Associated Papers
Activation of RhoC by regulatory ubiquitination is mediated by LNX1 and suppressed by LIS1.
Kholmanskikh S et al.
Scientific Reports, 2022
Mutations in cytoplasmic dynein and its regulators cause malformations of cortical development and neurodegenerative diseases.
Lipka J et al.
Biochemical Society Transactions, 2013
Role of cytoskeletal abnormalities in the neuropathology and pathophysiology of type I lissencephaly.
Friocourt G et al.
Acta Neuropathologica, 2011
Functional interplay between LIS1, NDE1 and NDEL1 in dynein-dependent organelle positioning.
Lam C et al.
Journal of Cell Science, 2010
Genome-wide analysis to predict protein sequence variations that change phosphorylation sites or their corresponding kinases.
Ryu GM et al.
Nucleic Acids Research, 2009
Missense mutations resulting in type 1 lissencephaly.
Reiner O et al.
Cellular and Molecular Life Sciences : Cmls, 2005
Lis1 and doublecortin function with dynein to mediate coupling of the nucleus to the centrosome in neuronal migration.
Tanaka T et al.
The Journal of Cell Biology, 2004
Mutation screening in a cohort of patients with lissencephaly and subcortical band heterotopia.
Torres FR et al.
Neurology, 2004
Interaction of reelin signaling and Lis1 in brain development.
Assadi AH et al.
Nature Genetics, 2003
Clinical and molecular basis of classical lissencephaly: Mutations in the LIS1 gene (PAFAH1B1).
Cardoso C et al.
Human Mutation, 2002
LIS1 missense mutations cause milder lissencephaly phenotypes including a child with normal IQ.
Leventer RJ et al.
Neurology, 2001
NudE-L, a novel Lis1-interacting protein, belongs to a family of vertebrate coiled-coil proteins.
Sweeney KJ et al.
Mechanisms of Development, 2001
The location and type of mutation predict malformation severity in isolated lissencephaly caused by abnormalities within the LIS1 gene.
Cardoso C et al.
Human Molecular Genetics, 2000
LIS1 regulates CNS lamination by interacting with mNudE, a central component of the centrosome.
Feng Y et al.
Neuron, 2000
Lissencephaly associated mutations suggest a requirement for the PAFAH1B heterotrimeric complex in brain development.
Sweeney KJ et al.
Mechanisms of Development, 2000
Analysis of lissencephaly-causing LIS1 mutations.
Sapir T et al.
European Journal of Biochemistry, 1999
Biochemical characterization of various catalytic complexes of the brain platelet-activating factor acetylhydrolase.
Manya H et al.
The Journal of Biological Chemistry, 1999
Point mutations and an intragenic deletion in LIS1, the lissencephaly causative gene in isolated lissencephaly sequence and Miller-Dieker syndrome.
Lo Nigro C et al.
Human Molecular Genetics, 1997