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The mechanism by which SIRPα modulates chemokine-induced cell spreading and actin polymerization is unknown although several possibilities exist: a) directly activates protein phosphatase and initiates signal pathways that attenuate filament actin polymerization and cell spreading, and b) binding to integrin-associated protein CD47 and modulating the integrin functions.
Comm is known to bind to Robo receptors to help clear it from the membrane via endocytosis and sorting pathways [27] [30], although more recent data suggest that Comm may also initiate intracellular signaling pathways that attenuate midline repulsion independent of its ability to clear Robo from the membrane [31].
The cellular pathways that attenuate hepatic ER stress have been the focus of many recent studies, but the role of microRNAs (miRNA) in this process remains unknown.
In particular, core pathways that attenuate pathologic protein aggregation are remodeled, including small heat shock proteins and components of cytosolic HSP70/HSP90 chaperoning pathways.
At the same time, feedback pathways that attenuate these signaling readouts may play a major role in enhancing the development of drug resistance.
We developed a method to isolate and characterize infected cells that arrest after this early burst of proliferation and integrated gene expression and metabolic profiling to gain a better understanding of the pathways that attenuate immortalization.
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Thus, by upregulating ATF4, Gem activates apoptosis resistance, and oxidative and nutrient stress response pathways that are attenuated by ISRIB.
However, the internalization of metal-based nanoparticles by cultured cells and the subsequent changes in cellular biochemistry [14] suggest there is also a possibility for disruption of intracellular pathways that could ultimately attenuate viral replication.
Insulin resistance is associated with upregulation of the same inflammatory pathways that can be attenuated by insulin sensitization treatment.
In addition, cells and tissues from beagles with MLS may help to elucidate the mechanisms and pathways that normally prevent or attenuate skin and joint fibrosis.
Potential mechanisms for resistance to trastuzumab include steric inhibition imposed by other extracellular factors, molecular changes in the target receptor itself (ErbB2), alterations in the regulation of downstream signaling components, and crosstalk with other pathways that could compensate for attenuated ErbB2 signaling.
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