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- What are the components from which the methyl groups, needed for all biological methylation, reactions come from? Methonin → S-adenosylhomocysteine
- Describe the metabolic cycling of methionine that is a key pathway of many biological methylation reactions. Subsequent to methyl donation, the product S-adenosylhomocysteine (SAH) becomes homocysteine (Hcy), which is then either catabolized or remethylated to methionine. (Elevated Hcy is the cause of several damaging effects.)
- Describe some metabolic enzymes that are epigenetically regulated. CYP450 proteins ABC transporters SLC22A8 (solute carrier) organic anion transporter
- Describe the epigenetic effects of the “oncometabolite” D-2 hydroxygluterate (D- 2HG) produced by mutant isocitrate dehydrogenase (IDH1/2). Cancer-associated gain-of-function mutations enable mutant IDH1/2 (mIDH1/2) to catalyze the oxidation of αKG to D-2HG, using NADPH as a cofactor. • Because D-2HG is structurally similar to α-KG, its accumulation can modulate the activities of α-KG– utilizing dioxygenases. D-2HG can also stimulate the activities of Hypoxiainducible factor prolyl hydroxylases, leading to enhanced degradation and a diminished HIF response, which are associated with increased soft agar growth of human astrocytes
- Describe the epigenetic function of SIRT6 and its metabolic role. Mammalian SIRT1 has been found to facilitate heterochromatin formation by histone hypoacetylation, particularly deacetylation of histone lysine residues. Transcription factors/cofactors, such as p53, FOXO, or a TATA-box binding protein TAF (I), are an outstanding type of protein known to be modified by sirtuin. SIRT6 deficiency promotes a state of glucose addiction, a hallmark of cancers undergoing aerobic glycolysis. SIRT6 inhibits the initiation and progression of colorectal cancer in vivo by repressing aerobic glycolysis and ribosomal gene expression
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