyamines generated by SSAT and releases toxic by-products such as H(2)O(2) and aldehydes, prevented cytochrome c release, caspase activation, and apoptosis. Polyamines 83-93 spermidine/spermine N1-acetyltransferase 1 Homo sapiens 107-111