Differential regulation of actin microfilaments by human MICAL proteins
Plexin
Actin remodeling
Growth cone
Myofilament
DOI:
10.1242/jcs.089367
Publication Date:
2012-02-14T01:46:44Z
AUTHORS (4)
ABSTRACT
The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling. also involved in regulating myofilament organization synaptic structures, serves as an actin disassembly factor downstream of plexin-mediated repulsion. In mammalian cells there are three known isoforms, MICAL1, MICAL2 MICAL3, well MICAL-like proteins MICAL-L1 MICAL-L2, but little their function, information comes almost exclusively from neural cells. this study we show non-neural human MICALs required normal organization, all regulate stress fibers. Moreover, provide evidence generation reactive oxygen species by crucial actin-regulatory function. However, although MICAL1 auto-inhibited its C-terminal coiled-coil region, remains constitutively active affects These data suggest differential complementary roles microfilament regulation.
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