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VE-cadherin is integral to maintain vessel integrity.
Therefore, we hypothesize that SLITs maintain vessel integrity via SLIT2/ROBO1 ROBO4 interaction and because of more efficient binding of SLIT2 with ROBO1, it preferentially binds to ROBO1, leading to the deficiency of free SLIT2.
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Binding of the agonist Ang-1 maintains vessel integrity, inhibits vascular leakage, suppresses inflammatory gene expression, and prevents recruitment and transmigration of leukocytes [ 3].
ANG-1 signalling through TIE-2 maintains vessel integrity through the recruitment of pericytes, while ANG-2 blocks ANG-1/TIE-2 signalling, loosening the vascular structure and exposing the endothelium to inducers of angiogenesis such as VEGF [ 45].
Binding of the agonist Ang-1 to the endothelial Tie2 receptor maintains vessel integrity, inhibits vascular leakage, suppresses inflammatory gene expression, and prevents recruitment and transmigration of leukocytes [ 7, 8].
Therefore, the interaction of extracellular domain of ROBO4 with extracellular domain of UNC5B may be required to maintain the vessel integrity.
MSC appear to exert yet another pertinent function, namely maintaining blood vessel integrity [ 2,3 ].
In conclusion, our study demonstrates that CD34 promotes tumor growth at an early time-point (day 14), by playing a key role on vasculature, maintaining appropriate vessel integrity.
These findings demonstrate increased vascular dye leakage in Cd34−/− mice, suggesting a role for CD34 in maintaining tumor vessel integrity and demonstrate that CD34 is required for optimal early tumor growth.
It promotes angiogenesis, blood vessel permeability and maintains tumour vessel integrity (Shweiki et al, 1992; Yancopoulos et al, 2000).
Cadherin-5, which is also called vascular endothelial cadherin, is found in endothelial cells and is part of the adherens junction that maintains blood vessel integrity.
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