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The in vivo cellular microenvironment is regulated by a complex interplay of soluble factors and signaling molecules secreted by cells and it plays a critical role in the growth and development of normal and diseased tissues.
The inflammatory microenvironment is regulated by a balance between release of proinflammatory and anti-inflammatory cytokines [ 29].
The inflammatory microenvironment is regulated by epidermal growth factor/epidermal growth factor receptor (EGF-EGFR) signaling and is associated with development of hepatocellular carcinoma (HCC).
Recent work showed that effective communication between a cell and its microenvironment is regulated not only by the coordinate activity of cell-surface receptors, such as β1 integrin and epidermal growth factor receptor, but also by changes in nuclear architecture, as was demonstrated in experiments probing the functional contributions of the nuclear matrix protein NuMA.
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There is mounting evidence that these perturbations in the cellular microenvironment are regulated by the Ca2+-permeable transient receptor potential vanilloid 4 (TRPV4) channel.
We further found that the ILK-mediated phenotypes induced by stiff and hypoxic microenvironments are regulated by PI3K/Akt.
To gain further insights into how these microenvironments are regulated in vivo, we performed a candidate gene screen designed to identify factors that restrict BMP signal production to the cap cells that comprise the germline stem cell (GSC) niche of Drosophila ovaries.
Within the complex three-dimensional (3-D) in vivo microenvironment, hMSC migration is regulated through a myriad of extracellular cues.
The microenvironment in vivo is regulated through complex interactions between tumour and stromal cell types.
Our results show that the expression of Csf-1r is greatly reduced after culture in vitro (data not shown), suggesting that expression of CSF-1R is regulated by microenvironment-dependent epigenetics.
Whether or not stem cells self-renew or differentiate is regulated by the microenvironment.
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