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• W2001281440 startingPage "6977" @default.
• W2001281440 abstract "Forming the structure of the human brain involves extensive neuronal migration, a process dependent on cytoskeletal rearrangement. Neuronal migration is believed to be disrupted in patients exhibiting the developmental brain malformation lissencephaly. Previous studies have shown that LIS1, the defective gene found in patients with lissencephaly, is a subunit of the platelet-activating factor acetylhydrolase. Our results indicated that LIS1 has an additional function. By interacting with tubulin it suppresses microtubule dynamics. We detected LIS1 interaction with microtubules by immunostaining and co-assembly. LIS1-tubulin interactions were assayed by co-immunoprecipitation and by surface plasmon resonance changes. Microtubule dynamic measurements in vitro indicated that physiological concentrations of LIS1 indeed reduced microtubule catastrophe events, thereby resulting in a net increase in the maximum length of the microtubules. Furthermore, the LIS1 protein concentration in the brain, measured by quantitative Western blots, is high and is approximately one-fifth of the concentration of brain tubulin. Our new findings show that LIS1 is a protein exhibiting several cellular interactions, and the interaction with the cytoskeleton may prove to be the mode of transducing a signal generated by platelet-activating factor. We postulate that the LIS1-cytoskeletal interaction is important for neuronal migration, a process that is defective in lissencephaly patients." @default.
• W2001281440 created "2016-06-24" @default.
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• W2001281440 date "1997-12-01" @default.
• W2001281440 modified "2023-10-13" @default.
• W2001281440 title "Reduction of microtubule catastrophe events by LIS1, platelet-activating factor acetylhydrolase subunit" @default.
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• W2001281440 doi "https://doi.org/10.1093/emboj/16.23.6977" @default.
• W2001281440 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1170301" @default.
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