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Why the Met-Glu-Glu-Gly-Met-Met-Val-Leu-His Amino Acid Can Be Dangerous - Lab Report Example

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The paper “Why the Met-Glu-Glu-Gly-Met-Met-Val-Leu-His Amino Acid Can Be Dangerous?” gives portrays the amino acid gene, the inheritance of which can provoke the particular pathology in a child while its timely detection in the fetus helps to prevent the disease in the next kid of the given parents…
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Why the Met-Glu-Glu-Gly-Met-Met-Val-Leu-His Amino Acid Can Be Dangerous
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Download file to see previous pages The Met-Glu-Glu-Gly-Met-Met-Val-Leu-His amino acid may be encoded by several triplets; the use of the different oligonucleotide probes is often required.  For the methionine the codon is AUG. So the probe constructed must have the starting code as TAC. The Glutamic acid has the two triplet codons. GAA and GAG. The Glycine has four triplet codons. GGU, GGC, GGA, and GGG. The valine has four triplet codons GUU, GUC, GUG, and GUA. The leucine has six triplet codons namely CUU, CUC, CUG CUA, UUA, and UUG. Histidine has two triplet codons namely CAU and CAC. Therefore the peptide sequence Met-Glu-Glu-Gly-Met-Met-Val-Leu-His  corresponds to ( 1 x 2 x 2 x 4 x 1 x 1 x 4 x 6 x 2 = 768 ) 768 possible DNA sequences. After the designing of the probe, this is a part of the DNA or RNA that is used to detect specific nucleic acid sequences by the hybridization technique. The probes are radioactively labeled and these hybridized probes can be identified by using the autoradiography. Autoradiography is used for analyzing the extend to which the hybridization with the radiolabeled probes occurs and to monitor the in-situ hybridization level. (Tenover, 1989). The human genomic library (Clontech) can be used to identify the gene of interest because this human genomic library of Clontech is widely used for the rapid screening of the adenovirus associated gene therapy.
Glycogen storage disease type 1 a (GSD 1 a) disease is caused by the deficiency in the synthesis of an enzyme called Glucose 6 phosphatase (G6Pase). A g6pase enzyme is a key enzyme in the glucose homeostasis. Glucose homeostasis is the maintenance of the balance between glyconeogenesis and glycogenolysis. GSD 1a is characterized by hypoglycemia, liver and kidney enlargement, hyperlipidemia, hyperuricemia and retardation of growth. The lack of Glucose 6 phosphatase is an autosomal recessive disorder. G6Pase catalyzes the terminal steps in gluconeogenesis and glycogenolysis. The glucose 6-Phosphate is concerted into Glucose molecule and phosphate. (Zingone, 2000). G6Pase is present in the endoplasmic reticulum as a membrane-spanning protein. The active site of this protein is presently facing the lumen. G6Pase requires a transporter molecule to transport the Glucose-6- phosphate from the cytoplasm to the endoplasmic reticulum. The organ transplantation and its effect on the GSD 1a were studied separately for kidneys and liver. It was found that the kidney replacement was not able to eradicate or reduce neither the hypoglycemia nor the hyperuricemia. When the liver was transplanted to the GSD 1a patients they found that they were able to reduce the hypoglycemia and its abnormalities and were able to have an improvement. Thus the gene therapy target was chosen as the liver. After the gene therapy target was selected, the selection of the vector was considered into account. The use of the adenovirus-mediated gene targeting was chosen. The efficiency of the helper-dependent mediated (HDAd) hepatic delivery of the G6Pase was tested and found to be the suitable model for the prolonged survival and the sustained correction of the metabolic abnormalities. (Koeberl, 2007). When the HDAd vector was administered along with the G6Pase into a 2-week old G6Pase knock out mice and tested, it was observed that the survival rate of the test animal was an average of 7 months as compared to the control that died after 3 weeks of age. The reduction in the accumulation of Glycogen, the increase in the growth as that of the wild type, minimal or no symptoms of hypoglycemia and hypercholesterolemia are the results of the gene therapy. As the success rate is very high for the mice, the same amount of success can be expected for the humans also. Here the conclusion is yes, we can clone the mouse gene into the human gene as they both resemble each other. ...Download file to see next pagesRead More
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