A single glycine residue in a conserved domain of the C. elegans CED-10 is crucial for controlling neurite outgrowth in a partially non-redundant manner. When CED-10 function is diminished the adaptor protein NAB-1 and its interacting partner SYD-1 can act as inhibitors of axon outgrowth.
we show that CED-10 binds to the RAB-5 GTPase activating protein TBC-2 that CED-10 contributes to recruitment of TBC-2 to endosomes and that recycling cargo is trapped in recycling endosomes in ced-12 ced-10 and tbc-2 mutants
mutations in GAP domain of CYK-4 lead to cytokinesis defects mimicking centralspindlin loss of function; defects could be rescued by depletion Rac; inactivation of Rac by centralspindlin functions in parallel with RhoA activation in cytokinesis
CED-10 GTPase acts to mediate corpse removal functionally linking two engulfment pathways and identifying the CED-1 -6 and -7 signalling module as upstream regulators of Rac activation
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