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Because of receptor adaptation, the amplitude varied during each treatment.
9 We hypothesise that because of receptor redundancy a generalised defect in adhesion due to 77H is unlikely to be an important pathogenic mechanism in SLE.
However, in practice, these slightly larger responses might be difficult to detect because of receptor saturation and desensitization effects at these concentrations.
The reason for the differences in cell specificity ex vivo is currently unclear but may be because of receptor expression distribution and levels and/or differences in surgical approaches to graft harvest and treatment.
In malignant gliomas, activity of this signaling network is frequently increased because of receptor tyrosine kinase over-activity, loss of PTEN tumor suppressor, and/or mutated oncogenic PI3K subunits [ 6].
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This is because down regulation of receptor signaling provides a means to attenuate proliferation and minimize cell growth.
However, because the number of receptor cells is limited, some of the cells must express more than one type of receptor protein.
The use of these agents may be compromised because of emergence of receptor mutations during therapy or increased expression of cofactors which potentiate agonistic effects of hydroxyflutamide, such as CREB-binding protein (CBP) or gelsolin (Culig et al. 2005).
Because the results of receptor imaging studies have a large variability, this article has chosen two model cases that could be representatives of the results.
Our data suggest, furthermore, that these Abs can also activate angiotensin and endothelin receptors across both species because of high receptor homology [ 34, 35].
Because of these characteristics of receptor desensitization, true steady-state responses could not be determined.
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