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WVSOM COMLEX Biochem
biochem review from First Aid and Kaplan
| Question | Answer |
|---|---|
| What is the structure of Chromatin? | It is negatively charged DNA that loops twice around a histone octamer to form a nucleosome bead. |
| What is unique about H1 histone protein? | H1 is the only histone that is not in the nucleosome core. |
| What is the function of H1 histone? | H1 ties nucleosomes together in a string. |
| When does DNA condense to form mitotic chromosomes? | DNA condenses during mitosis |
| What is heterochromatin | Condensed, transcriptionally inactive DNA. Think: " HeteroChromatin= Highly Condensed" |
| What is Euchromatin | Less condensed, transcriptionally active Think: "Eu= true, truly transcribed" |
| What are the 4 nucleotides? | Adenine, Thymine, Guanine, Cytosine |
| What are the purines? | A and G, Think: "PURe As Gold: PURines" |
| What are the pyrimidines? | C and T, Think: CUT the Py(pie): PYrimidines |
| Which nucleotides have two rings in their structure? | Purines |
| Which nucleotides have one ring in their structure? | Pyrimidines |
| What is special about Guanine? | it has a ketone |
| What is special about Thymine? | It has a methyl group attached. Think: "THYmine has a meTHYl" It is also found in DNA |
| What is special about Cytosine? | Deamination of cytosine makes Uracil |
| Where is Uracil found | RNA |
| Which has a stronger bond: G-C or A-T? | G-C because it has 3 H bonds. The more G-C bonds a DNA stand contains the higher the melting point of the strand. |
| What are the amino acids necessary for purine synthesis? | Glycine, Aspartate, Glutamine |
| What makes up a nucleoside? | base + ribosome |
| What makes up a nucleotide? | base + ribosome + phosphate, linked by a 3'-5' phosphodiester bond |
| How are purines made de novo? | purines are made from IMP precursor |
| How are pyrimidines made de novo? | Pyrimidines are made from orotate precursor with PRPP added later |
| What is made first: ribonucleotides or deoxyribonucleotides? | Ribonucleotides are synthesized first and are converted to deoxyribonucleotides by RIBONUCLEOTIDE REDUCTASE |
| The conversion of PRPP to IMP (AMP and GMP) requires what? | Glycine, Aspartate, Glutamine and THF |
| Conversion of Carbamoyl phosphate to Orotic Acid (precursor of pyrimidines) requires what? | Aspartate |
| What enzyme is required to convert dUMP to dTMP? | Thymidylate synthase |
| What enzyme is required to convert DHF to THF? | Dihydrofolate reductase |
| What is DNA transition? | Substitution of a purine for a purine or a a pyrimidine for a pyrimidine. Think: "TransItion = Identical type" |
| What is DNA transversion | Substituting a purine for pyrimidine. Think: "TransVersion = conVersion between types" |
| Features/Characteristics of the Genetic Code? | The genetic code is: - unambiguous - Degenerate/Redundant - Commaless, nonoverlapping - Universal |
| What does it mean to say that the genetic code is unambiguous? | Each codon specifies only 1 amino acid |
| What does it mean to say that the genetic code is degenerate/redundant? | More than 1 codon may code for the same amino acid |
| What is the only amino acid that is coded by only one codon? | Methionine is encoded by only one codon (AUG) |
| What does it mean to say that the genetic code is Commaless, nonoverlapping? | DNA is read from a fixed starting point as a continuous sequence of bases. However some viruses are an exception. |
| What does it mean to say that the genetic code is universal? | Genetic code is conserved throughout evolution. Exceptions include mitochondria, archaebacteria, Mycoplasma, and some yeasts. |
| What is a silent mutation | It is a mutation that produces the same amino acid and is often due to a base change in the 3rd position of the codon. Due to tRNA wobble |
| What is a Missense mutation? | mutation that results in a different amino acid being produced. |
| What is a Nonsense mutation? | mutation that results in the production of an early STOP codon. Think: "STOP the NONSENSE" |
| What is a Frameshift mutation? | a mutation that causes a misreading of all nucleotides downstream, usually resulting in a truncated, nonfunctional protein. |
| Which is the most severe DNA mutation? What is the least severe? | Most severe = Nonsense Least Severe = silent |
| What do single stranded binding proteins do? | Prevent strands from reannealing |
| What does DNA topoisomerases do? | create a nick in the helix to relieve supercoils created during replication |
| Primase | makes an RNA primer on which DNA polymerase III can initiate replication |
| DNA polymerase III | only found in prokaryotes only. Functions to elongate leading strand by adding deoxynucleotides to the 3' end. Elongates lagging strand until it reaches primer of preceding fragment. 3'-5' exonuclease activity profreads each added nucleotide |
| DNA polymerase I | prokaryotic only, degrades RNA primer and fills in the gap with DNA. DNA polymerase I excises RNA primer with 5'-3' exonuclease |
| DNA ligase | Seals |
| Nucleotide excision repair | Specific endonucleases release the oligonucleotide-containing damaged bases; DNA polymerase and ligase fill and reseal the gap |
| Base excision repair | Specific glycosylases recognize and remove damaged bases, AP endonuclease cuts DNA at apyrimidinic site, empty sugar is removed and the gap is filled and resealed. |
| Mismatch repair | Unmethylated, newly synthesized string is recognized, mismatched nucleotides are removed and the gap is filled and resealed |
| Nonhomologous end joining | Brings together 2 ends of DNA fragments. no requirement for homology |
| mRNA | longest type of mRNA, start codon = AUG, stop codon = UGA, UAA, UAG, made by RNA polymerase II |
| rRNA | most abundant type, made by RNA polymerase I |
| tRNA | smallest type, 75-90 nucleotides long, secondary structure is cloverleaf form made by RNA polymerase III |
| Promotor region | 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) |
| Mutation in promotor region commonly causes: | dramatic decrease in amount of gene transcribed |
| Enhancer region | stretch of DNA that alters gene expression by binding transcription factors |
| Silencer region | site where negative regulators (repressors) bind |
| Eukaryotic RNA polymerases | RNA polymerase I makes rRNA RNA polymerase II makes mRNA as well as opens DNA at promoter site RNA polymerase III makes tRNA RNA polymerase has no proof-reading functions but can initiate chains |
| RNA processing | Occurs in nucleus. After transcription: 1) capping on 5' end 2) polyadenylation on 3' end 3) Splicing out of introns Initial transcript is called heterogeneous nuclear RNA (hnRNA) Capped and tailed transcript is called mRNA |
| Exons | contain actual genetic information coding for protein, different exons can be combined by alternative splicing to make unique proteins in different tissues |
| Introns | intervening noncoding segments of DNA |
| tRNA wobble | accurate base pairing is required only in the 1st two nucleotide positioning of an mRNA codon, so codons differing in the 3rd 'wobble' position may code for the same tRNA/amino acid |
| Steps of protein synthesis | Initiation, elongation, termination |
| Proteasomal degradation | attachment of ubiquitin to defective proteins to tag them for breakdown |
| CDK cell cycle regulator | Cyclin dependent kinase, constitutive and inactive |
| Cyclins cell cycle regulator | Regulatory proteins that control cell cycle events, phase specific, activate CDKs |
| Cyclin-CDK complexes | must be both activated and inactivated for cell cycle to progress |
| Tumor suppressors | Rb and p53 normally inhibit G1 to S progression, mutations in these genes result in unrestrained growth |
| Permanent Cell type | remains in G0, regenerates from stem cells, Ex of permanent cell types: neurons, skeletal, cardiac muscle and RBCs |
| Stable (quiescent) cell type | Enter G1 from G0 when stimulated to grow Ex of stable cell types: Hepatocytes, lymphocytes |
| Labile cell type | Never go into G0, divide rapidly with a short G1 Ex: Bone marrow, gut epithelium, skin, hair follicle |
| Rough Endoplasmic Reticulum (RER) | site of synthesis of secretory proteins and of N-linked oligosaccharide addition to many proteins. Nissl bodies in neurons synthesize enzymes and peptide neurotransmitters |
| Smooth endoplasmic Reticulum (SER) | site of steroid synthesis and detoxification of drugs and poisons |
| Where is there a high concentration of RER | Mucus-secreting goblet cells of the small intestine and antibody secreting plasma cells |
| Where is there a high concentration of SER | liver hepatocytes and steriod hormone producing cells of the adrenal cortex |
| Golgi Apparatus function | 1) distrubution center of proteins and lipids from ER to plasma membrane, lysosomes and secretory vesicles 2) Modifies N-oligosaccharides on aspariagine 3) Adds O-Oliogosaccharides to serine and threonine 4) addition of mannose-6-phosphate to specific lys |
| I cell disease | inherited lysosomal storage disorder, failure of addition of mannose-6-phosphate to lysosome proteins |
| Microtubule | cylindrical structure composed of a helical array of polymerized dimers of alpha and beta tubulin, each dimer has 2 GTP bound. Grows slowly and collapses quickly |
| molecular motor proteins | transport cellular cargo toward opposite end of microtubular tracks Dynein = retrograde to microtubule Kinesin = anterograde to microtubule |
| Cilia Structure | 9+2 arrangement of microtubules Axonemal dynein- ATPase that links peripheral 9 doublets and causes bending of cilium by differential sliding of doublets |
| Cytoskeletal elements | actin, mysoin, microtubules, intermediate filaments |
| Actin and Myosin | found in microvilli,involved in muscle contraction, cytokinesis, adhering junctions |
| Microtubules | Cilia, flagella, mitotic spindle, neurons, centrioles |
| Intermediate Filaments | Vimentin, desmin, cytokeratin, glail fibrillary acid proteins (GFAP), neurofilaments |
| Plasma membrane composition | Asymmetric fluid bilayer, contains cholesterol, phospholipids, sphingolipids, glycolipids and proteins High cholesterol or long saturated fatty acid content leads to increased melting temp and decreased fluidity |
| Vitemtin Stain | Immunohistochemical stain for Connective tissue |
| Desmin Stain | Immunohistochemical stain for muscle |
| Cytokeratin Stain | Immunohistochemical stain for epithelial cells |
| GFAP stain | Immunohistochemical stain for Neuroglia |
| Neurofilaments stain | Immunohistochemical stain for Neurons |
| Sodium Pump | Na-K ATPase is located in the plasma membrane with ATP site on cytoplasmic side. For each ATP consumed, 3 Na go out and 2 K come in. During cycle, pump is phosphorylated |
| Collagen | most abundant protein in the human body, extensively modified, organizes and strengthens extracellular matrix |
| Type 1 Collagen | most common type, found in the Bone, Skin, Tendon, dentin, fascia, cornea, late wound repair |
| Type 2 Collagen | Cartilage(including hyaline), vitreous body, nucleus pulposus |
| Type 3 Collagen | Reticulin, skin, blood vessels, uterus, fetal tissue, granulation tissue |
| Type 4 Collagen | Basement membrane or basal lamina |
| Vitamin C is required for what part of collagen synthesis | Its needed for hydroxylation of specific proline and lysine residues |
| Ehlers-Danlos Syndrome | Faulty collagen synthesis causing: hyperextensible skin, tendency to bleed, hypermobile joints. There are 6 types and inheritance and severity vary depending on the type. May be addociated with joint dislocation, berry aneurysm, organ rupture. |
| What type of collagen is most often affected in Elhers-Danlos Syndrome | Type 3 collagen |
| Osteogenesis Imperfecta | aka Brittle Bone Disease, most common form is autosomal Dominant with abnormal Type 1 collagen. Sx: multiple fractures, blue sclerae, hearing loss, dental imperfections |
| Alports Syndrome | due to a variety of gene defects resulting in abnormal type 4 collagen, most common is X linked recessive. Sx: progressive hereditary nephritis, deafness, ocular disturbances |
| Elastin | stretchy protein within lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava. rich in proline and gylcine, broken down by elastase which is normally inhibited by alpha 1 antitrypsin |
| Marfans syndrome | caused by a defect in fibrillin |
| Emphysema | can be caused by alpha 1 antitrypsin deficiency resulting in excess elastase activity |
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