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These experiments reveal a novel role for a Ras superfamily member in catalyzing cyclin E turnover during S phase, as well as an unexpected, essential role for the Golgi as a ubiquitylation platform for cell cycle control.
The F-box protein hCdc4 therefore appears to be the critical component for cyclin E turnover in normal cells.
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(D ) Quantification of the forespore specificity of σF activity based on CFP fused to the σF dependent spoIIQ promoter using strains as in C. (E ) Multiple turnover measurements of dephosphorylation of SpoIIAA-P.
To investigate E-cad turnover, we carried out FRAP experiments on E-cad-GFP to determine the stable fraction present in cell junctions in the tracheal system.
Given the fact that NDRG1 is induced by calcium ionophores [22] and E-cadherin turnover is calcium dependent, the location of NDRG1 and E-cadherin in DU-145 cells was investigated after calcium chelation and subsequent recovery in calcium supplemented media by immunoflourescence.
We saw no evidence for the core pathway affecting levels of E-cad transcription (Fig. 4M), suggesting that it might be altering E-cad turnover.
Importantly, the stable fraction of E-cad-GFP increased in branches of mutant embryos (Fig. 2D), consistent with reduced E-cad turnover.
We next investigated how the core pathway might regulate E-cad turnover.
Thus, we speculated that Rab11-mediated E-cadherin turnover is an important mechanism in colorectal tumor formation.
Taken together, Rab11 plays a role not just in E-cadherin turnover but also improves the cytoskeleton reorganization for cell migration.
To seek further evidence for planar-polarised E-cad turnover controlled by the core pathway, we looked in the embryonic epidermis.
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