Sickle Cell

In Unit 5 we learned how and why falciform cells preserve usual cells and how sickle-cell anemia occurs. We learned how its DNA differs from a normal cells DNA, how mutations chamberpot influence it, and how the order of amino group acids outhouse change the protein. Even the slightest mutations shadow change a patrimonial disorder.
During the process of transcription, mutations can occur which can effect in a catastrophic change. Changes in the hemoglobin, the red consanguinity cells protein, can cause the red blood cells to change to sickle of a C shape. Sickle-shaped cells do not effectively enjoy oxygen by blocking circulation in small blood vessels. If the alleles ar heterozygous for both normal and sickle-shaped cells, they can still live a normal lives, as the normal blood compensates for the sickle-shaped cells.
As a result of these changes, proteins properties are changed. Single point mutation occurs in sickle-cell anemia. In the character reference of sickle cell disease the codon for glutamic acid GAA has been substituted with a valine GUA in the protein.
This changes the composition of the hemoglobin and is the cause of this disorder. The hemoglobin folds differently because of the non-polar amino acid. This change results in sickle cell disease.




The order of amino acids can play a specific role in the development of a cell. If the codons are not properly matched to its antonymous bases, changes like the folding and stability of the protein can occur. In sickle-cell disease, the incorrect nucleotide can be added only for one in one hundred thousand bases. It can go unsteady in less than one in one billion.
In conclusion, it is apparent that even the smallest changes in amino acids can affect a normal cell and convert it to a disorder. For example, the switching of nucleotides in a normal cell can result in a sickle-shaped cell. This inhibits the passage of oxygen thence resulting with sickle-cell anemia.

Martin Nunez
Biology
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