the protein-protein interacting surface formed in MATa2:MATbeta complexes is explored to demonstrate that several quinolone-based compounds modulate the activity of MATa2 and its mutants providing a rational for chemical design/intervention responsive to the level of S-Adenosylmethionine in the cellular environment
The simultaneous downregulation of MAT1A and upregulation of MAT2A are necessary and sufficient for hepatocellular carcinoma metastasis in the process of M1-M2 switch.
METTL16 that controls MAT2A intron retention in response to intracellular SAM levels; splicing of the MAT2A retained intron is rapidly induced upon Met depletion and this effect requires a conserved hairpin which is a METTL16 m6A substrate.
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