The mouse facility sends you the wrongknockout mice. For fun, you check levels ofcholesterol and cholesterol precursors in themice and find that the mice you mistakenlyreceived have very low levels of cholesterol(similar to the case of dhcr7 (-/-) mice).These mice however have elevated levels ofsqualene in their serum and tissues. Theenzymes in the pathway have beennumbered for your convenience in theschematic below. Which enzyme number(enzyme 1-5) do you think is mutated in theknockout mouse you received? In one briefsentence, explain why you chose thatenzyme.Geranyl-PPEnzyme 1 -Farnesyl-PPEnzyme 2SqualeneEnzyme 3LanosterolEnzyme 47-DehydrocholesterolEnzyme 5 -Cholesterol

Knockout mice are created in the laboratory in which one or more genes have been deleted. Such mice…

Answered: The mouse facility sends you the wrong…

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter18: Glycolysis

Section: Chapter Questions

Problem 20P: Understanding the Mechanism of Hemolytic Anemia Genetic defects in glycolytic enzymes can have...

See similar textbooks

Similar questions

"Protein tyrosine phosphatases display exquisite specificity for their substrates, unlike most serine/threonine protein phosphatases, which have rather broad specificity" is true or false.
In acute lymphoblastic leukemia, the cancerous white blood cells typically lack the enzyme asparagine synthetase. Why is the administration of asparaginase an eff ective therapy for this type of cancer?
Homocystinuria is caused by a defect in cystathionine beta-synthase (or 13-synthase), which leads to an accumulation of homocysteine in the blood. This accumulation causes symptoms such as a tall, thin frame, flushed cheeks, and osteoporosis (thinning of the bones). These individuals should limit their intake of proteins that contain methionine, such as egg whites. Using your understanding of biochemistry, explain why people with Homocystinuria should not consume egg whites and other such proteins.
The “keto diet” is a dietary regimen in which carbohydrates are severely restricted, protein intake is low, and fat comprises 70–90% of daily calories. The diet causes “nutritional ketosis,” which is a different metabolic state than the ketosis that occurs in an untreated diabetic. The normal ketone body concentration is less than 0.6 mM. Explain why an individual on the keto diet may have a blood ketone body concentration of up to 3 mM. What biochemical pathways are active in an individual adhering to the keto diet? What pathways are largely inactive? Protein intake is kept low because a high-protein diet would inhibit ketosis. Explain why. Why might the keto diet lead to weight loss?
Hydroxyurea has been shown to increase the expression of fetal hemoglobin in adult red blood cells, by a mechanism that remains unclear. Explain why hydroxyurea can be a useful therapy for patients with sickle-cell anemia.
Mucins found on adenocarcinoma cells carry O-glycans terminated with sialic acids (such as the Sialyl Tn antigen) that are smaller and less branched than O-glycans found in healthy epithelial cells. Based on what you know about the biosynthetic pathway for O-glycans, explain this observation.
AMP- PNP is a non-hydrolyzable ATP analog that cannot be metabolized by cells. Taurocholate is a bile acid that helps emulsify fats. When taurocholate is added to hepatocyte cell culture, it accumulates in those cells. The graph below shows the rate of cellular accumulation of the drug taurocholate in the presence of either ATP, ATP, or AMP-PNP. Based on this date, describe the mechanism by which taurocholate enters the cell. Justify the answer.
Acid phosphatases are an important group of enzymes that can be detected in human blood serum. Under slightly acidic conditions (pH 5.0), this group of enzymes can hydrolyze biological phosphate esters as follows in the picture Acid phosphatases are produced and can be detected in erythrocytes, kidney, spleen, the liver, and prostate gland. The enzyme from the prostate gland is clinically important because an increased activity in the blood is frequently an indication of cancer of the prostate gland.Tartrate ion can strongly inhibit the phosphatase from the prostate gland, but not acid phosphatases from other tissues. How can you use the information above to develop a specific procedure for measuring the activity of the acid phosphatase of the prostate gland in human blood serum?
Compare and contrast the c4 pathway and the malate–aspartate shuttle in bullet format, meaning list the similarities and differences.
A 65-year-old man with severe atherosclerotic coronary artery disease comes to the emergency department because of a 12-hour history of chest pain. Plasma activity of the MB isozyme of creatine kinase (MB-CK) is markedly increased. Which of the following processes is the most likely explanation for the increased plasma MB-CK? (A) Cell membrane damage (B) Endoplasmic reticulum dilation (C) Mitochondrial swelling (D) Polysome dissociation (E) Sodium pump dysfunction
A genetic defect in coagulation factor IX causes hemophilia b, a disease characterized by a tendency to bleed profusely after very minor trauma. However, a genetic defect in coagulation factor XI has only mild clinical symptoms. Explain this discrepancy in terms of the mechanism for activation of coagulation proteases shown in Box.
Suppose a new patient, patient HLU, presents with fatigue and failure to thrive within a few days. Upon further investigation, it is discovered that HLU has hypoglycemia between feedings and lactic acidosis right after feeding. In addition, isoelectric focusing of the protein transferrin from his bloodstream, transferrin being a heavily glycosylated protein, reveals that HLU has erroneous N-linked glycosylation of transferrin. Biosynthesis of N-linked glycosylated glycoproteins require UDP-glucose and UDP-galactose for construction of the oligosaccharide that gets added to the protein in the endoplasmic reticulum. Muscle biopsy later in life reveals that he has a glycogen storage disease – there are excess amounts of normally structured glycogen in muscle cells. Early in life, he was subjected to the Beutler test and misdiagnosed with galactosemia because NADPH levels did not increase as readily as wild type patient upon administration of galactose. Which enzyme is deficient in…

SEE MORE QUESTIONS

Recommended textbooks for you

Biochemistry

ISBN:

9781305577206

Author:

Reginald H. Garrett, Charles M. Grisham

Publisher:

Cengage Learning

Human Heredity: Principles and Issues (MindTap Co…

Biology

ISBN:

9781305251052

Author:

Michael Cummings

Publisher:

Cengage Learning

Biochemistry

ISBN:

9781305577206

Author:

Reginald H. Garrett, Charles M. Grisham

Publisher:

Cengage Learning

Human Heredity: Principles and Issues (MindTap Co…

Biology

ISBN:

9781305251052

Author:

Michael Cummings

Publisher:

Cengage Learning

SEE MORE TEXTBOOKS

The mouse facility sends you the wrong knockout mice. For fun, you check levels of cholesterol and cholesterol precursors in the mice and find that the mice you mistakenly