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Lapatinib blocks ligand-activated signaling from multiple receptor combinations, including homo-and heterodimers of EGFR and HER2 [5]; preclinically, it inhibits the proliferation of trastuaumab-resistant cancer cells [2], [6].
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Because epidermal growth factor (EGF -related ligands activatEGF -relatedHER receptors, and most tumours of epitheligandsigin express multiple HER receptors activatexpress one or more of the HER-relatedifferent, multiple HER receptorscombinandons mosttumourstive in a tumofr.
As these ligands activate different erbB receptors, it is possible that multiple erbB receptor combinations might be active in a tumor, a characteristic that could influence its response to an erbB-targeted therapeutic (Karunagaran et al, 1996).
In addition, ligands can bind to multiple receptor and/or co-receptor combinations to stimulate different downstream target gene expression.
Indeed, GSCs display elevated activity in multiple receptor tyrosine kinases, and the combination of sunitinib and gefitinb as well as sunitinib and sorafenib is effective in vitro.
The second type is referred to docking with multiple receptor structures, using pre-generated receptor conformers (Knegtel et al. 1997).
*Sorafenib and Sunitinib target multiple receptor tyrosine kinases (RTKs) in addition to the aforementioned receptors.
Moreover, in vertebrates, Notch signaling processes typically utilize combinations of multiple receptors and ligands.
Combination therapy can target multiple receptors and signaling pathways.
Although these BMP receptors and R-Smads are promiscuous and signal for multiple BMP subtypes, published data suggest that there is an optimal receptor combination for each BMP (Yu et al, 2008).
Each receptor can bind multiple chemokines within its class and each chemokine can bind multiple receptors.
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