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Thus our patient group may not manifest the shift of receptor expression.
For example, a shift of receptor labelling from inside the cell and towards the cell membrane might be explained by an increase in the LD of the membrane (reflecting an increase in receptor concentration) or in the total amount of membrane (due to an increase in the surface area of cell membrane rather than a change in receptor concentration).
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Moreover, the E6/E7-transfected keratinocytes exhibit a shift of TNF receptor profile from type 1 to type 2 and weakened apoptotic response to TNF-α stimuli, when compared with the normal control.
The phase shift of the receptor activity increases to π at high frequencies, indicating that the activity simply follows the output (a negative sign is due to the negative response of the activity to attractant concentration [ 28]).
Curiously, after a single episode of kainate-induced seizures in immature rats, there is a long-term shift of GluA1 receptor from the membrane to the intracellular compartment and a loss of total GluN2A in the rat hippocampus [ 40], changes that may increase hyperexcitability of the cellular membrane, but that would be undetectable when studying global tissue levels of expression.
A shift of the receptor-binding specificity of the avian virus HA from Neu5Acα2-3Gal recognitoon to Neu5Acα2-6Gal recognition is thought to be a prerequisite for the generation of pandemic viruses [ 25, 26, 47], however, no functional changes in the avian NAs of 1918 and 1957 viruses have been identified so far.
A shift of the receptor-binding specificity of the HA from Neu5Acα2-3Gal recognitoon to Neu5Acα2-6Gal recognition is believed to be essential for the emergence of these pandemic viruses [ 25, 26, 47], whereas functional changes in their NAs have not been identified.
The fluoride binding leads to red shift in the absorption spectrum of receptor and SO42− binding causes blue shift.
The corresponding UV‐vis measurements showed a bathochromic shift of the 395 nm band of receptor 1 to ~ 500 nm for fluoride and pyrophosphate.
This inhibition may be caused by a shift of the TNF-α receptors at the surface to lipid rafts.
This must be due to a shift of the interface between different receptor dimers, within previously suggested trimers of dimers, or even higher order complexes.
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