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Literature summary for 2.3.2.23 extracted from

  • Yokota, K.; Shibata, H.; Kurihara, I.; Kobayashi, S.; Suda, N.; Murai-Takeda, A.; Saito, I.; Kitagawa, H.; Kato, S.; Saruta, T.; Itoh, H.
    Coactivation of the N-terminal transactivation of mineralocorticoid receptor by Ubc9 (2007), J. Biol. Chem., 282, 1998-2010.
    View publication on PubMed
Search for more literature for 2.3.2.23

Cloned(Commentary)

Cloned (Comment) Organism
expression in Escherichia coli Homo sapiens

Protein Variants

Protein Variants Comment Organism
C93S sumoylatzion-defective mutant Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Synonyms

Synonyms Comment Organism
SUMO-1-conjugating enzyme Ubc9
-
 Homo sapiens
Ubc9
-
 Homo sapiens

General Information

General Information Comment Organism
physiological function reduction of Ubc9 protein levels by small interfering RNA attenuates hormonal activation of a mineralocorticoid receptor reporter construct as well as an endogenous target gene by mineralocorticoid receptor. A sumoylation-inactive mutant Ubc9 (C93S) similarly interacts with mineralocorticoid receptor and potentiates aldosterone-dependent mineralocorticoid receptor transactivation. An mineralocorticoid receptor mutant in which four lysine residues within sumoylation motifs are mutated into arginine (K89R/K399R/K494R/K953R) fails to be sumoylated, but Ubc9 similarly enhances transactivation by the mutant mineralocorticoid receptor. Coexpression of Ubc9 and steroid receptor coactivator SRC-1 synergistically enhances mineralocorticoid receptor-mediated transactivation in transient transfection assays Homo sapiens