Summary
Cells, physiology and pharmacology summary for exam
- Module
- Pharmacy
- Institution
- University Of East Anglia
Pharmacy - cells, physiology and pharmacology 1st and 2nd semester Bullet point summary of keys details for the exam
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Genetics miRNA- control gene expression
rRNA- 60% of ribosome
mRNA- codes for proteins
tRNA- adaptor for protein synthesis
8 histone proteins- H1 packs them together and 2 copies of H2A, H2B, H3 and H4
Introns- non-coding (regulatory) and exons are coding
Promoter upstream of gene- controls gene expression, transcription factors and
TATA box (RNA polymerase transcription complex)
DNA Replication
Topoisomerase de-coils DNA
DNA Helicase unwinds DNA requires ATP
DNA polymerase III creates the daughter strand 5’ to 3’
Parent strand reformed 3’ to 5’ by DNA ligase
DNA primase attaches RNA primer
Telomerase replicates DNA at the end of the chromosome
Origin of replication
Replication fork can emerge on both ends as replication is bidirectional
Initiation:
Primase attaches RNA primer which is removed by RNaseH and gap filled by
polymerase I
Primase in primosome and substitutes 3’ OH for polymerase
Elongation:
Leading strand 3’ to 5’ (exonuclease) and lagging 5’ to 3’ (polymerisation)
Okazaki fragment each requires RNA primer from discontinuous replication
Termination:
When replication forks meet
Telomerase produces telomeres at the end of DNA
Transcription
RNA polymerase reads 3’ to 5’ (no primer)
RNA polymerase I (rRNA), II (protein coding) and III (tRNA)
RNA polymerase II requires TFII (transcription factors)
TFII positions polymerase, pulls strands apart and allows polymerase to leave
TFIID binds to TATA box
TFIIH uses ATP to pull DNA strand apart and releases RNA polymerase II by
phosphorylating it
Enhancers bind to activator proteins to switch on transcription
Enhancers attract RNA polymerase towards TFII
Repressors bound to DNA dissociate from it so transcription begins
Activators and repressors bind to alpha helices in major groove (helix turn helix
motif or leucine zipper)
Histone deacetylase relax chromatin and allow activators to bind
Co-activators activator proteins or TFs and induce or enhance transcription
mRNA modification:
Capping 5’-add guanine with methyl group (protects from RNases)
Polyadenylation 3’- 250+ adenines added protects degradation by exonuclease
Pre-mRNA splicing- splicesome cuts out introns
Translation
, AUG start and UAA/UAG/UGA stop
tRNA anticodon and single strand on 3’
Aminoacyl tRNA synthetase forms ester bond
Ribosome sites E (exit), P (peptide) and A (amino acid)
Translation Initiation:
Initiation factors, UAC anticodon binds to P site and subunits
Elongation:
tRNA joins amino acid at A site
Second tRNA moves to P site (translocation)
Termination:
Release factor binds to site and ribosome dissociates
Chaperones- protein folding GroEl and GroES
N terminal sequences targets protein site
Protein modifications:
Proteolysis- removal of signal sequence
Glycosylation- oligosaccharide covalently bonded
Insertion of cofactor
Formation of disulphide bonds
PEST (Pro,Glu, Ser and Thr) proteins degraded quickly
Protein degradation: lysosome (protease), ubiquitins or proteasome
DNA Mutation and Repair
Point mutation- missense (changes meaning of code), nonsense (produces stop)
and silent (no effect)
Insertion- if not 3bp causes frame-shift
Deletion- if not 3bp causes frame-shift
Inversion- section reversed
Reciprocal translocation- segments of 2 non-homologous chromosomes switch
Exogenous agents (environmental) and Endogenous (bodily)
UV radiation causes thymine dimers
Deamination effects DNA structure
Depurination, oxidation or methylation
DNA repair Excision, resynthesis and ligation:
DNA glycosylase creates abasic site
AP endonuclease and phosphodiesterase recognise abasic site
Enzyme complex recognises damage- exonuclease excises nucleotides and DNA
helicase removes it
Non-homologous recombination- in G1, broken ends of DNA juxtaposed and
DNA ligates together but loses nucleotides
Homologous recombination- S/G2 phase but sister chromatid used to replicate
and repair
Stem Cells
Molecular cloning- loss of function, reporter gene and lineage tracing
Stem cell niche- microenvironment: direct contact, soluble factor and
intermediate cell
Stem cell: self renew, divide rarely and high potency
Committed progenitor- multipotent, divide rapidly and don’t self renew
Drug Interactions
When the effects of one drug are changed by the presence of another drug,
herbal medicine, food, drink or environmental chemical agent
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