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It has been observed that cellular proteins that are strongly associated with the DSS1 molecule are resistant to SDS treatment or denaturation.
Furthermore, it has been observed that cellular membrane electrolyte transporter Na+-K+-ATPase dysfunction in diabetic subjects, can be secondary to hyperglycemia [ 39].
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First, a clear relationship between partition coefficient (log D7.4 value) and cellular uptake was observed; that is, lower log D7.4 corresponded with higher uptake.
It has been observed that a cellular capacity wall of 350 Mb/s/cell [6] is on the horizon.
It has been observed that the cellular uptake increases monotonically at the beginning and gradually reaches a plateau within several hours, indicating the obtainment of thermodynamic equilibrium [13], [14].
Before the UPR was discovered, it had already been observed that different types of cellular stress like viral transformation, inhibition of glycosylation and calcium ionophore treatment induced the expression of a select group of proteins.
Recently, it has been observed that this protein interferes with cellular autophagy (Gannage et al., 2009).
It has been observed that proteins involved in the cellular disassembly, such as hydrolases, proteases, and enzymes implicated in membrane degradation, are produced during PCD in Streptomyces.
However, under cellular conditions it has been observed that some subsystems can present chaotic local activities.
It was observed that during cellular reduction of molybdate, cells precipitated together with the molybdenum blue product preventing cellular growth.
It was observed that the cellular response to the diversion of metabolites for product formation, is at multiple levels directed both at growth rate and protein production.
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