Explain the defect in protein of Sickle-cell disease?

In sickle cell disease, a genetic mutation leads to a defect in the production of the beta-globin chain of hemoglobin, which is the oxygen-carrying protein in red blood cells. The normal beta-globin gene produces a protein called beta-globin, which combines with alpha-globin to form hemoglobin A, the most common form of hemoglobin in adults.

In sickle cell disease, a single nucleotide change in the DNA of the beta-globin gene results in the production of a defective beta-globin protein called beta-S globin. This change causes the hemoglobin molecule to become elongated and stiff, forming abnormal sickle-shaped red blood cells.

These sickle-shaped red blood cells have a shorter lifespan compared to normal red blood cells, which are typically round and flexible. They also tend to clump together, which can block small blood vessels and lead to various complications, including episodes of pain, tissue damage, and organ failure.

The defect in the protein in sickle cell disease affects the overall function of hemoglobin and the ability of red blood cells to carry oxygen effectively to different parts of the body. This can lead to a range of symptoms and complications that characterize sickle cell disease, including anemia, fatigue, infections, and other long-term health problems.