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Indeed, these axons might be too far anterior to the source of Wnt in the tail, and thus be unable to activate the non-canonical pathway to promote termination.
Although acute innate pathway inflammatory responses promote termination of infection and wound healing, chronic activation of this pathway can lead to tissue damage and fibrosis and contribute to various disease states such as atherosclerosis, arthritis, inflammatory bowel disease and even cancer [1], [2], [3].
This preference is expected given that uORFs with strong signals would promote termination.
Interestingly however, they tend to avoid strong stop signals which would promote termination, instead allowing re-initiation of the ribosomal machinery to continue scanning.
They contribute to the desensitization of the GPCR after phosphorylation by G-protein coupled receptor kinases (GRKs) and thus promote termination of the G-alpha signal.
In inflammation, when the infection is already eliminated, but there are still many proinflammatory mediators in the microenvironment, in this case, the M1/M2 phenotype will promote termination of inflammation as a result of the negative feedback formation and increased production of the anti-inflammatory cytokines.
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Similarly, elegant studies have shown that Mmi1 selectively promotes termination of lncRNAs involved in developmental and environmental control of gene expression.
These results suggest that Mmi1 promotes termination of regulatory lncRNAs via a mechanism independent of its interaction with Erh1 or EMC formation.
In wild-type sepals, ROS accumulate in maturing cells and limit organ growth, suggesting that ROS are endogenous signals promoting termination of growth.
The increase in length of the base-paired region from six to ten matches as a result of this slippage event may have promoted termination of the CAN1 sequence at breakpoint 1.
Geminin facilitates the action of TopoIIα, thereby promoting termination of DNA replication at the same time it inhibits initiation.
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