Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
AMP-Activated Protein Kinase Kinases
-
Amino Acid Sequence
-
Animals
-
Cell Division* / genetics
-
Cell Division* / physiology
-
Cell Polarity*
-
Gene Expression Regulation, Enzymologic*
-
Genes, Tumor Suppressor
-
Humans
-
Molecular Sequence Data
-
Peutz-Jeghers Syndrome / enzymology
-
Peutz-Jeghers Syndrome / genetics
-
Phosphorylation
-
Protein Kinases / genetics
-
Protein Kinases / metabolism*
-
Protein Prenylation
-
Protein Processing, Post-Translational
-
Protein Serine-Threonine Kinases / chemistry
-
Protein Serine-Threonine Kinases / genetics
-
Protein Serine-Threonine Kinases / metabolism*
-
Protein Structure, Tertiary
-
Sequence Homology, Amino Acid
Substances
-
Protein Kinases
-
Protein Serine-Threonine Kinases
-
STK11 protein, human
-
AMP-Activated Protein Kinase Kinases