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The integrity and functions of blood-brain barrier (BBB) are regulated by the expression and organization of tight junction proteins.
The sorted cells were characterized by immunohistochemistry to evaluate the expression and organization of α-SMA, SM-MHC and calponin filaments.
The expression and organization of other adhesion complexes, in particular tight junctions, was then investigated in both cell systems.
These results strongly support that LOXL2 negatively modulates the expression and organization of cell polarity complexes in basal-like carcinoma cells.
Together, these data indicate a negative role for LOXL2 in the expression and organization of tight junction complexes of basal-like carcinoma cells.
To obtain further insights into the regulation of EMT mediated by LOXL2 in basal-like carcinoma cells, we next studied the expression and organization of cell polarity components.
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The specific expression and organization of those ion channels form the basis for the membrane and Ca2+ clocks, both of which contribute to the spontaneous diastolic depolarization of phase 4. Pacemaker cells do not express Kcnj2, which is highly expressed in all contractile cardiomyocytes.
These restrictive properties are bestowed upon the BBB by unique features of the microcapillary endothelium such as: 1) expression and organization of intercellular tight junction (TJ) complexes [ 2, 3]; 2) polarized expression of specialized carrier systems for selective transport of essential nutrients; 3) non-selective drug efflux pumps [ 4, 5].
The DHAC method is a general solution to this problem and provides a multi-resolution view of dynamic expression and organization of the proteome.
Amongst other factors, the inducers of EMT, ZEB and SNAI downregulate the expression and functional organization of core polarity complexes.
In contrast, epithelial signature expression and organization of E-cadherin and F-actin were absent in MCF-7-MEK5 and MDA-MB-231 cells.
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