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TRP channel activity can be modulated by receptor signaling triggered by both growth factor receptors and G protein-coupled receptors.
Phosphorylation by protein kinase C (PKC) provides a key mode of regulation for synaptic GABAARs underlying phasic inhibition; however, less attention has been focused on the plasticity of tonic inhibition and whether this can also be modulated by receptor phosphorylation.
It is becoming clear that the regulation of the GPCR itself – its location, stability, and signal duration – is a key component of the signaling process [ 1, 2] The length of a GPCR signal can be modulated by receptor desensitization (decrease in receptor responsiveness) and receptor internalization (trafficking of receptors to endocytotic vesicles).
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Moreover, the angiotensin receptor function might be modulated by receptor-associated proteins such as AT1 receptor-associated protein (ATRAP), AT1 receptor associated protein 1 (ARAP1) for the AT1R and AT2 receptor interacting protein (ATIP) or AT2 receptor binding protein of 50 kDa for the AT2R (the topic is discussed extensively elsewhere [ 86]).
VGSCs can be modulated by receptors coupled to intracellular signalling molecules through the activation of cytoplasmic protein kinases to phosphorylate the specific residues on the α-subunit of the VGSCs.
The function of NR is modulated by receptor coactivators, it was therefore important that we were also able to demonstrate expression of mRNAs for PGC1α and β.
1, 2 Both ligand-dependent and ligand-independent activation of the ERα is modulated by receptor phosphorylation, and receptor phosphorylation is enhanced by ligand binding.
Both ligand-dependent and ligand-independent activation of estrogen receptor (ER)α is modulated by receptor phosphorylation and results in activation of the ERα-dependent pathways that are involved in endometrioid endometrial cancer (EEC) pathogenesis.
The response of a leukocyte to immune complexes (ICs) is modulated by receptors for the Fc region of IgG (FcγRs), and alterations in their affinity or function have been associated with risk of autoimmune diseases, including systemic lupus erythematosus (SLE).
Our findings indicate that behavioral sensitization to cocaine may be modulated by 5-HT1B receptor ligands in the accumbens shell, but not into the core.
26, 33 Second, the increase in GAP-43 proteins could be modulated by NMDA receptor activation.
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