How is Pyruvate Kinase Deficiency (PKD) inherited? What gene is responsible for the expression of the PK enzyme?
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How is Pyruvate Kinase Deficiency (PKD) inherited? What gene is responsible for the expression of the PK enzyme?
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- The brain is fueled almost exclusively by glucose. Using this fact, would it be a good idea to express glucose-1-phosphatase in muscle? What type of phenotype would be exhibited by a mouse expressing glucose-1-phosphatase in muscle?Leigh syndrome is characterized by psychomotor regression: that is, the progressive loss of mental andmovement abilities. Patients also suffer from lacticacidosis, a condition in which mitochondrial respiration is deficient, so their tissues metabolize glucoseanaerobically, leading to the buildup of lactate. Somepatients with Leigh syndrome have a mutation in themitochondrial gene MT-CO3, which encodes a subunit of the electron transport complex cytochromec oxidase. Other patients diagnosed with Leigh syndrome have a loss-of-function mutation in the nucleargene SURF1, which encodes a factor needed for theassembly of this same enzyme complex.a. How can the same symptoms result from mutationsin a mitochondrial gene and from mutations in anuclear gene?What are the current treatments for Pyruvate Kinase Deficiency (PKD) patients?
- What does the fact that the two histograms overlap as much asthey do indicate about the extent to which PCSK9 determinesplasma LDL cholesterol levels?BACKGROUND Pyruvate kinase deficiency (PKD) can be inherited in an autosomal recessive manner, which means that a child must inherit a gene with the disease-causing mutation from both parents in order for the disorder to be inherited. The PLKR gene regulates the synthesis of the pyruvate kinase enzyme, which is located in the liver and red blood cells. Pyruvate kinase deficiency (PKD) is a rare genetic disorder characterized by the premature destruction of red blood, which is called hemolytic anemia. The altered red blood cell has a shortened lifespan leading to hemolytic anemia. Initial lab tests may be performed to determine whether anemia is present and whether it is due to hemolysis. QUESTION In the RBCs of the patient described above, which of the following would be expected? A. ADP to ATP ratios would be elevated above anormal. B. NADP+ would increase relative to NADPH. C. Ribulose 5-phosphate levels would decrease. D. NADH to NAD+ ratios would decrease. E. Methemoglobin levels…Increased ROS levels are a hallmark for Alzheimer's Disease. This is accurately described by all but which of the following statements? ROS production is upregulated because of the activity of the enzyme NADPH oxidase Oxidative phosphorylation is increased, leading to enhanced ROS generation via the ETC Amyloid precursor protein is converted in higher amounts to the amyloid peptide facilitating greater amounts of aggregation BACE1 levels are transcriptionally increased via hypoxia inducible factor Mitochondrial pyruvate flux is reduced 00000
- How would a mutation in ras that leads to formation of a Ras proteinwith no GTPase activity affect a cell’s response to insulin?The Gq-protein and phospholipase C pathway are responsible for stimulating gluconeogenesis and glycogenolysis. What effect would an agonist or an antagonist have on gluconeogenesis and glycogenolysis?What is the biological function of the Neurofibromin-1 (NF1) protein?
- Individuals with the hereditary disorder ataxia telangiectasia suffer from neurodegeneration, immunodeficiency, and an increased incidence of cancer. The genetic basis for ataxia telangiectasia is a loss-of-function mutation in the gene encoding ATM (ATM; ataxia telangiectasia mutated). Besides p53, what other substrate is phosphorylated by ATM? How does the phosphorylation of this substrate lead to inactivation of CDKs to enforce cell cycle arrest?There are several congenital disorders of fructose metabolism resulting from a variety of enzyme deficiencies. These patients have difficulty using fructose for a variety of reasons, of course depending on the specific deficient gene product. Fructose is regularly consumed by humans because of their omnivorous diet that includes fruits (…and other sweets). FBPase-1 deficiency is one example of a deficiency that leads to a disorder of fructose metabolism. Explain why these patients present with hypoglycemia and lactic acidosis during fasting. Which one of these will work to treat a FBPase-1 deficient patient and which one will not? Treatments: Lactose Sucrose Ribose GlycerolThe serine residues in acetyl CoA carboxylase that are the target of the AMP-activated protein kinase are mutated to alanine. What is a likely consequence of this mutation?