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Biochemistry
| Question | Answer |
|---|---|
| Gene mutation associated-onset diabetes of the young (MODY) | Glucokinase |
| 1st step of BOTH Glycolysis and Glycogen synthesis | Phosphorylation of glucose to yield glucose-6-P |
| NADPH is used in | *Anabolic processes (fatty acids and cholesterol synthesis) *Respiratory burst *Cytochrome P-450 system *Glutathione reductase |
| Universal electron acceptors | 1. Nicotinamides (NAD+ from vitamin B3, NADP+) 2. Flavin nucleotides (FAD+ from vitamin B2). |
| Hexokinase vs. Glucokinase | Hexokinase: everywhere, LOW Km, LOW Vmax, NOT induced by insulin Glucokinase: Liver+ Beta cells of Pancres; HIGH Km, HIGH Vmax, induced by insulin |
| Cofactor for enzymes that participate in the synthesis of Tyrosine, DOPAI and Serotonin as well as NO | Tetrahrydrobiopterin (BH4) |
| Cofactor used in transamination (e.g., ALT and AST), decarboxylation reactions, glycogen phosphorylase. | Vitamin 86 (pyridoxine) |
| Necessary for the synthesis of cystathionine, heme, niacin, histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine, and GABA. | Vitamin 86 (pyridoxine) |
| ONLY purely ketogenic amino acids | Lysine and Leucine |
| Neurologic defects, lactic acidosis, increased serum alanine starting in infancy | Pyruvate dehydrogenase complex deficiency |
| Pyruvate dehydrogenase complex deficiency; TREATMENT | Increase intake of KETOGENIC nutrients (e.g high fat content or high LYSINE or LEUCINE) |
| Metabolic processes that take place in the BOTH; mitochondria and cytoplasm | 1. Heme synthesis 2. Urea Cycle 3. Gluconeogenesis |
| Metabolic processes that take place in the Mitochondria | 1. Fatty acid oxidation (Beta-oxidation), 2. Acetyl CoA production, 3. TCA cycle, 4. Oxidative phosphorylation. |
| Metabolic processes that take place in the Cytoplasm | 1. Glycolysis, 2. Fatty acid synthesis, 3. HMP shunt, 4. Protein synthesis (RER), 5. Steroid synthesis (SER), 6. Cholesterol synthesis. |
| Most common inherited blood disorder in the US | Sickle Cell anemia (HbS) |
| Hemoglobin S (HbS) aggregates in the | Deoxygenated state |
| Non polar amino acid Valine replaces the charged amino acid Glutamate at the position 6 of the Beta globin chain | Sickle Cell anemia (HbS); nucleotide substitution, changed amino acid= MISSENSE mutation |
| Is the most common non-nuclear DNA found in the eukaryotic cells and its derived completely from the mother | Mitochondrial DNA (mtDNA) |
| Mitochondrial enzyme complex linking Glycolyisis and TCA cycle | Pyruvate dehydrogenase complex |
| Cofactors required for pyruvate dehydrogenase complex and alpha-ketoglutarate dehydrogenase complex reactions | l. Pyrophosphate (B1, thiamine; TPP) 2. FAD (B2, riboflavin) 3. NAD (B3, niacin) 4. CoA (B5, pantothenate) 5. Lipoic acid |
| Administration of glucose to a thiamine (Vit B1) deficient patient (e.g malnutrition, ALCOHOLICS) results in | Wernicke Encephalopathy |
| Diagnosis of Thiamine (Vit B1) deficiency | Increase in RBC transketolase activity following Vit B1 administration |
| Thiamine pyrophosphate (TPP), is a cofactor for several dehydrogenase enzyme reactions | • Pyruvate dehydrogenase (links glycolysis to TCA cycle) • Alpha-ketoglutarate dehydrogenase (TCA cycle) • Transketolase (HMP shunt) • Branched-chain amino acid dehydrogenase |
| Causes a buildup of PYRUVATE that gets shunted to lactate (via LDH) and alanine (via ALT) | Pyruvate dehydrogenase complex deficiency |
| Function of PDH (Pyruvate dehydrogenase) | Convert pyruvate to acetyl-CoA for metabolism in the TCA cycle |
| Necessary cofactor in the synthesis of alpha-aminolevulonic acid (which is elevated in cases of Lead Poisoning) | Pyridoxal phosphate (B6) |
| To treat cyanide poisoning, use | 1) Nitrites to oxidize Hb to methemoglobin, which binds cyanide. 2) Thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted. |
| Oxidized form of hemoglobin (ferric, Fe3+) that does not bind 02, but has high affinity for cyanide. | Methemoglobin |
| Iron in hemoglobin is normally in a | reduced state (ferrous, Fe2+). |
| Methemoglobinemia can be treated with | Methylene blue |
| Nitrites cause poisoning by | Oxidizing Fe2+ to Fe3+ |
| Autosomal-recessive; defective neutral amino acid (e.g, Tryptophan) transporters on proximal renal tubular cells and on enterocytes. | Hartnup disease |
| Essential amino acid precursor for nicotinic acid, serotonin and melatonin | Tryptophan |
| Cerebellar ataxia, pellagra-like symptoms, photosensitivity, neutral aminoaciduria | Hartnup disease |
| Treatment for Hartnup disease | 1) High protein diet 2) Nicotinic acid (Niacin,B3) |
| Nicotinic acid (Niacin,B3) is synthesized from | Tryptophan |
| Niacin, Vitamin B3; DEFICIENCY | 1) Glossitis 2) Pellagra: Diarrhea, Dementia (also hallucinations), Dermatitis (e.g, Casal necklace or hyperpigmentation of sun-exposed limbs) |
| Niacin, Vitamin B3; CAUSES | 1) Hartnup disease (decreased tryptophan absorption) 2) Malignant carcinoid syndrome (increased tryptophan metabolism) 3. Isoniazid (decreased vit B6) |
| Constituent of NAD+, NADP+ (used in redox reactions). Derived from tryptophan. Synthesis requires vit B2 and B6. Used to treat dyslipidemia; lowers levels of VLDL and raises levels of HDL | Niacin, Vitamin B3 |
| Niacin, Vitamin B3; EXCESS | 1) Facial flushing (induced by PROSTAGLANDINS, not histamine) 2) Hyperglycemia (Acanthosis nigricans) 3) Hyperuricemia (exacerbates Gout) |
| The 3 D´s of B3 | 1) Diarrhea 2) Dementia (also hallucinations) 3) Dermatitis (e.g, Casal necklace or hyperpigmentation of sun-exposed limbs) |
| Most significant causes of Vitamin A (retinol) deficiency | 1) Malnourishment 2) Fat malabsorption (e.g Cystic Fibrosis, Cholestatic liver disease) |
| Vitamin A (retinol); FUNCTIONS | 1) Antioxidant 2) Retinal 3) Normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells); prevents squamous metaplasia. 4) Treat measles and AML, subtype M3. |
| Vitamin used to treat measles and AML, subtype M3 | Vitamin A (retinol) |
| Vitamin that prevents squamous metaplasia | Vitamin A (retinol) |
| Vitamin A (retinol); DEFICIENCY | 1) Night blindness (nyctalopia) 2) Dry, scaly skin (xerosis cutis) 3) Alopecia 4) Corneal degeneration (keratomalacia) 5) Immune suppression |
| Vitamin A (retinol); EXCESS | 1) Sore throat 2) Skin changes (e.g, scaliness) 3) Cerebreal edema 4) Pseudotumor cerebri 5) Hepatic abnormalities (hypertriglyceridemia, hyperlipidemia) 6) Teratogenic (cleft palate, cardiac abnormalities) |
| Swollen gums, bruising, hemarthrosis, anemia, poor wound healing, perifollicular and subperiosteal hemorrhages ¨corkscrew¨ hair | Scurvy; Vitamin C (ascorbic acid) deficiency |
| Vitamin C deficiency causes scurvy due to | Collagen synthesis defect. Hydroxylation of specific proline and lysine residues requires vitamin C |
| Vitamin C (ascorbic acid); FUNCTIONS | 1) Antioxidant. 2) Iron absorption by reducing it to Fe2+ 3. Hydroxylation of proline and lysine in collagen synthesis. 4. Dopamine Beta-hydroxylase, which converts dopamine to NE. |
| ONLY DNA polymerase that has 5´to 3 exonuclease activity; excises RNA primer and damaged DNA sequences which are identified by endonucleases | DNA polymerase I |
| Cut DNA at very specific DNA sequences within the molecule | Endonucleases |
| Removal of supercoils | Topoisomerase II |
| Unwinding of double helix | Helicase |
| Stabilization of unwound template strands (bind only to ssDNA) | Single-stranded binding proteins (SSB) |
| Synthesis of RNA primer | Primase (RNA polymerase) |
| DNA synthesis: LEADING strand | DNA polymerase III |
| DNA synthesis: LAGGING strand | DNA polymerase III |
| Removal of RNA primer and replacement of RNA with DNA (proof reading) | DNA polymerase I (5´-exonuclease) |
| Joining of Okasaki fragments (lagging strand) | DNA ligase |
| Y-shaped region along DNA template where leading and lagging strands are synthesized. | Replication fork |
| RNA-dependent DNA polymerase | Telomerase |
| Adds DNA to 3´ends of chromosomes to avoid loss of genetic material with every duplication | Telomerase (only found in EUKARYOTES) |
| Thyroid hormones alter gene transcription by binding to receptors situated inside of the | NUCLEUS |
| hyperextensible skin, tendency to bleed (easy bruising), and hypermobile joints | Ehlers-Danlos syndrome |
| Ehlers-Danlos syndrome associated with | joint dislocation, berry and aortic aneurysms, organ rupture. |
| Problems with collagen cross-linking | Ehlers-Danlos syndrome |
| Vitamin B5 (pantothenate) | Essential component of CoA (a cofactor for acyl transfers) and fatty acid synthase. |
| Biologically active form of pantothenic acid | Coenzime A |
| Excess of this vitamin can lead to calcium oxalate nephrolithiasis | Vitamin C (ascorbic acid) |
| Excess of this vitamin can increase iron toxicity in predisposed individuals (e.g,those with transfusions, hereditary hemochromatosis) | Vitamin C (ascorbic acid) |
| Converts glucose to sorbitol | Aldose Reductase |
| Tissues that have both enzymes aldose reductase and sorbitol dehydrogenase | Liver, lens, ovaries, and seminal vesicles |
| Intracellular sorbitol accumulation, can cause | Osmotic damage (e.g., cataracts, retinopathy, and peripheral neuropathy seen with chronic hyperglycemia in diabetes). |
| Tissues that have only aldose reductase. | Schwann cells, Retina, Lens, Kidneys |
| In bacteria, one mRNA codes for several proteins. This is means it´s | Bacterial mRNA can be polycistronic |
| Ensures fast and effective DNA replication in Eukaryotic cells | MULTIPLE origins of replication |
| In Eukaryotic there are 5 major DNA polymerases | alpha, beta, delta, gamma and epsilon |
| Hypoxia-induced lactic acidosis is caused by | LOW activity of pyruvate dehydrogenase (oxidative phosphorilation pathway) and a HIGH activity of lactate dehydrogenase |
| Anaerobic glycolysis produces only | 2 net ATP per glucose molecule. |
| Aerobic metabolism of glucose produces | 32 ATP via malate-aspartate shuttle (heart and liver), 30 ATP via glycerol-3-phosphate shuttle (muscle). |
| End of anaerobic glycolysis | Lactate |
| Anaerobic glycolysis (Cori cycle) is the major pathway in | RBCs, leukocytes, kidney medulla, lens, testes, and cornea) |
| Cofactor for lactic acid dehydrogenase | Vitamin B3 (niacin) |
| Has higher affinity for oxygen due to less avid binding of 2,3 BPG. | Fetal hemoglobin (HbF); this allows HbF to extract O2 from (HbA) maternal hemoglobin across the placenta |
| The most important stimulator of insulin release | Glucose |
| Allows facilitated diffusion of glucose into beta cells | GLUT 2 (glucose transporter 2) |
| Insulin-DEPENDENT glucose transporters | GLUT-4: adipose tissue, skeletal muscle |
| Insulin-INDEPENDENT glucose transporters | GLUT-1: RBC´s , brain, cornea GLUT-5 (FRUCTOSE): spermatocytes, GI tract GLUT-2 (BIDIRECTIONAL): beta islet cells, liver, kidney, small intestine |
| ALWAYS utilize glucose because they lack mitochondria for aerobic metabolism | RBC´s |
| Insulin and C-peptide are INCREASED in | Insulinoma; whereas EXOGENOUS insulin LACKS C-peptide |
| Closes K+ channels in beta cells | INCREASE in ATP/ADP ratio generated from glucose metabolism within beta cells |
| Defects of the KATP channel gene can result in | Type II diabetes |
| Regulatory substance that stimulates KATP channel closure in insulin-producing pancreatic beta cells | ATP |
| Anabolic effects of insulin; INCREASE: | • Glucose transport (skeletal muscle, adipose tissue) • Glycogen synthesis/storage • Triglyceride synthesis/storage • Na+ retention (kidneys) • Protein synthesis (muscles, proteins) • Cellular uptake of K+ and amino acids |
| Anabolic effects of insulin; DECREASE: | • Glucagon release |
| is used by the brain during starvation | Ketone bodies |
| 3 polypeptide alpha-chains held together by hydrogen bonds to form a rope-like triple helix | Collagen (most abundant protein in the human body) |
| MOST abundant amino acid in the collagen molecule. It occurs AT LEAST every third amino acid position. | GLYCINE |
| Is derived from amino acids (valine, isoleucine, methionine, threonine), odd chain fatty acids and cholesterol | Propionyl-CoA (propionic acid) |
| Congenital deficiency of propionyl-CoA carboxylase the enzyme responsible for converting propionyl-CoA to methylmalonyl-CoA leads to | Propionic acidemia |
| Variety of hormones that exert their intracellular effects via the IP3 second messenger system | GnRH, Oxytocin, ADH (V1 receptor), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin |
| Hemoglobin carries carbon dioxide as | Carbamate |
| High fidelity replication of DNA is accomplished by | 3´to 5´ ¨proofreading¨exonuclease activity of DNA polymerase |
| The Shine-Dalgarno sequence is UNIQUE to | Prokaryotes |
| Are responsible for accuracy of amino acid selection | Aminoacyl-tRNA synthetase and binding of charged tRNA to the codon |
| 40S + 60S --> 80S | Eukaryotes |
| 30S + 50S ---> 70S | Prokaryotes |
| Absence of galactose-1-phosphate uridyltransferase. | Classic galactosemia |
| Failure to thrive, jaundice, hepatomegaly, infantile cataracts, mental retardation. | Classic galactosemia |
| Deficiency of galactokinase. | Galactokinase deficiency |
| Treatment: exclude galactose and lactose (galactose + glucose) from diet. | Classic galactosemia |
| Classic galactosemia can lead to | E.coli sepsis in neonates |
| Galactose appears in blood and urine, infantile cataracts. May initially present as failure to track objects or to develop a social smile. | Galactokinase deficiency |
| Most common cause of Homocystinuria | Deficiency of cystathionine synthase |
| Refers to the 1 to 4 residues remaining on a branch after glycogen phosphorylase has already shortened it | ¨Limit dextrin¨ |
| Enzime activation responsible for the rapid glycogen degradation in skeletal muscle after the onset of contraction | Ca2+ |
| Messenger mRNA is produced from | DNA by RNA polymerase II |
| mRNA is composed of 3 sequential bases known as | CODONS |
| Calls for the termination of synthesis of the polypeptide chain | STOP codons: UGA: u go away UAA: u are away UAG: u are gone |
| mRNA start codon | AUG (methionine) |
| Nucleotide substitution resulting in early stop codon. | Nonsense mutation |
| 3 IRREVERSIBLE enzymes of Glycolysis | Hexokinase (Glucokinase); Fructokinase; Pyruvate kinase |
| Activates GLYCOLYSIS by inducing PFK-1 and inhibits GLUCONEOGENESIS by inhibiting Fructose-1,6BP | Fructose-2,6-BP |
| IRREVERSIBLE enzimes, Gluconeogenesis | 1) Pyruvate carboxylase 2) Phosphoenolpyruvate carboxykinase 3) Fructose-1,6-biphosphatase 4) Glucose-6-phosphatase |
| 2 important pathophysiologic differences between the 2 forms of bilirubin | Direct bilirubin-conjugated with glucuronic acid; water Indirect bilirubin-unconjugated; water insoluble, tightly complexed to serum albumin (cannot be excreted in urine even when blood levels are high) |
| If energy dependent organic ion transport across hepatocellular membrane is selectively inhibited which is the most likely result | Increase bilirubin excretion in the urine |
| P50 | Partial pressure of O2 in the blood at which Hb is 50% saturated; normal: 26mmHg |
| 3 variables affect O2 content of blood: | Hb level; % O2 saturation of Hb (SaO2); Dissolved O2 (PaO2) |
| shift to RIGHT (increase P50); facilitates unloading | 1) BPG (2,3-BPG) 2) Altitude 3) Temperature 4) Acid (pH); DECREASED 5) C02 6) Exercise |
| O2 capacity | Maximal amount of O2 that can bind to Hb |
| O2 content | Total O2 in blood (bound+dissolved)= (O2 binding capacity X saturation% ) + dissolved O2 |
| O2 delivery to tissues= | O2 delivery to tissues= CO X O2 content of blood |
| shift to LEFT (increase P50); facilitates loading | 1) BPG (2,3-BPG) 2) CO poisoning 3) Temperature 4) Acid (pH); INCREASED 5) Fetal Hb 6) Methemoglobin |
| CO poisoning (Carboxyhemoglobin) is dangerous for 3 reasons: | 1) Left shift; decreasing P50 and O2 unloading in tissues 2) 240x greater affinity than 02 for Hb, decreasing O2 content of blood. 3) Inhibits cytochrome oxidase |
| Insulin acts via a | Tyrosine kinase mechanism |
| Tyrosine kinase leads to activation of protein phosphatase within cells, and protein phosphatase directly modulates the activity of enzymes in the metabolic pathways regulated by | INSULIN |
| Maintain plasma glucose levels for only a few hours of fasting until glycogen stores are depleted | Glycogenolysis |
| Predominant method used by the body to maintain blood glucose concentrations | Gluconeogenesis |
| Gluconeogenesis. IRREVERSIBLE enzymes | 1) Pyruvate carboxylase (mitochondria) 2) Phosphoenolpyruvate carboxykinase (cytosol) 3) Fructose-1,6-biphosphatase (cytosol) 4) Glucose-6-phosphatase (ER) |
| The activity of pyruvate carboxylase is increased by | Acetyl-CoA |
| Pyruvate carboxylase converts pyruvate to oxaloacetate in the mitochondria in a reaction that requires | Biotin + ATP |
| In cytosol. Fructose-1 ,6-bisphosphate is converted to fructose-6-P by Fructose-1,6-biphosphatase. This reaction is inhibited and activated by | (+) Citrate (-) Fructose 2,6-biphosphate |
| Deficiency of the key gluconeogenic enzymes causes | Hypoglycemia. |
| Muscle cannot participate in gluconeogenesis because it lacks | Glucose-6-phosphatase |
| Membrane-enclosed organelle involved in beta-oxydation of very long fatty acids (VLCFA), branched-chain fatty acids and amino acids. | Peroxisomes |
| Infant suffering from hypotonia and seizures shows and impaired ability to oxidize yew long chain fatty acids (VLCFA) and phytanic acid | Peroxisomal diseases (neurologic defects; improper CNS myelination) |
| Urea´s nitrogen in the urea cycle is derived from | NH3 and Aspartate |
| Rate-limiting enzyme in the urea cycle and is activated by | Carbamoyl phosphate synthetase I (CPS I) activated by N-acetylglutamate |
| required cofactor for Carbamoyl phosphate synthetase I (CPS I) | N-acetylglutamate |
| 3 main circulating catecholamines | Dopamine, NE, Epi |
| Phenylethanolamine-N-methyltransferase (PNMT) is responsible for the synthesis of epinephrine in the adrenal medulla, is under control of | Cortisol |
| Enzymes responsible for the metabolism of catecholamines | Cathecol-O-methyltransferase (COMT), Monoamine oxidase (MAO) |
| Fructose is rapidly absorbed in the proximal small bowel by the hexose transporter | GLUT 5 |
| Disorders of fructose metabolism | Essential fructosuria; Fructose intolerance |
| Involves a defect in fructokinase | Essential fructosuria (defect in fructokinase) |
| Fructose appears in blood or urine | Essential fructosuria (defect in fructokinase) |
| Hereditary deficiency of aldolase B. Fructose-1-phosphate accumulates, causing a decrease in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis | Fructose intolerance (deficiency of aldolase B) |
| Infant with hypoglycemia, jaundice, cirrhosis, vomiting. Symptoms presented 20-30mins after fructose consumption | Fructose intolerance (deficiency of aldolase B) |
| Hereditary deficiency of aldolase B | Fructose intolerance (deficiency of aldolase B) |
| Fructose intolerance; TREATMENT | decrease intake of both fructose and sucrose (glucose + fructose) . |
| Receptor proteins are either | 1) Extracellular (located on cell surface): majority of receptors 2) Intracellular (located in the cytoplasm or nucleus): Steroid hormones |
| The majority of receptor proteins are extracellular, which is the intracellular exception | Steroid hormones |
| The steroid resceptor is a | Zinc finger protein |
| Increase in melting temperature of DNA | Increase in G-C (3H bonds) content |
| Uracil found in | RNA |
| Thymine found in | DNA |
| Amino acids necessary for purine synthesis | GAG Glycine Aspartate Glutamine |
| Nucleoside | Base+ (deoxy) ribose (Sugar). |
| Nucleotide | base + (deoxy) ribose (Sugar) + phosphate; linked by 3´-5´phosphodiester bond |
| Carbamoyl phosphate is involved in 2 metabolic pathways: | De novo pyrimidine synthesis and the urea cycle. |
| retardation, self-mutilation, aggression, hyperuricemia, gout, dystonia. | Lesch-Nyhan syndrome; X-linked recessive |
| Defective purine salvage owing to absent HGPRT, which converts hypoxanthine to IMP and guanine to GMP. Results in excess uric acid production and de novo purine synthesis. X-linked recessive. | Lesch-Nyhan syndrome; X-linked recessive |
| Lesch-Nyhan syndrome; TREATMENT | Allopurinol or febuxostat (2nd line) |
| Purine salvage deficiencies | 1. Adenosine deaminase deficiency 2. Lesch-Nyhan syndrome |
| One of the major causes of autosomal recessive SCID | Adenosine deaminase deficiency |
| Deletion or insertion of a number of nucleotides NOT divisible by 3, resulting in misreading of all nucleotides downstream= truncated, nonfunctional protein. | Frameshift mutation |
| Early stop codon | Nonsense mutation |
| Histone octamer | 2 copies of H2A, H2B, H3, and H4 |
| Between adjacent nucleosomes | Histone H1 |
| Difference between 10nm and 30nm chromatin is presence or absence of | Histone H1 |
| Euchromatin | • Loose • Accessible • Active |
| Heterochromatin | • Condensed • Inaccessible • Inactive |
| Telomerase | • Inactive in somatic cells (skin, blood, connective tissue) • Prokaryotes have single circular chromosomes, hence no telomerases • Inappropriately present in cancer cells |
| Nicks the phosphodiester backbone of damaged strand | Excision endonuclease |
| Site where RNA polymerase and multiple other transcription factors bind to DNA upstream from gene locus (AT-rich upstream sequence with TATA and CAAT boxes). | Promoter |
| Promoter mutation commonly results in dramatic decrease in level of | Gene transcription |
| Process that occurs on the NUCLEUS following transcription | 1) Capping on 5' end (addition of 7-methylguanosine cap); 2) Polyadenylation of 3' end ("" 200 A´s); 3) Splicing out of introns (non-coding regions) |
| Capped, tailed and spliced transcript is called | mRNA |
| opens DNA at promotor site | RNA polymerase II |
| most numerous RNA | rRNA |
| RNA polymerase I makes | rRNA (most numerous RNA, rampant) |
| RNA polymerase II makes | mRNA (largest RNA, massive) |
| Largest RNA | mRNA |
| RNA polymerase III makes | tRNA (smallest RNA, tiny) |
| Smallest RNA | tRNA |
| l RNA polymerase (multisubunit complex) makes all 3 kinds of RNA. | Prokaryotes |
| Molecular motor proteins | Dynein=RETROGRADE to microtubule (+to -) Kinesin=ANTEROGRADE to microtubule (-to +) |
| Transport cellular cargo toward opposite ends of microtubule tracks. | Molecular motor proteins |
| Drugs that act on microtubules | 1)Mebendazole (antihelminthic) 2)Griseofulvin (antifungal) 3)Vincristine/vinblastine (anti-cancer) 4)Paclitaxel (anti-breast cancer) 5)Colchicine (anti-gout) |
| Male infertility and decreased female fertility, bronchiectasis, and recurrent sinusitis; associated with situs inversus. | Kartagener's syndrome (primary ciliary dyskinesia) - immotile cilia clue to a dynein arm defect. |
| Dynein arm defect | Kartagener's syndrome (primary ciliary dyskinesia) |
Created by:
heidy39
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