The Expression Of Glycine Receptor Type 4A (Glr4A) In Mammalian Cells
Abstract
Kidney diseases damage the kidney's ability to filter blood which can lead to chronic symptoms that can deteriorate to kidney failure and then possibly death. One-in-six people who suffer from a kidney disease, suffer from kidney disease focal segmental glomerulosclerosis (FSGS), the goal in this study is to better understand some of the mechanisms underlying it. This specific area is very novel as the mutation of glycine receptor type 4a (GLR4a) was just recently discovered to contribute to FSGS and the amount of research done on glycine receptors in the kidneys is very scarce. Procedures carried out in this investigation included: multiplying bacterial cells with DNA that carried the targeted gene, isolating the DNA, quantifying the DNA, and assuring its purity before then inserting the DNA into mammalian cells and visualizing the proteins in cells using confocal microscopy. After visualization of the proteins it was evident that protein was structured and clustered in the cytoplasm of the mutant-type (cells with the targeted mutant gene) and more concentrated than the wild-type, while contrasting with the control-type cells in which protein was evenly distributed throughout the cell. This data would need to be further verified with more visualizations, but it does indicate that the mutant-type of GLR4a has an effect on the distribution of protein within the cell and further research could extend off of the findings of this research to find future solutions.
The Expression Of Glycine Receptor Type 4A (Glr4A) In Mammalian Cells
114 A
Kidney diseases damage the kidney's ability to filter blood which can lead to chronic symptoms that can deteriorate to kidney failure and then possibly death. One-in-six people who suffer from a kidney disease, suffer from kidney disease focal segmental glomerulosclerosis (FSGS), the goal in this study is to better understand some of the mechanisms underlying it. This specific area is very novel as the mutation of glycine receptor type 4a (GLR4a) was just recently discovered to contribute to FSGS and the amount of research done on glycine receptors in the kidneys is very scarce. Procedures carried out in this investigation included: multiplying bacterial cells with DNA that carried the targeted gene, isolating the DNA, quantifying the DNA, and assuring its purity before then inserting the DNA into mammalian cells and visualizing the proteins in cells using confocal microscopy. After visualization of the proteins it was evident that protein was structured and clustered in the cytoplasm of the mutant-type (cells with the targeted mutant gene) and more concentrated than the wild-type, while contrasting with the control-type cells in which protein was evenly distributed throughout the cell. This data would need to be further verified with more visualizations, but it does indicate that the mutant-type of GLR4a has an effect on the distribution of protein within the cell and further research could extend off of the findings of this research to find future solutions.
