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. Author manuscript; available in PMC: 2022 May 1.
Published in final edited form as: Biochem Pharmacol. 2020 Nov 6;187:114321. doi: 10.1016/j.bcp.2020.114321

Figure 1: Biochemical pathways controlled by ADK.

Figure 1:

Simplified scheme showing compartmentalization of the ADO system and major pathways controlled by ADK (for a comprehensive description of ADO metabolizing pathways, please see [7]). The main route for the extracellular production of ADO is degradation of ATP through a system of ectonucleotidases, with CD39 and CD73 shown here. Extra- and intracellular levels of ADO are equilibrated through equilibrative nucleoside transporters (ENT). Therefore, intracellular ADO metabolism through ADK can control adenosine receptor (AR) activation. In the intracellular compartment the ADO-ADK system is linked to S-adenosylmethionine (SAM) dependent methyltransferase (MT) reactions, which yield S-adenosylhomocysteine (SAH), which is a substrate for S-adenosylhomocysteine hydrolase (SAHH). By removing adenosine ADK-S in the cytoplasm and ADK-L in the nucleus drives the flux of methyl groups through the transmethylation pathway. In the intranuclear compartment ADK-L activity is needed to maintain DNA methyltransferase (DNMT) activity and DNA methylation.