You can directly edit the membrane receptor, if the defective for any reason, it is possible to prevent signal transduction to cause disease. Specific disease is caused by a membrane receptor dysfunction caused by failure or defect of the receptor caused by changes in the gene encoding the protein receptor. The TM4SF5 membrane receptor recently, scientists have discovered that it has something to do with the migratory capacity of liver cancer and liver cells. Peel and characteristics of membrane fluidity changes in NMDA receptors and in Alzheimer’s disease. Further, if it is infected with non-enveloped viruses, the virus binds to membrane receptors specific for the first, the film of endosomal vesicles or cell membranes of certain viruses, the cells other in some way subviral components virus or thereafter I finished on the cytoplasmic side of the cell membrane of. In the case of poliovirus, can lead to structural reorganization of the virus that results in the release of one of the proteins of the virus are known, and thus interaction with the receptor in vitro, hydrophobic myristylated VP4 of VP4 it. called The N-terminus. As a result of the introduction of myristic acid, available structural changes induced by the binding of the receptor to the formation of channels that VP4 could RNA cell membranes and does not enter the cells.
In addition to participating in acute signaling function, GPCR has long-term effects on cell proliferation and gene expression. Signaling pathways involved in cell proliferation transmit signals from the plasma membrane to the cytoplasmic space ultimately to the nucleus, and are stimulated by extracellular ligand few. I can as well as the tyrosine kinase-associated receptor, GPCR to intracellular activation Signaling relationship with a mitogenic effect. GA-protein GAQ, GPCR-trigger proliferation of these effects and Guy / move, is mediated by BD dimer and the corresponding class Ga12/Ga13 and gas. Growth-promoting activation of the GPCR.
The mitogen-activated protein kinase cascade, to regulate the expression of genes necessary for growth eventually. This can be done through the mechanism of may not include also include the GTPbinding G protein Ras’s or small. Further, a family of related marks enzymes modulate the activity of transcription factor c-JUNprotein phosphorylation and selectively to (due June kinase closely Specific GPCR, expression of genes related to under the influence) growth response of mediated effect, related to the low molecular weight GTP-binding by Russ Of Cdc42 and protein RAC1.
From the foregoing description, the structural change of the receptor molecule, that results in a functional change of GPCR-G-protein system is clear or residue of the major G-protein. Thus, mutation of the region involved in the binding of a ligand, usually
Whereas can lead to either mutation in the site involved in the activation of G protein-coupled receptors or the loss will be recognized (lossof function mutation) and activation signaling molecules The resulting receptor molecules on the receptor can be, modified (and activation in the absence of amplification offunction mutated ligand) activation or permanent functional. The other mutations, can cause decreased expression of membrane receptor molecule improper folding, and abnormal intracellular transport. Meanwhile, the function of G-proteins may be varied by the number of disease states
As a result of changes in expression level maladaptive mechanism and adaptive containing a mutation of the gene encoding the G-protein subunit of G-protein
Post-translational modification of G protein or mRNA or protein subunit. That both the germline mutations in the gene encoding the G-protein GPCR and body cause disease in humans has been found. Some examples of effects on cell function and intracellular signaling and mutation of these, I will explain in the next section.
The partition both organelles and whole cells and their fencing destruction of membrane function, can lead to pathological consequences different not surprising it. For role in regulating components or cytoskeletal anchoring fibers of the extracellular matrix, the binding site for the catalyst and enzyme transported out of the intracellular region of cells or for providing selective sensitivity by protein receptor When providing a film and to enable the organelle movement or target cell does not work, you can be anything else. In fact, when most diseases do not include a film of any shape, it is possible to say that much more.
According to the head Werner Kramer, metabolic disorders, sanofi-aventis, this diversity and the nature and function, to stop the reaction of more than one, that there is no unifying theme at all by classifying the disease caused by changes in cell membrane I mean. In fact, it is complicated by the endpoint similar the best for any or are likely to identify understand how drugs treat the work of them and some mechanism, underlying them suffer from the medical condition of the membrane-based I look like a break of a few you need to design further.
For example, membrane traffic may be interrupted by a change in the protein component of the cytoskeleton or bilayer lipid ubiquitous. As a result of the change in the number of proteins to populate structural parts receptors, transporters, and enzymes, and membrane function, example of a number of diseases or disorders are present. Target drugs, is moved to the logical target membrane these defects, disease of the target membrane protein-based, for example, the block, there is a tendency to cure or enhance the action of a protein, called to imitate. Second occurrences that interfere with traffic film, generated lipid membrane modification composition first when defect impairs membrane function in cytoskeleton parts: of what may be referred to as a disease-based film “real” by Kramer probably There are two categories.
While reducing the number of neutrophils to help the adhesion of sickled cells major drug therapy, the vessel wall sickle cell anemia, the hydroxy for, it is in order, because it reduces the formation of sickle hemoglobin, and improve the structural efficiency Then I considered. However, recent studies are hydroxyurea, may act directly on the plasma membrane was suggested. the drug to reduce the expression of adhesion molecules in red blood cells is known, one of them, phosphatidylserine is expressed on the outer surface of red blood cells in some of the abnormal sickle cell anemia. The study, which reduce the level of phosphatidylserine in a blood sample of his greatly sickle cell anemia in patients receiving hydroxy of 12 months of treatment.
In DMD, mutations in the dystrophin gene, affect the ability to add protein product cytoskeletal elements of the membrane surface. Adding damage and immune response of the following: – structural support is lost, pressure permeability, intracellular elevated cell membrane, it is cell “explosion”. It is considered effective for DMD gene therapy, but to be present in the eye to bring benefits to people already diagnosed is not expected. The mouse model is a pretty good understanding of the DMD, the role of the potential to find a way to increase the production of dystrophin-related protein utrophin and dystrophin abnormal and normal might be the first step to effective treatment.