Bacteria, cell membrane protein content

The abnormal deposits found in the brains of CJD victims consist of an abnormal isoform of PrP. Prion protein is normally found in cells. Detailed structural studies show that normal cellular PrP (PrP ) is a soluble protein whose conformation is rich in a-helices with very little P-sheet. The PrP protein extracted from the brains of CJD victims (i.e., PrP ) is identical in primary amino acid sequence to the normal PrP (PrP ). However, PrP has a much greater content of P-sheet conformation with little a-helical structure. Thus PrP is neurotoxic because of its three-dimensional structure. When the prion protein is predominantly in an a-helical conformation it is nontoxic when the prion protein is predominantly in a P-sheet conformation, it kills neurons. The prion protein is thus made neurotoxic not by its amino acid composition but by its conformation. This concept is both fascinating and terrifying. Prion diseases are transmissible thus prions are infectious agents. However, prions are not like bacteria or viruses, or other infectious microbes—they are simply protein molecules. Prions are not microbes with cell membranes and nucleic acids they are not living things. Indeed, prions are not even infectious molecules, they are infectious molecular shapes. 

Bacteriolysis. Bacteriolysis is a complement-mediated reaction. The last Five proteins in the cascade scif-asscmble to produce a membrane attack complex (hat disrupts the cell membranes of bacteria, acting like bacitracin or amphotericin B. The cell membranes lose integrity, cell contents leak... 

A membrane in a cell wall fulfills a number of functions. It acts as a barrier to prevent the contents of a cell from dispersing and also to exclude external agents such as viruses. The membrane, however, does not have a purely passive role. It also enables the transport of ions and chemicals such as proteins, sugars and nucleic acids into and out of the cell via the membrane proteins. Membranes are important not only as the external cell wall, but also within the cell of eukaryotes (plants and animals, but not most bacteria) where they subdivide the cell into compartments with different functions. 

Therefore, if the recipient cell does not express the specific lipids required by the receptor (which may concern the acyl chain content of sphingolipids), or an adequate cholesterol-sphingolipid balance, the transfection experiment may lead to an abxmdant expression of a totally inactive receptor. In 2003, Opekarova and Tanner published a list of more than 30 membrane proteins whose activity is specifically affected by lipids. The list covered a broad range of proteins expressed by various bacteria, yeasts, insect, and mammalian cells. The problem is particularly acute when mammalian receptors or transporters are expressed in bacteria. For instance, the failure to express fxmctional serotonin transporters in E. coli has been attributed to the lack of cholesterol in bacteria. Moreover, the recovery of fully active neurotensin and adenosine receptors in transfected bacteria required the presence of choles-teryl hemisuccinate (a cholesterol derivative) during solubilization. Paradoxical results have also been obtained for some proteins whose activity requires cholesterol but can be fxmctionally expressed in bacterial hosts. In this case, one can exclude a direct interaction of cholesterol with the protein but rather consider a more general effect of the sterol on membrane properties. As a matter of fact, we are just at the beginning of our comprehension of the complex molecular ballet that involves bofh lipid and protein actors in the plasma membrane of excitable cells. 

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