Mutations in the F8 and F9 genes cause hemophilia. Changes in the F8 gene are responsible for hemophilia A, while mutations in the F9 gene cause hemophilia B. The F8 gene provides instructions for making a protein called coagulation factor VIII. A related protein, coagulation factor IX, is produced from the F9 gene. Coagulation factors are proteins that work together in the clotting process. After an injury, blood clots protect the body by sealing off damaged blood vessels and preventing further blood loss. Mutations in the F8 or F9 gene lead to the production of an abnormal version of coagulation factor VIII or coagulation factor IX. The altered protein cannot participate effectively in the blood clotting process and, in some cases, the protein does not work at all. A shortage of either protein prevents clots from forming properly in response to injury. These problems with blood clotting lead to excessive bleeding that can be difficult to control. Some mutations almost completely eliminate the activity of coagulation factor VIII or coagulation factor IX, resulting in severe hemophilia. Other mutations reduce but do not eliminate the activity of one of these proteins, which usually causes mild or moderate hemophilia. The other, rare form of this condition, acquired hemophilia, results when the body makes specialized proteins called autoantibodies that attack and disable coagulation factor VIII. The production of autoantibodies is sometimes associated with pregnancy, immune system disorders, cancer, or allergic reactions to certain drugs. In about half of cases, the cause of acquired hemophilia is unknown. Read more about the F8 and F9 genes. Hemophilia A and hemophilia B are inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier. She can pass on the altered gene to her children, but usually does not experience signs and symptoms of the disorder. In about 10 percent of cases, however, females who carry one altered copy of the F8 or F9 gene will experience mild problems with bleeding. From: http://ghr.nlm.nih.gov/condition=hemophilia
Mutations on recessive genes return to normal in an organism
Somatic mutations occur in non-reproductive cells and are not passed on to offspring because they do not affect the germline cells (sperm and eggs) that give rise to the next generation. Only mutations in the germline cells can be inherited by offspring.
Muscular dystrophy is a genetic condition caused by mutations in genes responsible for the structure and function of muscles. These mutations lead to muscle weakness, wasting, and degeneration over time. There are many different types of muscular dystrophy, each caused by mutations in specific genes.
Hemophilia is most often caused by mutations in the F8 gene, located on the X chromosome. This gene provides instructions for making a protein called factor VIII, which is essential for blood clotting. Mutations in the F8 gene can result in reduced or absent levels of factor VIII, leading to the characteristic bleeding problems seen in hemophilia.
Traits like colorblindness, hemophilia, and Duchenne muscular dystrophy are carried on the X chromosome. These traits are caused by mutations in specific genes located on the X chromosome, such as the OPN1LW and OPN1MW genes for colorblindness and the F8 and F9 genes for hemophilia.
No, none of them do that. F7 starts a spell check. F8 starts a selection. F9 recalculates the spreadsheet. F10 starts the menu system.
fart for 43 hrs and then press f5 f8 f9 f7 f5 and f1 f2 f3 f4 f5 f6 f7 f8 f9 f10 f11 f12
esc, f1, f2, f3, f4, f5, f6, f7, f8, f9 :)
Mutations in the F8 and F9 genes cause hemophilia. Changes in the F8 gene are responsible for hemophilia A, while mutations in the F9 gene cause hemophilia B. The F8 gene provides instructions for making a protein called coagulation factor VIII. A related protein, coagulation factor IX, is produced from the F9 gene. Coagulation factors are proteins that work together in the clotting process. After an injury, blood clots protect the body by sealing off damaged blood vessels and preventing further blood loss. Mutations in the F8 or F9 gene lead to the production of an abnormal version of coagulation factor VIII or coagulation factor IX. The altered protein cannot participate effectively in the blood clotting process and, in some cases, the protein does not work at all. A shortage of either protein prevents clots from forming properly in response to injury. These problems with blood clotting lead to excessive bleeding that can be difficult to control. Some mutations almost completely eliminate the activity of coagulation factor VIII or coagulation factor IX, resulting in severe hemophilia. Other mutations reduce but do not eliminate the activity of one of these proteins, which usually causes mild or moderate hemophilia. The other, rare form of this condition, acquired hemophilia, results when the body makes specialized proteins called autoantibodies that attack and disable coagulation factor VIII. The production of autoantibodies is sometimes associated with pregnancy, immune system disorders, cancer, or allergic reactions to certain drugs. In about half of cases, the cause of acquired hemophilia is unknown. Read more about the F8 and F9 genes. Hemophilia A and hemophilia B are inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier. She can pass on the altered gene to her children, but usually does not experience signs and symptoms of the disorder. In about 10 percent of cases, however, females who carry one altered copy of the F8 or F9 gene will experience mild problems with bleeding. From: http://ghr.nlm.nih.gov/condition=hemophilia
Genes produce proteins that cause traits.
Defective genes are genes that have mutations or alterations that can lead to abnormal function or health conditions in individuals. These mutations can disrupt the normal processes controlled by the gene, potentially resulting in genetic disorders or diseases.
Mutations on recessive genes return to normal in an organism
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Cis mutations occur on the same strand of DNA, while trans mutations occur on different strands. Cis mutations affect nearby genes, while trans mutations can affect genes located far apart.
Somatic mutations occur in non-reproductive cells and are not passed on to offspring because they do not affect the germline cells (sperm and eggs) that give rise to the next generation. Only mutations in the germline cells can be inherited by offspring.