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We recently published data suggesting that PI5P may regulate actin dynamics in cell migration.
Cdc42 may regulate actin and membrane trafficking to target secretory vesicles containing cell-wall synthases, cell-wall precursors, and membrane to the growth site [ 45].
This suggests that WT and H1047R MUT p110 α of PI3K may regulate actin cytoskeleton and cell migration by cooperation with Bcl-2 through distinct molecular mechanisms.
In germinated zygotes, FdRac1 localizes in the cortex at the rhizoid tip, suggesting that it may regulate actin assembly and dynamics.
This led us to postulate that besides actin, microtubules may contribute to the organisation of membrane raft architecture/clustering or that DIMs may regulate actin and microtubule function in pollen tubes.
A more likely scenario is that other palmitoylated proteins than ROPs may regulate actin MF dynamics in root hairs, as was reported for some receptor kinases during neuronal growth [ 6].
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Lastly, LAMTOR1 may also regulate actin remodeling by activating RhoA and RhoC through its binding to p27kip1.
A role for dendritic mitochondria is to buffer synaptic calcium; excess calcium may negatively regulate actin-binding proteins that are required for maintaining for spine density and plasticity (discussed below) [ 12, 57].
Additional evidence comes from proteomic data where up-regulation of multiple proteins in a coordinated signaling network may regulate the actin cytoskeleton dynamics as depicted in our proposed pathway model.
When over-expressed in the cytoplasm, p120-catenin may regulate the actin cytoskeleton and cell motility, through Rho GTPase activity [ 102].
These data led us to hypothesize that Lpd and Ena/VASP proteins may regulate the actin cytoskeleton at CCPs to support CME of the EGFR.
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