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Literature summary for 3.4.22.B72 extracted from

  • Yu, X.; Lao, Y.; Teng, X.L.; Li, S.; Zhou, Y.; Wang, F.; Guo, X.; Deng, S.; Chang, Y.; Wu, X.; Liu, Z.; Chen, L.; Lu, L.M.; Cheng, J.; Li, B.; Su, B.; Jiang, J.; Li, H.B.; Huang, C.; Yi, J.; Zou, Q.
    SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation (2018), Nat. Commun., 9, 3157 .
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Mus musculus Q9EP97
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
SUMOylated transcription factor BACH2 + H2O
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 Mus musculus ?
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General Information

General Information Comment Organism
physiological function SENP3 is a pivotal regulator of regulatory T cells (Treg cells) that functions by controlling the SUMOylation and nuclear localization of transcription factor BACH2. Treg cell-specific deletion of Senp3 results in T cell activation, autoimmune symptoms and enhanced antitumor T cell responses. SENP3-mediated BACH2 deSUMOylation prevents the nuclear export of BACH2, thereby repressing the genes associated with CD4+ T effector cell differentiation and stabilizing Treg cell-specific gene signatures. SENP3 accumulation triggered by reactive oxygen species is involved in Treg cell-mediated tumor immunosuppression Mus musculus