Finding a better drug for epilepsy: the mTOR pathway as an antiepileptogenic target.
New York City, United States. In Epilepsia, 2012
These include tuberous sclerosis, which is due to mutations in TSC1 or TSC2 genes; mutations in phosphatase and tensin homolog (PTEN) as in Cowden syndrome, polyhydramnios, megalencephaly, symptomatic epilepsy syndrome (PMSE) due to mutations in the STE20-related kinase adaptor alpha (STRADalpha); and neurofibromatosis type 1 attributed to neurofibromin 1 mutations.
Emerging roles of pseudokinases.
Dundee, United Kingdom. In Trends Cell Biol, 2006
We review evidence that the pseudokinase STRAD controls the function of the tumour suppressor kinase LKB1 and that a single amino acid substitution within the pseudokinase domain of the tyrosine kinase JAK2 leads to several malignant myeloproliferative disorders.
LKB1-dependent signaling pathways.
Dundee, United Kingdom. In Annu Rev Biochem, 2005
We discuss evidence that the cellular localization and activity of LKB1 is controlled through its interaction with a catalytically inactive protein resembling a protein kinase, termed STRAD, and an armadillo repeat-containing protein, named mouse protein 25 (MO25).
LKB1 tumor suppressor protein: PARtaker in cell polarity.
Utrecht, Netherlands. In Trends Cell Biol, 2004
Recently, mammalian LKB1 was found to be active only in a complex with two other proteins--STRAD and MO25--and to induce complete polarization of intestinal epithelial cells in a cell-autonomous fashion.