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MCB Phys-Biochem

MCB Physiology

Histones Nucleosome=H2A, 2B, 3, 4. H1 is solo & ties nucleosomes. Hetero: Condensed, inactive chromatin. Eu: Less condensed, active chromatin.
Purines 2 Rings. Guanine & Adenosine. Requires Gly, Glut, Asp AAs from IMP precursor. Guanine has a Ketone.
Pyrimidine 1 Ring. Cytosine, Thymidine (methyl), Uracil. Orotate+ PRPP.
Nucelotide v. Nucleoside -side: Base + ribose. –tide: Base + ribose + Pi
Transition v. Transversion Transition: purine -> purine. Transversion: purine/pyrimidine -> pyrimidine/purine
Unambiguous, Degenerate/Redundant, Commaless/Non-overlapping, Universal Know it. Exceptions to universal code: Mitochondiria, archaebacteria, mycoplasma, some yeast.
Silent Mutation Same AA due to 3rd base wobble
Missense Mutation AA change
Nonsense Mutation AA-> Stop Codon (UGA, UAA, UAG)
DNA Gyrase Prokaryote-only Topoisomerase.
DNA Pol I, DNA Pol III, Primase DNA Pol I: Replaces RNA primer w/ DNA. DNA Pol III: Starts on a primer, 5-3 Polymerization 3-5. PRIMASE: Makes RNA Primer.
Nucleotide excision repair Endonucleases rip out portion of strand containing damaged bases. DNA pol & Ligase clean it up. Mutated in Xeroderma pigmentosum
Base Excision Repair DNA Glycosylase recognizes mutant base & pulls it off the backbone, AP Endonuclease IDs the baseless site & cleaves the backbone to be replaced by a POL.
Mismatch Repair Mutated in HNPCC
DS Break Repair Non-homologous end-joining
Protein Polymerization N to C
Start & Stop Codons Start: AUG-> methionine (eukaryotes), formyl-Met (prokaryotes). STOP: UAA, UAG, UGA.
Promoter Sequence Where DNA Pol +/- some transcription factors bind in front of gene (includes TATA boxes)
Enhancer Sequence Where transcription factors bind (anywhere)
Silencer Sequence Where negative regulators/repressors bind.
RNA Pol I, II, & III In eukaryotes only. RNA Pol I: rRNA. RNA Pol II: mRNA (inhibited by alpha-amantin in shrooms) RNA Pol III: tRNA. Prokaryotes have 1 RNA Pol that does it all.
RNA Processing heterogenous nuclear RNA (hnRNA) 5’Cap: Methyl-Guanosine; 3’ Poly A Tail (mRNA)
Spliceosome snRNPs. Consider alternative splicing (beta-thalassemia mutation)
tRNA 3’ end has CCA sequence & is where AA binds. Charged by Aminoacyl-tRNA synthase (2 ATP)
Ribosome Eu [60S + 40S-> 80s]. Pro [50s + 30s -> 70s]. Activated by GTP hydrolysis, IFs. A Site(Accepts tRNA), P Site (Peptide elongation), E site (Empty tRNA). Polymerization requires 2 GTP/AA added.
Protein Trimming Cleave N or C peptides to activate zymogens/pro-enzyme
G1-> S Regulation Buided by Rb & p53.
Nissl Bodies Synthesize secretory enzymes in neurons
SER Steroid synthesis & chemical detox, lot of SER in liver & steroid-producing cells.
Golgi Protein Modification adds O-oligosaccharides to Serine & Threonine, modifies N-oligosaccharides on asparagines. Addition of M6P -> lysosome. COP I: golgi -> ER. COP II RER-> golgi. Clathrin: Golgi -> everywhere but ER.
Drugs that act on microtubules Mebendazole/Thiabendazole (helminth), Pacitaxel (BRCA), Griseofulvin (Antifungal), Vincristine/Vinblastine (Cancer), Colchicine (gout). Cheidak-Higashi: polymerization defect-> less phagocytosis.
Phosphatidylcholine RBC membrane, myelin, bile, surfactant.
Vimentin Stain Connective tissue
Desmin Stain Muscle
GFAP Stain Neuroglia
Type 1 Collagen Most abundant protein in body. bONE, tendon, Skin, dentin, fascia , cornea.
Type 2 Collagen Cartilage, nucleus pulposus
Type 3 Collagen AKA reticulin. Skin, blood vessels, uterus, fetus, granulation tissue
Type 4 Collagen Basement membrane/Basal lamina
Pre-Secretory Collagen Synthesis 1) Synthesis in RER: Preprocollagen (Glycine + Proline/Hydroxylproline/Hydroxylysine) 2) Hydroxylation of non-gly AAs in ER (vitamin C-dependent) 3) Glycosylation of lysine in ER: (Osteogenesis Imperfecta) -> pro-collagen
Post-Secretory Collagen Synthesis 4) Secretion + cleavage of terminal procollagen-> tropocollagen 5) Lysyl oxidase cross-links lysine & hydroxylysine (Ehlers-Danlos).
Ehlers Danlos Syndrome Type III Collagen. Hyperextensible skin, bleeding, hypermobile joints. Variable inheritance & forms.
Osteogenesis Imperfecta Most are AD Collagen 1 synthesis disorder. Col1A1 & A2. Type 2 is in-utero fatal. Multiple fractures, blue sclera, hearing loss (bones), dental imperfections.
Elastin Lungs, large arteries, ligaments, vocal cords. Lots o’ proline, glycine. Fibrillin is scaffolding protein. Marfan: Fibrillin defect. Alpha1 antitrypsin: inhibits elastase.
Glycolysis Result 32 ATP in heart & liver (malate-aspartate shuttle), 30 ATP via G3P shuttle in muscle.
NADPH Generated by HMP shunt. Use: steroid & FA synthesis (anabolic processes), P-450, respiratory bursts:
NAD+ Catabolic processes
Hexokinase & Glucokinase Irreversible 1st step of glycolysis. HEXOKINASE: ubiquitous. high affinity & low Vmax, feedback inhibited by G6P, insulin. GLUCOKINASE: pancreatic beta cells & liver. Induced by insulin. Low affinity & high Vmax & sequesters glucose.
Enzyme-Deficiency Hemolytic Anemia LOF Pyruvate kinase >> Phosphoglucose Isomerase. RBCs can’t do anaerobic metabolism -> no Na/K ATPase -> cell lysis.
Pyruvate DeH & Alpha Ketoglutarate DeH Complexes Co-Factors: B1,2,3,5, Lipoic Acid. Arsenic --| Lipoic Acid -> -> Vomiting, rice water stools, garlic breath. B1 Def-> ->ATP depletion -> SM relaxation -> High output cardiac failure.
Pyruvate DeH Deficiency Pyruvate & Alanine backup -> Lactic Acidosis & neuro defects. Congenital or acquired (alcoholic B1 deficiency). Tx: High ketogenic diet (Fat, and lysine & Leucine)
Regions of Anaerobic Glycolysis RBCs, Leukocytes, Kidney medulla, Lens, Testes, cornea.
Ox Phos Poisons Electron Transport Inhibitors: CN, CO, Antimycin A, Rotenone. ATPase Inhibitors: Oligomycin. Uncouplers: 2,4 DNP, Aspirin, thermogenin in brown fat.
Incomplete Penetrance v. Variable Expression Incomplete penetrance: binary phenotype of a given genotype. Variable Expression: phenotype is along a spectrum
Pleiotropy Multiple genes affect a phenotype
Dominant Negative Mutation Normal allele is disrupted by mutant allele (ie- Osteogenesis Imperfecta)
Locus heterogeneity Mutations at different loci can produce the same phenotype (ie-albinism)
Heteroplasmy Presence of normal & mutated mtDNA-> variable expression patterns in mitochondrial diseases
Uniparental disomy 2 copies of a chromosome from 1 parent, 0 from the other.
Imprinting 1 of 2 genes is permanently inactivated by methylation. Prader-Willi: Deletion of normally active paternal. Angelman: Deletion of normally active maternal allele.
APKD1 Chromosome 16. AD
Von Hippel Lindau AD. Hemangioblastomas, renal cell carcinoma. VHL gene deletion (Ch 3)
Huntington’s Disease AD. Reduced GABA & ACh. Chromosome 4.
Familial Adenomatous Polyposis AD. Adenomatous polyps in colon by puberty->-> colon cancer. Chromosome 5 Del (# in “polyp”)
Achondroplasia AD. Fibroblast GF receptor 3 LOF-> dwarfism, short limbs, normal trunk. Assoc. w/ advanced paternal age.
Things I don’t know about CF Chromosome 7. Def. of fat-soluble vitamins (ADEK), N. Acetylcysteine loosens mucous plugs. Meconium ileus in newborns
X-Recessive Diseases that I don’t know Bruton’s Agammaglobulinemia, Wiskott-Aldrich Syndrome, G6PD def, Ocular albinism, . Lesch-Nyhan Syndrome, Fabry’s Disease, Hunter’s Syndrome
Fragile X Syndrome CGG repeat -> overmethylation of the region -> inactivation of FMR1 gene -> #2 cause of MR, Macro-orchidism…
Myotonic Dystrophy Myotonic grip, balding, cataracts, testicular atrophy. Trinucleotide repeat -> sequesters splicing factors -> deficiency in other gene expression.
Edward’s Syndrome Prominent occiput, small jaw, low ears, clenched hands, rocker bottom-feet. Trisomy 18 (Election age). Severe MR, <1 yr life expectancy.
Patau’s Syndrome Micropthalmia, microcephaly, cleft lip/palate, polydactyly, rocker-bottom feet. Trisomy 13 (Puberty age). Severe MR & <1yr life expectancy.
PerIcentric v. ParAcentric Chromosomal Inversion ParIcentric: involves centromere, can go through meiosis. ParAcentric: Doesn’t involve centromere, doesn’t go through meiosis
Cri-du-chat Syndrome Chromosome 5 arm deletion-> MR & Microcephaly, high pitch crying, epicanthal folds, cardiac probs.
22q11 Syndrome DiGeorge: thymic aplasia, heart defects, hypocalcemia. Velocardiofacial Syndrome: Cleft palate, abnormal facies, heart defects
Created by: Kyle Tiemeier



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