Tubby, N-terminal (IPR005398)

Short name: Tubby_N

Overlapping homologous superfamilies


Domain relationships



A mutation in the mouse tub gene causes maturity-onset obesity, insulin resistance and sensory deficits [PMID: 8612280, PMID: 8606774]. By contrast with the rapid juvenile-onset weight gain seen in diabetes (db) and obese (ob) mice, obesity in tubby mice develops gradually, and strongly resembles the late-onset obesity observed in the human population [PMID: 8606774]. Excessive deposition of adipose tissue culminates in a two-fold increase of body weight. Tubby mice also suffer retinal degeneration and neurosensory hearing loss. The tripartite character of the tubby phenotype is highly similar to human obesity syndromes, such as Alstrom and Bardet-Biedl. Although these phenotypes indicate a vital role for tubby proteins, no biochemical function has yet been ascribed to any family member [PMID: 10591637], although it has been suggested that the phenotypic features of tubby mice may be the result of cellular apoptosis triggered by expression of the mutuated tub gene.

Mammalian tub is a hydrophilic protein of ~500 residues. Tub carries a nuclear localisation signal and is able to activate transcription [PMID: 11801719]. The N-terminal portion of the protein is conserved neither in length nor sequence, but the C-terminal 250 residues are highly conserved. The C-terminal extremity contains a cysteine residue that might play an important role in the normal functioning of these proteins. The C-terminal is represented by IPR000007.

Contributing signatures

Signatures from InterPro member databases are used to construct an entry.