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Literature summary for 1.14.11.53 extracted from

  • Yu, F.; Wei, J.; Cui, X.; Yu, C.; Ni, W.; Bungert, J.; Wu, L.; He, C.; Qian, Z.
    Post-translational modification of RNA m6A demethylase ALKBH5 regulates ROS-induced DNA damage response (2021), Nucleic Acids Res., 49, 5779-5797 .
    View publication on PubMedView publication on EuropePMC

Protein Variants

Protein Variants Comment Organism
K86R/K321R ROS-induced global mRNA m6A modification is completely blocked by mutant K86R/K321R overexpression Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q6P6C2
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Posttranslational Modification

Posttranslational Modification Comment Organism
sumoylation ROS promotes ALKBH5 sumoylation, which blocks m6A demethylase activity by inhibition of substrate accessibility. Overexpression of sumoylation-deficient ALKBH5 blocks ROS-induced mRNA m6A methylation, leading to a significant delay of DNA repair and increase of cell apoptosis Homo sapiens

General Information

General Information Comment Organism
physiological function ROS significantly induces global mRNA N6-methyladenosine levels by modulating ALKBH5 post-translational modifications, leading to the rapid and efficient induction of thousands of genes. DNA damage repair genes are ALKBH5 downstream targets induced by ROS. ROS promotes ALKBH5 SUMOylation through activating ERK/JNK signaling, leading to inhibition of ALKBH5m6A demethylase activity by blocking substrate accessibility Homo sapiens