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The quantity of ECM relative to cell mass is very high during embryonic development and declines towards the time of birth, while the composition of matrix proteins also changes.
Matrix proteins also serve as reservoirs for molecules released from wall-residing cells that promote communication between different layers.
Our previous comparative proteomic analysis for uterine fluid and eggshell matrix proteins also identified that many bone-development related proteins were up-presented in strong eggshell group [ 15].
Previous studies showed that chemokines produced by thymic microenvironmental cells, together with extracellular matrix proteins (also secreted by the thymic microenvironment), have a pivotal role in thymocyte migration, and data suggest a combinatorial role for these molecules in this migratory process [3], [28], [29].
In parallel, up-regulation of extracellular matrix (ECM) components, as well as increased cross-linking of matrix proteins, also occurs postnatally, leading to an overall stiffening of the heart tissue (Janmey and Miller, 2011; Swift et al., 2013; Majkut et al., 2014).
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Fibulin-1 is an elastin- and basement membrane-associated extracellular matrix protein also present in plasma.
One promising candidate is COMP (cartilage oligomeric matrix protein, also called thrombospondin-5), originally isolated and characterized in cartilage [ 13].
Quantitatively, more minor components (e.g. type IX, XI and VI collagens, biglycan, decorin and cartilage oligomeric matrix protein) also have important roles in controlling the supramolecular organization of the matrix [ 3].
Quantitatively more minor components (for example, type IX, XI, and VI collagens, biglycan, decorin, and cartilage oligomeric matrix protein) also have important roles in controlling matrix structure and organisation [ 2].
Quantitatively more minor components (for example, type IX, type XI and type VI collagens, biglycan, decorin, cartilage oligomeric matrix protein) also have important roles in controlling the supramolecular organization of the matrix.
As well as changes to bone matrix proteins we also investigated whether key bone regulatory genes were also altered that might be driving the osteoproliferative response.
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