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S-methyl-5'-thioadenosine degradation

General Background : 5-METHYLTHIOADENOSINE (MTA) is a side product in the biosynthesis of several important compounds. An important case is polyamine synthesis, where : MET is consumed through the utilization of : S-ADENOSYLMETHIONINE (SAM) in a reaction that releases MTA (see the pathway :POLYAMINSYN3-PWY). MTA is a strong inhibitor of polyamine biosynthesis and transmethylation reactions, and its concentration needs to be tightly regulated. Another example is found in the pathogen : TAX-287, where MTA is a by product in the synthesis of the autoinducer compounds : CPD-10783 and : CPD-10784 (see : PWY-6157). To ensure that the pathways that produce MTA as a byproduct are not blocked, the organism must remove this compound. The most common way of achieving it is through the : PWY-4361 "methionine salvage" pathway, in which MTA is recycled through a series of reactions back to AMP and : MET. While the methionine salvage pathway is widely conserved, its initial steps, converting MTA to :CPD-444, differ among microorganisms and plants (such as the bacteria : TAX-573 and : TAX-1423 ), protozoans (such as : TAX-5741 and : TAX-5833 ) and mammalian cells. The different routes employed by these organisms are described in the different pathways under : Methylthioadenosine-Degradation. About This Pathway Higher eukaryotes possess the enzyme : CPLX-1163 (: 5-METHYLTHIOADENOSINE-PHOSPHORYLASE-RXN "EC"), which converts : 5-METHYLTHIOADENOSINE into : CPD-444 in a single step. The enzyme draws special interest since it has been shown that all normal tissues (and cell lines established from normal tissues) show clearly detectable MTAPase activity, while a large number of cell lines derived from malignancies and primary tumors completely lacks the phosphorylase activity . This may make it possible to administer drug therapies that would only affect tumor cells .

from BIOCYC source record: HUMAN_PWY-6756
Type: pathway
Taxonomic scope
organism-specific biosystem
Homo sapiens

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