Protein cell stabilisation

The application of synthetic glycopolymers in signal transduction and protein/cell stabilisation has emerged as a relatively new area for such materials. The impact of glycopolymer structure on... 

Such damage is more likely to occur when DNA is stripped of the proteins that stabilise it (e.g. histones). Consequently, the concentration of p53 is high in rapidly dividing cells but low in quiescent cells. 

In an other hand, NO inhibits iNOS expression. When NO provokes the p53 accumulation, this one could in return inhibit iNOS gene transcription [154], Repression is observed in DLD-1 cells (human colon carcinoma) or Calu 6 cells (human pulmonary carcinoma) which express wild type p53. High NO concentration leads to p53 nitrosylation and inhibits the repression [114]. The wild type but not the mutated or the nitrosylated protein binds the iNOS gene promoter. Moreover, exogeneous NO produced by NO donors can inhibit NFkB activity in whole cells and in acellular preparation [155-157]. Those results have been confirmed in endothelial cells in which NO produced by eNOS inhibits NFkB activity and iNOS gene transcription [158], The inhibition can be explain in parts by NFkB sub-unit p50 nitrosylation [155], but also by its cytoplasmic inhibitor protein IxBa stabilisation (IkB proteins functionally retain NF-... 

The MHC protein helps to stabilise the binding between the T-cell receptor and the peptide. 

There is a family of proteins (the Bcl-2 family) that can regulate the potential across the inner mitochondrial membrane, and its permeability. Hence, they can influence apoptosis. Some of this family stabilise the inner membrane and maintain the potential, so that they suppress apoptosis. They are known as cell survival molecules (e.g. the proteins, Bcl-2, Bcl-X). Other members of the family destabilise the mitochondria and decrease the membrane potential which facilitates apoptosis. They are known as cell killer proteins (e.g. the proteins, Bax, Bak). The mechanisms by which they have their effects on mitochondria are not known. They are, of course, of considerable interest for the development and control of growth of tumour cells (See Chapter 21). 

Figure 21.14 A summary diagram of how damaged DNA leads to arrest of the cell cycle. Damaged DNA activates a protein kinase which phosphorylates and hence stabilises p53, which stimulates transcription of the p21 gene which expresses a protein that arrests the cycle. CDK, cell cycle division kinase.

Behnke, O., Ammitzboll, T., lessen, H., Klokker, M., Nilhausen, K., Tranum-Jensen, H., et al. (1986) Non-specific binding of protein-stabilised gold sols as a source of error in immunocytochemistry. Eur. J. Cell Biol. 41, 326-338. 

Peloruside A 14 (Scheme 6.1 Part 2) was isolated from a New Zealand Mycale hentschei marine sponge and initially showed activity against P388 murine leukaemia cells at 10 ng/mL.98 Peloruside s cytotoxicity profile and structural similarity to bryostatin led to the examination of protein kinase C (PKC) as a possible mode of action.242 This was determined to be incorrect and it was soon established that the remarkable activity of peloruside was through the stabilisation of microtubules at a site distinct from the taxoid site.243... 

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