Anatomy, Biochem and Physiology Flashcards

1
Q

Central dogma of the genetics

A

DNA to protien

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2
Q

Building blocks of DNA

A

Sugar phosphate, base, and nucleotide

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3
Q

How are AT and GC bonded

A

AT w/ 2 H bonds

GC w/ 3 h bonds

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4
Q

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

A

covalently

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5
Q

The 5’ end is characterized by the

A

phosphate group

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6
Q

How is DNA packed in eukaryotes

A

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

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7
Q

Levels of DNA packing (eukaryotic)

A

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

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8
Q

What is the role of H1

A

It is a binds together other nucleosomes

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9
Q

How is prokaryotic DNA packed

A

HU protiens

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10
Q

Where does DNA synthesis being?

A

ORIC

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11
Q

Prokaryotic genomes are usually ____ so have ___ ORI

A

circular and have one

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12
Q

Eukaryotics chromosomes have ____ replication origin

A

multiple

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13
Q

Why does eukaryotics genomes have multiple ORC

A

Large amount of DNA to process

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14
Q

in e.coli what tow sequences are needed

A

13 nucleotide sequence(three in tandem array)

9 Nucleotide sequence

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15
Q

13 mer tandem sequence

A

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

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16
Q

the 9 nucleotide regions is needed for

A

DNA-A initiator proteins to bind

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17
Q

After DNA-A bind what is next

A

DNA-C protein delivers Helicase(DNA-B)

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18
Q

Single stranded binding protein(SSB)

A

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

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19
Q

what is a primosome

A

Has DNA-B and a primase

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20
Q

DNA Polymerase III fxn

A

to catalyze the formation of phosphodiester bond

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21
Q

3’=5’ proofreading exonuclease

A

to clip away any unpaired residues at the primer terminus

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22
Q

how does DNA encounter for the lagging strand

A

okazaki fragments

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23
Q

in bacteria how many RNA polymerases are there

A

one, the sigma factor

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24
Q

in eukaryotes how many RNA polymerases are there

A

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

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25
Q

Where will RNA polymerase bind in prokaryotic genes

A

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

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26
Q

In RNA what is the Sense and Anti-sense stands

A

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

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27
Q

In prokaryotic transcription how does it stop

A

Poly U and hairpin structure

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28
Q

Open reading Fram(ORF)

A

Used to see what the gene will be made into

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29
Q

Prokaryotic transcriptions and translation occurs

A

in the cytosol and simultaneously

30
Q

Transcription factor D

A

Used in TATA boxing binding

31
Q

t-RNA

A

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

32
Q

What couples a particular AA to is coresposning tRNA

A

aminoacyl tuna synthase

33
Q

Prokaryotes Large and small subunit size

A

70S but 50S and 30S

34
Q

Eukarotes subunit sizes

A

80 but 60s and 40s

35
Q

Ribosome structure

A

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

36
Q

In prokaryotes what is additionally on iniitating methionine

A

formyl group

37
Q

what are apoenzymes

A

enzymes w/o the coenzyme

38
Q

Catabolism

A

Break down

39
Q

Anabolism

A

build up of

40
Q
  • delta G
A

spontaneous rrxn

41
Q

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

A

energy of activation

42
Q

enzymes do not change the gibes energy just find alternate path

A
43
Q

Micheaelis eq

A

Vo=Vmax/KM+s

44
Q

KM is the

A

substrate concretion where half max velocity is reached Vmax/2

45
Q

Vmax increases when

A

higher enzyme concentration but the KM remains

so more product is formed w/ more enzymes but the affinity for binding is unchanged

46
Q

Michaelis menten kinetis curve is

A

hyperbolic

47
Q

allosteric curve is

A

sigmoidal

48
Q

Competitive reversible inhibition

A

When substrate and analog compete for same site

49
Q

How can competitive inhibition be overcome

A

w/ high substrate concentrations

50
Q

Competitive inhibition KM and Vmax/2

A

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

51
Q

Non competitive inhibition

A

finds and alternate site for binding

52
Q

non competitive inhibition km and max

A

No completion means low effort to VMAX KM same

53
Q

Un competitive inhibitor

A

competition is not present so max decrease but KM increases

54
Q

Reversible inhibition

A

inhibitor drugs bind non-covalently(weak bonds)

Competitive and non competitive

55
Q

inhibitor drugs or poison bind ___

A

covalently and interfere w/ cofactors

56
Q

NSAIDs are considered reversible inhibition but ASA(aspirin)

A

is not and is considered non reversible

57
Q

ASA irreversibly inhibits ___ and ___

A

COX1 and COX2 which are needed for thrombonxans synth

58
Q

ASA acrylates(give and acetyl group) to

A

Serine group on COX

this is done so close to the EBS that it is unable to bind anymore

59
Q

ASA is not selective

A

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

60
Q

Intercellular

A

Diffrent areas

61
Q

intracellular

A

in the same area

62
Q

endocrine signaling

A

via hormones

63
Q

4 types of receptors

A

Steroid, gated ion, Receptor(ligand) and GPCR

64
Q

Steroid hormones work bu

A

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

65
Q

Steroid receptor order of ops

A
  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
66
Q

gated Ion channel ex

A

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

67
Q

What type of receptor is tyrosine kinase

A

catalytic receptor

68
Q

Order of ops for TK

A
  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
69
Q

GPCR pathway

A

Secondary messenger

70
Q

GPCR order of ops

A
  1. First messenger(Cytokine or NT)

2. Heterotrimeric g-protein(A, B and Gamma) bound to GDP