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Indeed, Rab5-positive early endosomes (EE) can act as signaling platforms on which Rac is first GTP-loaded by the phosphatidylinositol 3-monophosphate (PIns(3 P)- and Ras-regulated guanyl exchange factor (GEF) T-lymphoma invasion and metastasis-inducing protein 1 (TIand) and then recycled to the plasma membrane in an Arf6-dependent manner to induce cell migration.
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Our results suggest a new mechanism in which RAC directly regulates protein translation by mechanically coupling cotranslational folding with the peptide-elongation cycle, and they lay the foundation for further exploration of regulatory roles of RAC in translation control.
Light-dependence of Rac activity was examined using a previously established biochemical method for assessing Rac activation, in which Rac was pulled down with the CRIB domain of the Rac effector p-21 activated kinase.
Activated Syk stimulates the guanine nucleotide exchange factor Vav3, the dominant isoform in osteoclasts, which transits Rac from its inactive GDP-bound form to active Rac-GTP [ 31].
For example, the enzyme lysyl oxidase (LOX) confers a motile phenotype on breast cancer cells by facilitating the formation of a p130Cas/Crk/DOCK180 complex, which sustains Rac activity and subsequent actin polymerization [ 19].
Proteins of the Rho GTPases family, which include Rac and Cdc42, function as molecular switches.
Two Rac-1 inhibitors were used: EHT1864 (Tocris), which places Rac-1 in an inert and inactive state [ 32] and NSC23677 (Calbiochem), which specifically inhibits Rac-1 GDP/GTP exchange activity [ 31].
The Primary Care Services Improvement Project (PCSIP) was a retrospective observational study, which used RAC-E methods to assign general practices to models of care based on observed differences in practice nurse activity in the provision of clinical-based services.
The ability of Rac to activate PAK is dependent on membrane translocation of Rac, which requires an integrin-dependent adhesion event.
To quantitatively determine the beta value for CC17 on amorphous cellulose (that is, the number of cellobiose lattices that was occupied by one molecule of CC17), we measured the TCAC based on regenerated amorphous cellulose (RAC), which was made by the dissolution in ice-cooled concentrated phosphoric acid followed by water precipitation.
Interestingly, the high RhoA activity in nocodazole-treated cells was slightly decreased upon CXCL12 stimulation, possibly reflecting an inhibitory effect of Rac (which is activated by CXCL12 [42]) on RhoA [43], [44].
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