Protein joins transport family

Article Abstract:

Cystic fibrosis is characterized by abnormally thick mucous secretions, especially in the lungs, which lead to infections and eventually death. The cystic fibrosis protein is similar to a group or family of identified proteins that are involved in the transport of molecules across the cell membranes. Cystic fibrosis patients cannot transport chloride ions, electrically charged molecules, across the cell membrane as efficiently as normal individuals. This results in decreased fluid secretion and abnormally thick mucous secretions in the lungs. The transport molecule in cystic fibrosis may be defective but a defect may also lie in the regulatory network that controls the transport. In greater than 60 percent of cystic fibrosis patients there was one amino acid, a building block of proteins, missing in the protein coded by the gene, in greater than 60 percent of the cystic fibrosis patients. The absence of the amino acid can lead to a protein that has either no function or an altered function. It appears that the protein in cystic fibrosis may have an altered function, in which case treatment of the disease may be possible. It is easier to modulate the function of a defective protein than to activate a protein that is not functioning at all. Using similar transport molecules as models, it may be easier to understand the defective function of the molecules involved in cystic fibrosis. The development of a treatment and perhaps a cure for cystic fibrosis may occur in the near future.

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Steady steps lead to the gene

Article Abstract:

Cystic fibrosis is an inherited disease which affects approximately one in 2,000 children born in Britain each year. Cystic fibrosis is characterized by abnormally thick mucous secretions, especially in the lungs, which lead to infections and eventually death. Approximately 5,000 children worldwide die each year from complications of the disease. The gene that codes for the molecule involved in cystic fibrosis was recently identified. It was localized by seeing if other genes already localized are inherited along with the gene for cystic fibrosis. The gene involved in cystic fibrosis codes for a protein molecule that is similar to other proteins that transport ions, electrically charged molecules, across the membranes of cells. There was one amino acid, a building block of proteins, missing in the protein coded by the gene in 70 percent of the cystic fibrosis patients. The absence of the amino acid can generate a defective protein molecule which can be involved in the disease process. Identification of the gene can be used for genetic screening of carriers of the defect and for prenatal diagnosis of cystic fibrosis. Knowing the structure and function of the defective protein may lead to new therapies and treatments and perhaps a cure for cystic fibrosis.

Reports, Genetic research

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Variation is now the theme

Article Abstract:

The development of human genetic linkage maps by two research groups clears the way for further progress in the Human Genome Project, the ambitious effort to determine the entire sequence of the human DNA molecule. Jean Weissenbach and co-workers derived a map from the 792 (C-A) repeat microsatellite markers including 600 markers that yield a plethora of genetic data. M. Guyer and a large number of multinational colleagues devised a map containing 1,416 loci embracing more than 90% of the genome. These maps are useful for linking genes with disease-causing phenotypes.

Forecasts and trends, Human genetics, Human Genome Project, Chromosome mapping

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