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. Author manuscript; available in PMC: 2022 Jul 1.
Published in final edited form as: Neurochem Int. 2021 May 5;147:105054. doi: 10.1016/j.neuint.2021.105054

Figure 2. Molecular, biochemical and epigenetic mechanisms regulated by ADK isoforms.

Figure 2.

Schematic shows intracellular adenosine metabolism via ADK-S, equilibration to the extracellular space via equilibrative (ENT) or concentrative (CNT) nucleoside transporters, and associated adenosine receptor-mediated mechanisms. On the other hand, nuclear ADK-L acts as an epigenetic regulator of DNA methylation. ADK-L promotes transmethylation reactions by adenosine conversion to 5’AMP causing a forward shift in S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) transformation, thereby promoting DNA methylation through DNA methyltransferases (DNMT).