Anatomy, Biochem and Physiology Flashcards by Adam Garza

Central dogma of the genetics

DNA to protien

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Building blocks of DNA

Sugar phosphate, base, and nucleotide

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How are AT and GC bonded

AT w/ 2 H bonds

GC w/ 3 h bonds

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How are nucleotides linked w/ through a sugar-phosphate backbone

covalently

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The 5’ end is characterized by the

phosphate group

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How is DNA packed in eukaryotes

Histones(portiens)
histones is comprised of 8 monomers
H2, H2b H3 and H4 x 2

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Levels of DNA packing (eukaryotic)

Nucleosomes, beads on a string, and 30nm(solenoid)

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What is the role of H1

It is a binds together other nucleosomes

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How is prokaryotic DNA packed

HU protiens

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Where does DNA synthesis being?

ORIC

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Prokaryotic genomes are usually ____ so have ___ ORI

circular and have one

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Eukaryotics chromosomes have ____ replication origin

multiple

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Why does eukaryotics genomes have multiple ORC

Large amount of DNA to process

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in e.coli what tow sequences are needed

13 nucleotide sequence(three in tandem array)

9 Nucleotide sequence

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13 mer tandem sequence

bonding at A-T is weaker and this means that seperation of DNA is easier

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the 9 nucleotide regions is needed for

DNA-A initiator proteins to bind

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After DNA-A bind what is next

DNA-C protein delivers Helicase(DNA-B)

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Single stranded binding protein(SSB)

bind to single stranded DNA to prevent reanneling or forming a secondary structure

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what is a primosome

Has DNA-B and a primase

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DNA Polymerase III fxn

to catalyze the formation of phosphodiester bond

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3’=5’ proofreading exonuclease

to clip away any unpaired residues at the primer terminus

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how does DNA encounter for the lagging strand

okazaki fragments

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in bacteria how many RNA polymerases are there

one, the sigma factor

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in eukaryotes how many RNA polymerases are there

3
RNA polymerase I:
RNA Polymerase II:
RNA polymerase III:

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Where will RNA polymerase bind in prokaryotic genes

will bind to the promoter regions also know as the Pribnow box

In RNA what is the Sense and Anti-sense stands

Sense: coding strand RNA should be identical besides the U replacement Anti: template

In prokaryotic transcription how does it stop

Poly U and hairpin structure

Open reading Fram(ORF)

Used to see what the gene will be made into

Prokaryotic transcriptions and translation occurs

in the cytosol and simultaneously

Transcription factor D

Used in TATA boxing binding

t-RNA

transfer RNA forms the clover w/ T Loop on right and D loop on left

What couples a particular AA to is coresposning tRNA

aminoacyl tuna synthase

Prokaryotes Large and small subunit size

70S but 50S and 30S

Eukarotes subunit sizes

80 but 60s and 40s

Ribosome structure

EPA side A for aninoacyl tuna where TRNA w/ AA P for peptide transferase E for Exit

In prokaryotes what is additionally on iniitating methionine

formyl group

what are apoenzymes

enzymes w/o the coenzyme

Catabolism

Break down

Anabolism

build up of

- delta G

spontaneous rrxn

enzyme provide an alternate reaction pathway and as a result can reside the

energy of activation

enzymes do not change the gibes energy just find alternate path

Micheaelis eq

Vo=Vmax/KM+s

KM is the

substrate concretion where half max velocity is reached Vmax/2

Vmax increases when

higher enzyme concentration but the KM remains | so more product is formed w/ more enzymes but the affinity for binding is unchanged

Michaelis menten kinetis curve is

hyperbolic

allosteric curve is

sigmoidal

Competitive reversible inhibition

When substrate and analog compete for same site

How can competitive inhibition be overcome

w/ high substrate concentrations

Competitive inhibition KM and Vmax/2

When your competitive you and your competition are equal max but your KM wants it more(but it is opposite)

Non competitive inhibition

finds and alternate site for binding

non competitive inhibition km and max

No completion means low effort to VMAX KM same

Un competitive inhibitor

competition is not present so max decrease but KM increases

Reversible inhibition

inhibitor drugs bind non-covalently(weak bonds) | Competitive and non competitive

inhibitor drugs or poison bind ___

covalently and interfere w/ cofactors

NSAIDs are considered reversible inhibition but ASA(aspirin)

is not and is considered non reversible

ASA irreversibly inhibits ___ and ___

COX1 and COX2 which are needed for thrombonxans synth

ASA acrylates(give and acetyl group) to

Serine group on COX | this is done so close to the EBS that it is unable to bind anymore

ASA is not selective

it still inhibits platelets synth and endothelia cells but also inhibits platelets synth

Intercellular

Diffrent areas

intracellular

in the same area

endocrine signaling

via hormones

4 types of receptors

Steroid, gated ion, Receptor(ligand) and GPCR

Steroid hormones work bu

inducing(up regulating) gene expression at the level of DNA

Steroid receptor order of ops

1. hormone is carried to target tissue via binding proteins 2. Hormone binds changes confirmation 3. Binding regulates transcription of adjacent gene 4. transcript and translation occur

gated Ion channel ex

Neurotransmitter results in a rush of ions through ion channel alterning membrane potential

What type of receptor is tyrosine kinase

catalytic receptor

Order of ops for TK

1. Alpha and beta dimmers are together 2. Insulin receptors bind Tyr w/ ATP 3. phosphorylated and ADP is related and Try w/ target protein goes through signiling

GPCR pathway

Secondary messenger

GPCR order of ops

1. First messenger(Cytokine or NT) | 2. Heterotrimeric g-protein(A, B and Gamma) bound to GDP