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Additionally, as insulin/insulin growth factor receptor is a general controller of cell size, presumably as the result of MAPK dependent control of the overall rate of translation [ 45], our observation that functional MAPK is required to produce protein the degradation observed in response to knockdown of most kinases suggests that our observations may be not specific to muscle.
The mTOR pathway involves two functional complexes: the mTOR complex 1 (mthat1) that is an important controller of cell growth and proliferation and plays a major role in controlling autophagy, and the mTOR complex 2 (mthat2) that is not directly implicated in autophagy modulation.
The Target of Rapamycin Complex is a central controller of cell growth and differentiation in eukaryotes.
The target of rapamycin (TOR) is a large (281 kDa) conserved Ser/Thr protein kinase that functions as a central controller of cell growth.
TOR (Target of Rapamycin) kinase is a highly conserved, central controller of cell growth [1] [3].
TOR (Target of Rapamycin) is a highly conserved protein kinase and a central controller of cell growth.
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Cell cycle_1 collects most of the canonical controllers of cell cycle progression and is linked to several DNA processing pathways, as discussed in the Results section.
These results indicate that oncogenes like Bcl-xL, besides regulating absolute death values, can have a novel role as active controllers of cell-cell variability and the extent of adaptation.
mTOR is recognized as a central controller of eukaryotic cell growth and proliferation, in that it senses nutritional status and mitogens in mammalian cells and allows for the progression from G1 to S phase, although it may not be the only target of rapamycin.
Since first discovered more than a decade ago [ 128,21] the Aurora kinase family has emerged as a major controller of the cell cycle and mitosis.
Ang-2, on the contrary, functions as an autocrine controller of endothelial cells in a context- dependent manner promoting either blood vessel growth or regression depending on the levels of other growth factors, such as VEGF-A [ 16, 17].
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