Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Molecular
First Aid - Biochem - Molecular
| Question | Answer |
|---|---|
| chromatin structure | DNA exists in the condensed chromatin form to fit into the nucleus -negatively charged DNA loops twice around positively charged histone octamer (2 sets of H2A, H2B, H3 and H4) to form a nucleosome bead -- HI ties nucleosome beads together in a string |
| heterochromatin | condensed, transcriptionally inactive, and sterically inaccessible |
| euchromatin | less condensed, transcriptionally active and sterically accessible |
| nucleotides | PURe As Gold: purines = adenine and guanine CUT the PY = pyrimidines = cytosine and thymine ---deamination of cytosine = uracil (RNA) G-C (3 H bonds) stronger than A-T (2 H bonds), so ^ G-C content means a higher melting temperature |
| purine salvage deficiencies | nucleic acids > GMP > guanosine >< guanine > xanthine > uric acid AMP > adenosine > inosine >< hypoxanthine > xanthine > uric acid |
| adenosine deaminase deficiency | excess ATP and dATP imbalance makes due to feedback inhibition of ribonucleotide reductase > prevents DNA synthesis and decreases lymphocyte count > major cause of severe combined immunodeficiency disorder |
| lesch-nyhan syndrome | defective purine salvage owing to absence of HGPRT, this converts hypoxanthine to IMP and guanine to GMP. results in excess uric acid production > retardation, self-mutilation, aggression, gout, hyperuricemia, choreoathetosis |
| Amino Acids - purine synthesis | GAG = glycine, aspartate, and glutamine are all necessary -Purines are made from IMP precursor |
| Pyrimidine synthesis | pyrimidines are made from orotate precursor, with PRPP added later -ribonucleotides are synthesized first and are converted to deoxyribonucleotides by ribonucleotide reductase |
| pyrimidine synthesis 2 | carbamoyl phosphate involved in de no pyr. syn and urea cycle, ornithine transcarbamoylase deficiency leads to an accumulation of carbamoyl phopsphate > converted to orotic acid |
| drugs that interfere with nucleotide synthesis | Hydroxyurea = inhibits ribonucleotide reductase, 6-mercaptopurine = blocks de novo purine syn ,5-fluorouracil - inhibits thymidylate synthase, Methotrexate = inhibits dihydrofolate reductase, Trimethoprin = inhibits bacterial dihydrofolate reductase) las3 |
| salvage path - nucleoside and nucleotides | salvage pathway = recover bases and nucleosides formed during DNA or RNA degradation, nucleosides (hypoxanthine, guanine, adenine) and nucleotides (IMP, AMP, GMP) |
| DNA replication - origin | particular sequence in genome where DNA replication begins |
| DNA replication - replication fork | Y shaped region along DNA template where leading and lagging strands are synthesized |
| DNA replication - helicase | unwinds DNA template at replication fork |
| DNA replication - single-stranded binding proteins | prevents strand from reannealing |
| DNA replication - DNA topoisomerases | create a nick in the helix to relieve supercoils created during replication |
| DNA replication - primase | makes an RNA primer to which DNA polymerase III can initiate replication |
| DNA replication - DNA polymerase III | prokaryotic - elongates leading strand by adding deoxynucleotides to the 3' end -- elongates lagging strand until it reaches primer of preceding fragment. 3' exonuclease proofreads each nucleotide |
| DNA replicaiton - DNA polymerase I | prokaryotic -- degrades RNA primer and fills in the gap with DNA |
| DNA replicaiton - DNA ligase | seals the DNA |
| DNA rep - Step 1 | helicases unwind the parental DNA double helix |
| DNA rep - Step 2 | single strand binding proteins stabilize the unwound parental DNA |
| DNA rep - Step 3 | the leading strand is syn continuously in the 5' - 3' by DNA polymerase |
| DNA rep - Step 4 | lagging strand syn discontinuously - primase synthesize short RNA primers that is extended by DNA polymerase to form an Okazaki fragment |
| DNA rep - Step 5 | RNA primer replaced by DNA by another DNA polymerase and DNA ligase puts together the Okazaki fragments to growing strand |
| Fluroquinolones | inhibit DNA gyrase (a specific prokaryotic topoisomerase) |
| Methods of single strand DNA repair | nucleotide excision repair, base excision repair, and mismatch repair |
| Methods of double strand DNA repair | nonhomologous end joining |
| nucleotide excision repair | specific endonucleases release the oligonucleotide containing damaged bases, DNA polymerase and ligase fill and reseal the gap, respectively |
| Xeroderma pigmentosum - nucleotide excision repair | no nucleotide excision repair - prevents repair of thymidine dimers from UV light > results in dry skin with melanoma and other cancers |
| Base excision repair | specific glycosylases recognize and remove damaged bases, AP endonuclease cuts DNA at apyrimidine 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 (mutated in HNPCC/Lynch) hMLH1 mutation (microsatellite instability) |
| Nonhomologous end joining | brings together 2 ends of DNA fragments -- no requirement for homology (error prone - can lead to translocations and telomere fusions) |
| DNA/RNA/protein synthesis direction | 5' - 3' / DNA syn requires a free 3' OH at add the next nucleotide -- drugs blocking DNA replication often have a modified 3' OH preventing addition of the next nucleotide (chain termination) |
| Functional organization of the gene | 5' promoter, enhancer, promoter (TATA), transcription initiation site, Coding Region (exon/intron) , AATAAA 3' |
| Promoter | 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 = dramatic decrease in amount gene transcribed |
| Enhancer | stretch of DNA that alters gene expression by binding transcription factors - (enhancers and silencers may be located close to far from or even within (in an intron) the gene whose expression it regulates |
| Silencer | site where negative regulators (repressors) bind |
| RNA processing | Nucleus: after transcription 1. capping on 5' end (7-methylguanosine) 2. polyadenylation on 3'end 3. splicing out of introns *capped and tailed transcript = mRNA - transported out of nucleus (AAUAAA polyadenylation signal) |
| Introns | Introns are intervening noncoding segments of the DNA - stay in the nucleus |
| Exons | contain the actual genetic information coding for protein, exons exit and are expressed |
| Alternative splicing (ex. Beta-Thal mutations) | different exons can be combined by alternative splicing to make unique proteins in different tissues (Beta-Thal mutations) |
| tRNA structure | secondary structure, cloverleaf formation, CCA at 3' end along with high % of chemically modified bases - amino acid covalently bound to 3' end of tRNA |
| tRNA charging | aminoacyl-tRNA synthestase examines aa before and after it binds, incorrect bond hydrolyzed, aa-tRNA energy for formation of peptide bond, mischarged tRNA reads usual codon but inserts wrong aa |
| Tetracyclines | aminoacyl-tRNA synthetase and binding of charged tRNA to the codon are responsible for accuracy of aa selection - Tetracyclines bind 30s subunit preventing attachment of aminoacyl-tRNA |
| protein synthesis - initiation | activated by GTP hydrolysis, initiation factors assemble 40S ribosomal subunit with initiator tRNA and released when mRNA and ribosomal subunit assemble with the complex |
| protein synthesis - elongation | 1. aminoacyl-tRNA binds to A site 2. ribosomal rRNA catalyzes peptide bond formation transfers growing polypeptide to aa in A site 3. ribosome advances 3 nucleotides toward 3' end of RNA, moves peptidyl RNA to P site |
| protein synthesis - termination | completed protein is released from ribosome through hydrolysis and dissociates |
| protein synthesis inhibitors | Clindamycin = binds 50S blocking translocation |
| Posttranslational modifications | trimming(removal of N or C terminal propeptides from zymogens to generate mature proteins), covalent alt(phosphorylation, glycosylation, hydroxylation), proteasome degradation(ubiquitin to defective proteins tagged for breakdown) |
Created by:
Smukadam
Popular USMLE sets