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Western blotting analysis of a number of different types of cells indicated that cultured human vascular smooth muscle cells express Tie2 under the experimental conditions, although the level of expression is much lower than that in endothelial cells.
This is indeed the case; however, despite the fact that arterial smooth muscle cells express multiple isoenzymes of the GRK family (22), only GRK2 expression has been reported to be elevated in both hypertensive patients (8) and in rodent models of hypertension (9, 10).
Instead, muscle cells express core ECM components, including all 19 collagen-encoding genes.
Muscle cells express both PW1 and Hsp70, and we show that these two factors interact.
We therefore propose two possible mechanisms: (1) upon differentiation, muscle cells express 'receptors' that are anchored to the nuclear surface and that bind centrosome proteins (Fig. 7A).
Ascidian muscle cells express homologs of vertebrate transcriptional regulators required for specification and differentiation of paraxial mesoderm, including Snail, Tbx6 and MyoD ([6]; reviewed in [7]).
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Inflammatory pathway activation and cytokine expression were analyzed in L6 muscle cells expressing myc-tagged GLUT4 (L6GLUT4 myc) exposed to 0.2 mM palmitate or palmitoleate.
Smooth muscle cells expressed smooth muscle markers (Actg2, Cnn1, and Des), but lacked myoFB markers Pdgfra and Ednrb.
Muscle cells expressed genes involved in protein secretion, but these genes did not display tissue-enriched expression (Supplementary Figs. 2 and 6, Supplementary Data 3).
The skeletal muscle cells expressed α-MHC and α-actinin (markers for both skeletal muscle and cardiomyocytes), and Nebulin (specific for skeletal muscle), but not Gata4 (specific for cardiomyocytes) (Supplementary information, Figure S7a).
Endothelial cells, macrophages, and skeletal muscle cells expressed TG throughout the healing process.
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