2016
DOI: 10.1074/mcp.m115.055772
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Methylthioadenosine (MTA) Regulates Liver Cells Proteome and Methylproteome: Implications in Liver Biology and Disease

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Cited by 35 publications
(21 citation statements)
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“…Indeed, polyamine catabolism and the production of ROS has been implicated in disease progression (e.g., ischemic reperfusion injury [ 53 ]). Moreover, MTA is a byproduct of S-adenosylmethionine (SAMe) metabolism and, like SAMe, it can act as a primary methyl donor for DNA and protein methylation [ 54 , 55 ]. MTA also has anti-inflammatory and antiproliferative effects [ 54 , 55 ].…”
Section: Discussionmentioning
confidence: 99%
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“…Indeed, polyamine catabolism and the production of ROS has been implicated in disease progression (e.g., ischemic reperfusion injury [ 53 ]). Moreover, MTA is a byproduct of S-adenosylmethionine (SAMe) metabolism and, like SAMe, it can act as a primary methyl donor for DNA and protein methylation [ 54 , 55 ]. MTA also has anti-inflammatory and antiproliferative effects [ 54 , 55 ].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, MTA is a byproduct of S-adenosylmethionine (SAMe) metabolism and, like SAMe, it can act as a primary methyl donor for DNA and protein methylation [ 54 , 55 ]. MTA also has anti-inflammatory and antiproliferative effects [ 54 , 55 ]. Whether polyamine catabolism is involved in the pathophysiology of PSC remains to be explored, but is testable in in vitro and in vivo models of disease.…”
Section: Discussionmentioning
confidence: 99%
“…In prokaryotic and eukaryotic systems, SAM provides methyl for a variety of protein, DNA, and RNA methylation reactions ( 56 61 ). In eukaryotic systems, modulation of methionine metabolism resulting in changes to the cellular MTA and SAM pools can have important consequences on protein, DNA, and RNA methylation ( 62 65 ). Therefore, we hypothesize that increased MTA alters methylation to repress the expression or function of critical virulence factors.…”
Section: Discussionmentioning
confidence: 99%
“…Further research involving in vivo, using orthotopic GBM models will be necessary to illuminate the functional interplay between MTAP loss and the function of innate immune cells in GBM, and how they collectively influence the adaptive immune characteristics within the tumor. One question raised by this study is what might be the long term impact of the uptake/accumulation of MTA (i.e., via nucleoside transporters) on the epigenomes and epiproteomes of immune cells, an aspect awaiting further investigation, though previous studies indicate this might play an important role (68)(69)(70). Furthermore, we note that the experimental results represent a limited view of the complex time scale of the signaling mechanisms and responses involved.…”
Section: Discussionmentioning
confidence: 86%