Carroll Kilpatrick, Gomez Carlos, Shapiro Lawrence
Department of Biochemistry and Molecular Biophysics, Columbia University, 701 West 168th Street, Room 712, New York, New York 10032, USA.
Nat Rev Mol Cell Biol. 2004 Jan;5(1):55-63. doi: 10.1038/nrm1278.
The tubby mouse, which shows late-onset obesity and neurosensory deficits, arises from a mutation in the Tub gene. Tub shares homology with the genes for tubby-like proteins Tulp1, Tulp2 and Tulp3. Ablation of Tub, Tulp1 or Tulp3 causes disease phenotypes that are indicative of their importance in nervous-system function and development. Despite this importance, the biochemical functions of tubby-like proteins are only now beginning to be understood. At present, data indicate that tubby-like proteins might function as heterotrimeric-G-protein-responsive intracellular signalling factors, although an array of data also implicates them in other processes.
肥胖小鼠表现出迟发性肥胖和神经感觉缺陷，它是由Tub基因的突变引起的。Tub与类Tubby蛋白Tulp1、Tulp2和Tulp3的基因具有同源性。Tub、Tulp1或Tulp3的缺失会导致疾病表型，这表明它们在神经系统功能和发育中具有重要性。尽管具有这种重要性，但类Tubby蛋白的生化功能直到现在才开始被了解。目前，数据表明类Tubby蛋白可能作为异源三聚体G蛋白反应性细胞内信号因子发挥作用，尽管一系列数据也表明它们参与其他过程。
