Boudeau Jérôme, Sapkota Gopal, Alessi Dario R
MRC Protein Phosphorylation Unit, MSI/WTB Complex, University of Dundee, Dow Street, Dundee DD1 5EH, UK.
FEBS Lett. 2003 Jul 3;546(1):159-65. doi: 10.1016/s0014-5793(03)00642-2.
LKB1 is a serine-threonine protein kinase mutated in patients with an autosomal dominantly inherited cancer syndrome predisposing to multiple benign and malignant tumours, termed Peutz-Jeghers syndrome. Since its discovery in 1998, much research has focused on identification and characterisation of its cellular roles and analysing how LKB1 might be regulated. In this review we discuss exciting recent advances indicating that LKB1 functions as a tumour suppressor perhaps by controlling cell polarity. We also outline the current understanding of the molecular mechanisms by which LKB1 is regulated in vivo, through interaction with other proteins as well as by protein phosphorylation and prenylation.
LKB1是一种丝氨酸-苏氨酸蛋白激酶,在患有常染色体显性遗传癌症综合征的患者中发生突变,该综合征易引发多种良性和恶性肿瘤,称为黑斑息肉综合征。自1998年发现以来,许多研究都集中在确定其细胞作用并进行特征描述,以及分析LKB1可能如何被调控。在这篇综述中,我们讨论了近期令人兴奋的进展,这些进展表明LKB1可能通过控制细胞极性发挥肿瘤抑制作用。我们还概述了目前对LKB1在体内如何通过与其他蛋白质相互作用以及通过蛋白质磷酸化和异戊二烯化进行调控的分子机制的理解。