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In this study, lectin-sensitive polymer gels showing volume changes in response to the formation of molecular complex between pendant carbohydrate and target lectin Con A were prepared.
A lectin-sensitive polymer gel that undergoes volume changes in response to the formation of molecular complex between 'pendant' carbohydrate and a 'target' lectin concanavalin A [Con A] was synthesized.
First, we will describe the preparation of a lectin-sensitive polymer gel that undergoes volume changes in response to the formation of molecular complex between carbohydrate and a lectin concanavalin A [Con A] (Figure 1).
LPA-induced molecular complex between LPA2 and Siva-1 plays a major role in the anti-apoptotic effect of LPA.
Thus, it is possible that the molecular complex between the triadins and Cav-3 requires a direct interaction of Cav-3 with the DHPR.
Using the Y1 andand Y1 A2 BiFC cell lines we were able to correlate our observations on the slowed diffusion of NPY stimulated Y1 receptors, with the behaviour of the underlying molecular complex between the receptor and arrestin proteins.
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The molar stoichiometry and the crystal structure of four molecular complexes between poly ethylene oxide) (PEO) and p-dichlorobenzene (PDCL), resorcinol (RES), hydroquinone (HYD) and p-nitrophenol (PNP) are compared.
It remains to be investigated whether formation of the molecular complexes between CAMs and Ca2+ channels directly influences the activity of the latter.
The formation of a multi-molecular complex between mTOR and regulatory-associated protein of mTOR (raptor) has a role in cell proliferation, survival and tumour angiogenesis (Le Tourneau et al, 2008).
The boost in the photocurrent density mainly is due to the molecular complex formation between DEOX and redox species in the electrolyte solution that promotes the electrochemical properties of electrolyte.
Recent reports have also pointed towards an alternative role of E-cadherin in carcinogenesis, which suggests that it may not just be that of a "sticky" molecular complex in between cells – the dysregulated over-expression of E-cadherin may participate in tumor progression through its associated cellular mechanisms [ 8– 10].
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