Manual High-Yield Cell and Molecular Biology (3rd Edition) (High-Yield Series)

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See all condition definitions - opens in a new window or tab Read more about the condition. About this product. I suspect what will happen is that many of the "traditional" courses will extend their discussion of various topics down to the molecular biology level. RNA processing Occurs in nucleus. After transcription: Only processed RNA is eukaryotes 1. Capping on 5 end 7-methyl-G transported out of the 2. Polyadenylation on 3 end As nucleus. Capped and tailed transcript is called mRNA.

All tRNAs, both eukaryotic and prokaryotic, have CCA at 3 end along with a high percentage of chemically modied bases. The amino acid is covalently bound to the 3 end of the tRNA. If and binding of charged incorrect, bond is hydrolyzed by synthetase. A mischarged tRNA reads usual codon but amino acid selection. Protein synthesis Met sits in the P sitepeptidyl. HINT: Competitive inhibitors cross each other competitively, while noncompetitive inhibitors do not.

Mitosis is usually shortest phase. Most cells are in G 0. Rapidly dividing cells have a shorter G 1. Nissl bodies Nissl bodies in neurons rough ER; not found in axon or axon hillock. Synthesize enzymes e. Smooth SER is the site of steroid synthesis and detoxication Liver hepatocytes and endoplasmic of drugs and poisons. Functions of Golgi 1. Distribution center of proteins and lipids from I-cell disease is caused by the apparatus ER to the plasma membrane, lysosomes, and failure of addition of secretory vesicles mannosephosphate to 2.

Modies N-oligosaccharides on asparagine lysosome proteins, causing 3. Adds O-oligosaccharides to serine and threonine these enzymes to be secreted residues outside the cell instead of 4. Proteoglycan assembly from proteoglycan core being targeted to the proteins lysosome.

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Characterized by 5. Sulfation of sugars in proteoglycans and of coarse facial features and selected tyrosine on proteins restricted joint movement. Basic Histology, 10th ed. New York:McGraw-Hill, A helical array of polymerized dimers of - 1. Each dimer antihelminthic has 2 GTP bound. Incorporated into agella, cilia, 2.

Taxol antibreast cancer mitotic spindles. Grows slowly, collapses quickly. Griseofulvin antifungal Microtubules are also involved in slow axoplasmic 4. Colchicine anti-gout Chdiak-Higashi syndrome is due to a microtubule polymerization defect resulting in phagocytosis. Kartageners syndrome is due Dynein is an ATPase that links peripheral to a dynein arm defect, 9 doublets and causes bending of cilium by resulting in immotile cilia.

High cholesterol or long saturated fatty acid content melting temperature. Only noncytoplasmic side of membrane contains glycosylated lipids or proteins i. Phosphatidylcholine Phosphatidylcholine lecithin is a major component of RBC membranes, of myelin, of function bile, and of surfactant DPPCdipalmitoyl phosphatidylcholine. Also used in esterication of cholesterol LCAT is lecithin-cholesterol acyltransferase. MAD 2s.

Functions to organize and strengthen extracellular matrix. Type III Reticulin skin, blood vessels, uterus, fetal tissue, granulation tissue. Type IVBasement membrane or basal lamina. Collagen synthesis Inside broblasts: and structure 1. ER hydroxylation of specic proline and lysine residues requires vitamin C 3.

Golgi glycosylation of pro--chain lysine residues and formation of procollagen triple helix of 3 collagen chains 4. Procollagen molecules are exocytosed into extracellular space Outside broblasts: 5. Procollagen peptidases cleave terminal regions of procollagen, transforming procollagen into insoluble tropocollagen 6.

Hyperextensible skin 2. Tendency to bleed easy bruising 3. Hypermobile joints 10 types. Inheritance varies. Associated with berry aneurysms. Osteogenesis Primarily an autosomal-dominant disorder caused May be confused with child imperfecta by a variety of gene defects, resulting in abnormal abuse. Clinically characterized by: Type II is fatal in utero and in 1.

Multiple fractures occurring with minimal the neonatal period. Blue sclerae due to the translucency of the connective tissue over the choroid 3. Hearing loss abnormal middle ear bones 4. Both Gluconeogenesis, urea cycle, heme synthesis. Anaerobic glycolysis produces only 2 net ATP per glucose molecule. ATP hydrolysis can be coupled to energetically unfavorable reactions. Activated carriers Phosphoryl ATP.

Acyl coenzyme A, lipoamide. CO 2 biotin. CH 3 groups SAM. Aldehydes TPP. Glucose UDP-glucose. Choline CDP-choline. Regeneration of methionine and thus SAM is dependent on vitamin B FructoseP fructose-1,6-bis-P via phosphofructokinase PFK , the rate-limiting enzyme of glycolysis. HMP shunt. Anabolic processes equivalents.

Respiratory burst 3. Hexokinase is found throughout body. Only hexokinase is feedback glucokinase GLucokinase is primarily found in the Liver inhibited by G6P. Glycolysis D-glucose Glucosephosphate GlucoseP. Glycolytic enzyme Hexokinase, glucose phosphate isomerase, aldolase, RBCs metabolize glucose deciency triosephosphate isomerase, phosphate glycerate anaerobically no kinase, enolase, and pyruvate kinase deciencies mitochondria and thus are associated with hemolytic anemia.

Pyrophosphate B 1 , thiamine; TPP dehydrogenase complex 2. FAD B 2 , riboavin same cofactors, similar 3. NAD B 3 , niacin substrate and action. CoA B 5 , pantothenate 5. Can be seen in purely ketogenic amino deciency alcoholics due to B 1 deciency. Findings: neurologic defects. Treatment: intake of ketogenic nutrients e. Pyruvate metabolism 6 ATP equivalents are needed to generate glucose from pyruvate. Alanine serves as carrier of amino groups from muscle to liver. Oxaloacetate can be used to replenish TCA cycle or in gluconeogenesis.

Electron transport inhibitors rotenone, antimycin A, CN. ATPase inhibitor oligomycin directly inhibits mitochondrial ATPase, causing an of proton gradient, but no ATP is produced because electron transport stops. Uncoupling agents 2,4-DNP permeability of membrane, causing a of proton gradient and O 2 consumption. ATP synthesis stops. Electron transport continues. Pyruvate oxaloacetate.

Requires biotin, ATP. Activated by acetyl-CoA. PEP carboxykinase In cytosol. Oxaloacetate phosphoenolpyruvate. Requires GTP. Fructose-1,6- In cytosol. Fructose-1,6-bisphosphate bisphosphatase fructoseP. Pathway Produces Glucose In cytosol. GlucoseP glucose. Fresh Glucose. Muscle cannot participate in gluconeogenesis. Hypoglycemia is caused by a deciency of the key gluconeogenic enzymes listed above e. Pentose phosphate Produces riboseP from G6P for nucleotide synthesis. All reactions of this pathway occur in the cytoplasm. No ATP is used or produced. Sites: lactating mammary glands, liver, adrenal cortexall sites of fatty acid or steroid synthesis.

NADPH is necessary prevalent among blacks. RBC defense against oxidizing agents fava beans, X-linked recessive disorder. Fructosephosphate accumulates, causing a in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis. Symptoms: hypoglycemia, jaundice, cirrhosis, vomiting.

Essential fructosuria Involves a defect in fructokinase and is a benign, asymptomatic condition. Symptoms: fructose appears in blood and urine. Disorders of galactose metabolism Galactosemia Absence of galactosephosphate uridyltransferase. Autosomal recessive. Damage is caused by accumulation of toxic substances including galactitol rather than absence of an essential compound. Symptoms: cataracts, hepatosplenomegaly, mental retardation.

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Galactokinase Causes galactosemia and galactosuria, galactitol accumulation if galactose is present in diet. Symptoms: bloating, cramps, osmotic diarrhea. Treatment: avoid milk or add lactase pills to diet. Essential amino Ketogenic: Leu, Lys. Arg and His are required during periods of growth. Basic amino Arg and Lys have an extra acid His at pH 7. NH 3 group. Arginine is the most basic amino acid. Arg and Lys are found in high amounts in histones, which bind to negatively charged DNA. Transport of ammonium by alanine and glutamine Urea cycle Degrades amino acids into amino groups.

Urea cycle occurs Are Also Frivolous About in the liver; carbamoyl phosphate incorporation Urination.

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In PKU, there is phenylalanine Phenylketonesphenylacetate, hydroxylase or tetrahydrobiopterin cofactor. Autosomal-recessive disease. Findings: mental retardation, growth retardation, Incidence , Disorder of aromatic amino Treatment: phenylalanine contained in acid metabolism musty aspartame, e.

High Yield Cell and Molecular Biology

Alkaptonuria Congenital deciency of homogentisic acid oxidase in the degradative pathway of tyrosine. Resulting alkapton bodies cause urine to turn black on standing. Also, the connective tissue is dark. Benign disease. May have debilitating arthralgias. Albinism Congenital deciency of either of the following: Lack of melanin results in an 1. Tyrosinase inability to synthesize melanin risk of skin cancer. Defective tyrosine transporters amounts of tyrosine and thus melanin Can result from a lack of migration of neural crest cells. Cystathionine synthase deciency treatment: in the urine. Cysteine Met and Cys in diet becomes essential.

Methionine synthase deciency downward and inward , and atherosclerosis stroke and MI. Excess cystine alkalinize the urine. Maple syrup urine Blocked degradation of branched amino acids Urine smells like maple syrup. I Love Vermont maple syrup. Causes -ketoacids in the blood, especially Leu.

Causes severe CNS defects, mental retardation, and death. This disease. X-linked recessive.

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Results in excess uric acid production. Findings: retardation, self-mutilation, aggression, hyperuricemia, gout, and choreoathetosis. Liver: fed state vs. Required for adipose Insulin moves glucose Into cells. Insulin inhibits glucagon Brain release by cells of pancreas. Cornea Anabolic effects of insulin: Kidney 1. Na retention kidneys 5. Glycogen storage 12 types, all resulting in abnormal glycogen metabolism and an accumulation of glycogen diseases within cells.

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Type I Von Gierkes diseaseglucosephosphatase The liver becomes a muscle. Think about it. Findings: severe fasting hypoglycemia, glycogen in liver, hepatomegaly, blood lactate. Findings: cardiomegaly and systemic ndings, leading to early death. Type III Coris diseasedeciency of debranching enzyme -1,6-glucosidase. Findings: milder form of type I with normal blood lactate levels. Findings: glycogen in muscle but cannot break it Very Poor Carbohydrate down, leading to painful cramps, myoglobinuria Metabolism.

Hunters aim for the X X-linked recessive. Urine test for Ketone bodies found in prolonged starvation and ketones does not detect diabetic ketoacidosis. Excreted in urine. Ketone bodies are metabolized by the by high redox state. Hormone-sensitive lipasedegradation of TG stored in adipocytes. C-IICofactor for lipoprotein lipase.

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EMediates Extra remnant uptake. Function and route Apolipoproteins Chylomicron Delivers dietary triglycerides to peripheral tissues and B mediates secretion. Secreted by intestinal As are used for formation of epithelial cells. Excess causes pancreatitis, lipemia new HDL. C-II activates lipoprotein lipase. E mediates remnant uptake by liver. VLDL Delivers hepatic triglycerides to peripheral tissues. B mediates secretion. Secreted by liver. Excess causes pancreatitis.

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Delivers triglycerides and cholesterol to liver, where they are degraded to LDL. LDL Delivers hepatic cholesterol to peripheral tissues. B mediates binding to cell Formed by lipoprotein lipase modication of surface receptor for VLDL in the peripheral tissue. Taken up by target endocytosis. Excess causes atherosclerosis, xanthomas, and arcus corneae.

Secreted from both liver and intestine. CETP mediates transfer of cholesteryl esters to other lipoprotein particles. Accumulation of intermediates causes porphyrias. Coproporphyrin and ALA accumulate in urine. Acute intermittent Deciency in uroporphyrinogen I synthetase. Polyneuropathy, tarda Uroporphyrin accumulates in urine tea-colored. Psychological disturbances, Photosensitivity. Precipitated by drugs.

Heme biliverdin bilirubin sparingly water soluble, toxic to CNS, transported by albumin. Bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted in bile. In the intestine it is processed into its excreted form. Some urobilinogen, an intestinal intermediate, is reabsorbed into blood and excreted as urobilin into urine. Hemoglobin Hemoglobin is composed of 4 polypeptide subunits Carbon monoxide has 2 and 2 and exists in 2 forms: greater afnity than O 2 1. T taut form has low afnity for O 2.

R relaxed form has high afnity for O 2 Hemoglobin exhibits positive cooperativity and negative allostery accounts for the sigmoid-shaped O 2 dissociation curve for hemoglobin , unlike myoglobin. Hemoglobin structure Cl. Fetal hemoglobin 2 and 2 subunits has lower afnity for 2,3-BPG than adult hemoglobin HbA and thus has higher afnity for O 2. CO 2 transport in CO 2 binds to amino acids in globin chain at N CO 2 must be transported from blood terminus but not to heme.

CO 2 binding favors T tissue to lungs, the reverse taut form of hemoglobin and thus promotes O 2 of O 2 occurs primarily in the unloading. Steps: 1. DNA is denatured by heating to generate 2 separate strands 2. During cooling, excess premade DNA primers anneal to a specic sequence on each strand to be amplied 3. The resulting double- stranded labeled piece of DNA is visualized when the lter is exposed to lm. Western blot Sample protein is separated via gel electrophoresis and transferred to a lter.