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400. C) he variation in proteins expressed by each cell re- lects cell-speciic expression and repression of speciic genes. Each cell contains the same DNA in the nucleus and the same number of genes, and thus diferentiation results not from diferences in the genes but from selective repression and/or activation of diferent gene promoter Join @Superspeciality for more questions and detailed explanation For all recent updates, join https://t.me/DocopsyPoint_Superspeciality

399. Explanation A) (B) Hemochromatosis is defined as a disorder in iron metabolism that is characterized by excess iron absorption, saturation of iron-binding proteins, and deposition of hemosiderin in the tissues. The primary affected tissues are the liver, pancreas, and skin. Iron deposition in the liver leads to cirrhosis and in the pancreas causes diabetes. The excess iron deposition leads to bronze pigmentation of the organs and skin. In fact, the bronze skin pigmentation seen in hemochromatosis, coupled with the resulatant diabetes lead to the designation of this condition as bronze diabetes. The primary cause of hemochromatosis is the inheritance of an autosomal recessive allele. The locus causing hemochromatosis has been designated HFE and is a major histocompatibility complex (MHC) class-1 gene. The gene encodes an alpha-chain protein with three immunoglobulin- like domains. This alpha-chain protein associates with beta-2-microglobulin. Normal HFE has been shown to form a complex with the transferrin receptor and in so doing is thought to regulate the rate of iron transfer into cells. A mutation in HFE will therefore, lead to increased iron uptake and storage. The majority of hereditary hemochromatosis patients harbor a mutation in HFE that results in the substitution of Cys 282 for a Tyr. This mutation causes loss of conformation of one of the immunoglobulin domains in HFE. Another mutation found in HFE causes a change of His 68 to Asp. DMT1 (choice A) is responsible for the intestinal absorption of dietary iron and thus, a deficiency in this protein would lead to reduced total body iron, not excess. Ferritin (choice C) is the intracellular iron binding and storage protein. A deficiency in ferritin would lead to less iron deposition, not excess. Ferroportin (choice D) is the iron transport protein that moves dietary iron from within intestinal enterocytes across the basolateral membrane to the circulation, therefore, a deficiency in this protein would have consequences similar to deficiencies in DMT1. Transferrin (choice E) is the iron transport protein of the blood that binds to the trasferrin receptor on cell surfaces, allowing cellular uptake of circulating iron. A deficiency in this protein would lead to less iron deposition not more. @Superspeciality

399. Explanation A) (B) Hemochromatosis is defined as a disorder in iron metabolism that is characterized by excess iron absorption, saturation of iron-binding proteins, and deposition of hemosiderin in the tissues. The primary affected tissues are the liver, pancreas, and skin. Iron deposition in the liver leads to cirrhosis and in the pancreas causes diabetes. The excess iron deposition leads to bronze pigmentation of the organs and skin. In fact, the bronze skin pigmentation seen in hemochromatosis, coupled with the resulatant diabetes lead to the designation of this condition as bronze diabetes. The primary cause of hemochromatosis is the inheritance of an autosomal recessive allele. The locus causing hemochromatosis has been designated HFE and is a major histocompatibility complex (MHC) class-1 gene. The gene encodes an alpha-chain protein with three immunoglobulin- like domains. This alpha-chain protein associates with beta-2-microglobulin. Normal HFE has been shown to form a complex with the transferrin receptor and in so doing is thought to regulate the rate of iron transfer into cells. A mutation in HFE will therefore, lead to increased iron uptake and storage. The majority of hereditary hemochromatosis patients harbor a mutation in HFE that results in the substitution of Cys 282 for a Tyr. This mutation causes loss of conformation of one of the immunoglobulin domains in HFE. Another mutation found in HFE causes a change of His 68 to Asp. DMT1 (choice A) is responsible for the intestinal absorption of dietary iron and thus, a deficiency in this protein would lead to reduced total body iron, not excess. Ferritin (choice C) is the intracellular iron binding and storage protein. A deficiency in ferritin would lead to less iron deposition, not excess. Ferroportin (choice D) is the iron transport protein that moves dietary iron from within intestinal enterocytes across the basolateral membrane to the circulation, therefore, a deficiency in this protein would have consequences similar to deficiencies in DMT1. Transferrin (choice E) is the iron transport protein of the blood that binds to the trasferrin receptor on cell surfaces, allowing cellular uptake of circulating iron. A deficiency in this protein would lead to less iron deposition not more. @Superspeciality