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Subsequently, targeted cell based in vitro studies have been conducted to identify the selectivity, potency and efficacy of environmentally relevant chemicals that can modify receptor function.
Here we show that this is the case for the channel blocking compound PXN, but increasing or decreasing the size of residue 16′ does not cause major changes to GABA-induced activation, indicating that the properties of the residue at this location do not significantly modify receptor function.
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Here we show that almost all of the known mouse exons have corresponding orthologs within the human OPRM1 gene locus and can be subject to genetic variability, which modifies receptor function and associated phenotypes.
In light of the receptor mechanism suggested above for Asc enhancement of adrenergic function, and since Asc modifies dopamine binding to its receptors [1], [18] and binds to the first extracellular loop of the histamine receptor [4], it was logical to search for an Asc binding site on the AR that could act allosterically to modify receptor sensitivity.
Our results also suggest that newly discovered alternative exons, rather than constitutive exons, may represent targets for genetic variability which modifies OPRM1 receptor function.
This was an intended result for this modified receptor.
We examined how structurally and functionally diverse compounds included in the Tox21 chemical space modify core nuclear receptor functions of VDR with respect to VDR heterodimerization with human RXRα, recruitment of coactivator (SRC-1) or corepressor (NCoR), and the ability to initiate/inhibit transactivation of CYP24A1.
Using conditioned place preference as the behavioral readout, we studied nicotine induced associate learning in a genetically modified mouse model where NMDA receptor function is selectively blocked in the dompaminergic neurons.
Admittedly, we cannot entirely rule out the possibility that DOP and MOP receptor are located in different neurons of a network and that decreasing DOP receptor function is sufficient to modify the input of this neuron on a MOP receptor-positive neuron to regulate its functions.
Inhaled drugs of abuse enhance serotonin-3 receptor function.
CD147 immunoglobulin superfamily receptor function and role in pathology.
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CEO of Professional Science Editing for Scientists @ prosciediting.com