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Literature summary for 3.4.19.12 extracted from

  • Suzuki, M.; Setsuie, R.; Wada, K.
    Ubiquitin carboxyl-terminal hydrolase l3 promotes insulin signaling and adipogenesis (2009), Endocrinology, 150, 5230-5239.
    View publication on PubMed

Protein Variants

Protein Variants Comment Organism
additional information Uchl3-deficient mice show reduced content of white adipose tissue and reduced adipogenesis due to attenuated insulin responses, ectopic expression of wild-type UCH-L3 restores the phosphorylation of insulin/IGF-I receptor and adipocyte differentiation in UCH-L3-/- mouse embyronic fibroblasts, overview. Hydrolase-deficient UCH-L3 does not enhance insulin signalling and expression of gluta4, fabp4, and adiponectin, resulting in impaired formation of large lipid droplets Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
embryo
-
Mus musculus
-
epididymis
-
Mus musculus
-
fibroblast embryonic Mus musculus
-

Synonyms

Synonyms Comment Organism
ubiquitin carboxyl-terminal hydrolase l3
-
Mus musculus
UCH-L3
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Mus musculus

General Information

General Information Comment Organism
additional information ectopic expression of UCH-L3 promotes the phosphorylation of insulin/IGF-I receptor and adipocyte differentiation in fibroblasts, overview Mus musculus
physiological function UCH-L3 promotes insulin signaling and adipogenesis Mus musculus