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MCM Final > DSA Readings > Flashcards

DSA Readings Flashcards

1
Q

DNA polymerases

A

add NT to strand growing in 5 to 3, copying a DNA temp in 3 to 5

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2
Q

Primase

A

syn RNA primer

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3
Q

Helicase

A

separate parental DNA strands, unwind double helix

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4
Q

Single strand binding proteins

A

prevent single strands of DNA from reassociating

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5
Q

topoisomerases

A

relieve torsional strain on parental duplex caused by unwinding

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6
Q

RNase H

A

hydrolyzes RNA of DNA RNA hybrids

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7
Q

Flap endonucleases 1

A

recognizes flap-created by poly z displacing primer as okazaki frag is syn, remove primers

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8
Q

DNA ligase

A

joins 2 adjacent DNA strands that are bound to the same template, form phosphodiester bond

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9
Q

Proliferating cell nuclear antigen

A

enhances processivity of DNA poly, binds many proteins at replication fork

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10
Q

Euchromatin vs heterochromatin

A

eu: loosely packed, hetero: tightly packed

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11
Q

AT and CG bonds

A

AT: 2 H, CG 3 H connecting bases

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12
Q

what causes DNA strands to seperate

A

heat and alkali (doesnt cause PD bonds to break, will in RNA)- only separates strands

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13
Q

Ecoli DNA structure

A

supercoiled and attached to RNA protein core

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14
Q

Nucleosomes

A

DNA bound to histones, looks like beads on a string- nucleosomes are the beads, bind together- solenoid stucture

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15
Q

Nucleosome core

A

DNA bound to histones, looks like beads on a string- nucleosomes are the beads with DNA coming from both sides

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16
Q

Euk mRNA general structure

A

starts with guanine cap at 5 end, start codon, stop codon, poly A tail (cap, tail- added after translation of mRNA)

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17
Q

Ribosome sizes

A

30S and 50S combine to for E 70S, 55S in mitochondria, 55S in bacteria- target of azithromycin (can also affect mito ribo)

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18
Q

tRNA modified NTs

A

ribothymine, dihydrouridine, pseudouridine

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19
Q

other RNAs

A

oligonucleotides: primer for DNA rep, small nuclear ribonucleoproteins: involved in splicing and mod. during maturation of RNA, microRNA: help w reg of gene expression

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20
Q

DNA rep in pro

A

bidirectional, start at origin of replication, 2 replication forks

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21
Q

DNA poly directions

A

copy strand 3 to 5, make new 5 to 3

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22
Q

DNA poly bond and energy

A

ester bond formed between new NT and chain- pyrophosphate released, cleaved- energy that drives polymerization rxn

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23
Q

Processivity

A

how much an enzyme stays attached to chain, DNA poly has high processivity

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24
Q

Ecoli DNA polyermase III

A

proofreading, 3 to 5 exonuclease activity

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25
Q

RNA primer

A

DNA poly needs OH group, needs RNA primer- made by RNA polymerase (primase) that copies the DNA strand

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26
Q

Leading vs lagging strand

A

lead: continous, 5 to 3
lagg: okazaki frag, 3 to 5, away from fork

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27
Q

Lagging strand process

A

RNA primer made by pol a and primase, poly S adds DORNT, stops when reach primer of previous fragment- removed by flap endonuclease I and RNase H, gap filled by poly S and ligase

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28
Q

Cigarette smoke mutagen

A

complex oxidized- form bulky adducts w ganine residues in DNA

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29
Q

UV mutagen

A

excitation of adjacent pyrimidine bases- form covalent bonds (thymine dimers)

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30
Q

general DNA repair mechanism

A

distortion removed, DNA poly syn strand 5 to 3, ligase

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31
Q

general DNA repair mechanism bacteria

A

NT not released, thymine dimer- protoactivate enzyme that cleaves bond using energy from visible light

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32
Q

nucleotide excision repair

A

mismatched bases or bulky adducts, specific repair endonuclease- cleave bond, remove region, DNA poly, , ligase

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33
Q

base excision repair

A

damage to single base, glycosylase cleaves N glycosidic bond that joins damaged base to deoxyribose, apurinic/apyrimidinic (AP) endonuclease cleaves sugar phosphate strand- DNA poly, ligase

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34
Q

mismatch repair

A

mismatch repair enzyme complex find mismatch and replace, in bact- parent strand is acetylated (A), complex goes over new strand before A, dont know how its done in E

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35
Q

General/homologous recombination

A

2 homo chomo/seg of DNA align- 1 strand of duplex 1 nicked by enzyme, invade strand of duplex 2- form displacement loop, nick duplex 2- displaced strand now base pairs with former partner of invading strand- Holliday structure that can move- cleaved and ligated- chromo w exchanged information

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36
Q

translocation

A

nonorganic break in chromo- free end reseal with free end of diff broken chromo- can have deleterious effects, seen in cancer

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37
Q

transposable elements

A

seg of DNA that can move from original position to new location in genome, contains genes for transposase, retrotransposons have these- but RNA used to make double strand copy of DNA and insert into host DNA

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38
Q

Reverse transcriptase

A

use single strand RNA template to make DNA copy, retrovirus contain to instert bacterial DNA Into host genome

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39
Q

Poly used when DNA is damaged 2 continue replication

A

polymerases L, k, n, l- no 5 exonuclease activity, bypass polymerases

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40
Q

DNA poly a

A 
function in replication and DNA repair, no exo
-primase associ with poly a - produces RNA primer, a addes 20 DORNT to RNA and diss from temp (low processivity)
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41
Q

DNA poly b

A

DNA repain, no exo

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42
Q

DNA poly y

A

DNA replication in mito, 3 to 5 exo

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43
Q

DNA poly S

A

*main, replication, DNA repain, 3 to 5 exo

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44
Q

DNA poly E

A

*main, replication, DNA repair, 3 to 5 exo

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45
Q

DNA poly K, n, z, L

A

DNA repair, bypass polymerase, no exo

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46
Q

AP-1

A

heterodimer formed by protein products of fos and jun families of proto oncogenes

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47
Q

MAPK pathway

A

MAPK induc myc and fos and AP1- act genes involved in cellular prolif and progression through cell cycle (same targets as myc)

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48
Q

C-myc

A

targets genes in cell prolif and progression through cell cycle, tightly regulated, only expressed during S phase, tumor/cancer- regulation lost, continuous prolif

49
Q

cyclin CDK

A

reg through phos and inh proteins- cyclin dependent kinase inhibitors (CKIs slow cell progression by inh cyclin CDK complex)

50
Q

cdk4 and cdk6

A

regulatory proteins, constitutively produced throughout cell cycle

51
Q

cyclin D

A

syn is induced only after growth factor stimulation, regulatory proteins

52
Q

retinoblastoma gene product (Rb)

A

regulatory protein

53
Q

E2F and proteins induced

A

regulatory protein, class of transciprtion factors, inh by binding Rb, induce cyclin E, cyclin A, cdc25A

54
Q

Rb/E2F pathway normal

A

Rb (tumor suppressor) bind E2F- supp. growth factor simulation- cyclin D induced, bind cdk4 and cdk6 - act protein kinases- target of CD/CDK= Rb, P of RB release from E2F- activation of tranc of genes required for entry to S phase

55
Q

once E2F is active

A

lead to prod of cyclin E1-Cdk2- hyperphos Rb protein-keeping inactive, cyclin a-Cdk2 complex- phos and inactivates E2F- signal not present for long

56
Q

CKIs categories

A

inh progress through cell cucle, Cip/Kip family and INK4, some induced by DNA damage to halt cell cycle for repair

57
Q

Cip/Kip

A

CKIs, p21, p27 and p57, broad specificity and inhib all cyclin CDKs

58
Q

INK4

A

CKI, p15, p16, p18, p19, specific for cyclin D -cdk4/6 family

59
Q

tumor suppressor gene

A

halt cell cycle if damage, contribute to development of cancer when both copies of gene are inactive

60
Q

retinoblastoma gene

A

G1-S phase, reg act of E2F family, inherit mut of Rb gene- 100% of developing retinoblastome (high prob of second allele gain mut)- familial retinoblastoma, dont inherit but develop- sporadic retinoblastoma

61
Q

p53

A

TF that regulates cell cycle and apop, loss of both allele f(x) found in more than 50% tumors, level rises in response to DNA damage

62
Q

p53 process

A

inc p53, inc transc of p21- inh cyclin CDK- prevent P of Rb- cant enter S phase, inc p53= inc transc of DNA repair enzymes

63
Q

p53 if dna repaired or nah

A

repair: induce own downreg through act of mdm2 gene, not repaired: act genes for apop including bax and insulinlike growth factor binding protein 3

64
Q

Ras

A

involved in signal transduction for many hormones and growth factors, oncogenic, bind NF1 to Ras- act GTPase domain of Ras- hyro GTP to GDP- inact Ras

65
Q

Patched and Smoothened

A

hedgehod class of signaling peptides, patched inhib smoo, binding of HH to pat (tumor suppressor) releases inhib of smoo- act smoo (protooncogene)

66
Q

Cadherin family of glycoproteins

A

mediates Ca dependent cell cell adhesion, anchored intracellulary by catenins, which bind actin filaments, loss of E cadherin exp- cancer cells to detach and migrate in metastisis

67
Q

Apop external vs internal signaling ex

A

Ex: tumor necrosis factor, deprivation of growth hormone,
In: dec mito integrity, irreparably damaged DNA

68
Q

Phases of apop

A

initiation, signal integration, excecution- carried out by proteolytic enzymes called capases

69
Q

Capases general

A

cysteine proteases that cleave peptide bond next to an aspartate- activated from procapases to capases by proteolytic cleavage

70
Q

Initiator capase vs execution capase

A

In: cleave other procapases, induced by death receptor pathway and mito integrity pathway
Ex: cleave other cellular proteins involved in maintaining cellular integrity

71
Q

formed elements of blood

A

rbc, wbc, platelets (hematocrit concentration of formed elements in blood 40%)

72
Q

blood plasma vs serum

A

plas: water, plasma proteins, ser: fluid portion of blood leftover after clot forms (plasma)

73
Q

albumin

A

imp in maintaining blood and interstitatial fluid VL

74
Q

globulins

A

a and b globulins - arise from liver and transport sustances

75
Q

y globulins

A

arise from plasma cells and include anitbodies

76
Q

clotting proteins

A

made by liver, involved in clot formation- prothrombin, fibrinogen

77
Q

complement proteins

A

initiate inflammation and destruction of foreign microorganisms

78
Q

plasma lipoproteins

A

chylomicrons, VLDL, LDL

79
Q

chylomicrons

A

transport triglycerides to liver

80
Q

VLDL

A

transport triglycerides from liver to body cells

81
Q

LDL

A

transport chol from liver to body

82
Q

hematopoiesis

A

development of blood cells

83
Q

diapedesis

A

process by which WBC leave BV

84
Q

WBC categories

A

granulocytes, agranulocytes

85
Q

granulocytes

A

specific granules (specific fx) and azurophilic granules (lysosomes) in cytoplasm

86
Q

agranulocytes

A

no azurophilic granules, have specific granules

87
Q

neutrophils

A

granulocyte, nucleus arranged in 3 lobes, combating bacterial infection

88
Q

eosinophils

A

granulocytes, kills parasitic worms

89
Q

basophils

A

granulocytes, lobed nucleus-hidden, immune response

90
Q

lymphocyte types

A

t cells, b cells, null cells

91
Q

t cells

A

lymphocytes, cellular immune response- rejecting of transplanted organ

92
Q

b cells

A

lymphocyte, humoral immune response-production of AB due to antigen

93
Q

null cells

A

lymphocyte, circulating stem cells and natural killer cells- kill virus infected cells

94
Q

monocytes

A

kidney shaped nuc, macrophages in connective tissue

95
Q

megakaryocytes

A

present in boine marrow, appear to be multinucleated- only large lobed nuc

96
Q

death receptor pathway 2 apop

A

trimer formed by Fas/CD95, TNF R1 and death receptor 3 bind to TNF 1- TNF receptor complex forms the scaffold for binding 2 molecules of procapase 8 (or 10)-cleave to form active capase 8/10- initiator capase activate execution cap 3, 6, 7

97
Q

capase 3

A

also cleaves Bcl 2 protein, Bid- act mitochondrial integrity pathway to apop

98
Q

mitochondrial integrity pathway to apop

A

release of cytochrome c from mito (no ETC)- bind Apaf in cyto- Apaf/cyto c binds capase 9 (initiator capase)- activate apoptosome - act cap 3,6,7

99
Q

Bcl 2 family

A

integrate pro death and anti death signals, antiapop factors- all 4 domains (BH1-BH4), proapop- 3 domains (BH1-BH3), proapop BH3

100
Q

antiapop Bcl 2 type proteins

A

Bcl 2, Bcl L, Bcl w- insert into outer mito memb- antagonize channel forming proapop factors- dec cytochrom c release, can also bind cyto Apaf- cant for apoptosome complex

101
Q

proapop Bcl 2 families

A

ion channel forming members, BH3 only members

102
Q

pro death, ion channel forming members

A

(Bcl 2) Bax, dimerize with proapop BH3- only memb in outer mito matrix- form ion channel that promotes cyto c release

103
Q

pro death, BH3 only members

A

(Bim and Bid) bind to other Bcl 2 family members, form channel, bind Apaf, inactivate antiapop members

104
Q

cancer signaling pathways that inhibit apop

A

PDGF/Akt/BAD pathways

105
Q

BAD/Akt pathway

A

non phos BAD acts like Bid. binding of growth factor to receptor activates P13K- P and act. serive threonine kinase AKT- act AKT- P/inh of prop apop BH3 only protein BAD- stop apop

106
Q

BAD/RSK pathway

A

MAP kinase kinase P/act another protein kinase, RSK- P/inh BAD - no apop

107
Q

centromere

A

sister chromatids are held together physically here, region of DNA associates w/ proteins to create kinetochore

108
Q

prophase

A

gradual condensation of chromosomes, formation of mitotic spindles, formation of a pair of centromeres

109
Q

prometaphase

A

nuclear memb dissolves, chorom attach kinetochores to MT of mitotic spindles

110
Q

metaphase

A

equatorial plate

111
Q

anaphase

A

chromosomes seperate at centromere

112
Q

telophase

A

chromo begin to decondense, nuclear memb begins to reform

113
Q

spermatogenesus

A

seminiferous tubules of testes- lines with spermatogenia (develop from primordial germ cells)

114
Q

sperm

A

found only after sexual maturity is reached

115
Q

primary spermatocyte

A

diploid germ cell that undergoes meiosis I to form 2 haploid secondary spermatocytes - enter meiosis II making 2 spermatids - differentiate into sperm

116
Q

oogenesis

A

begin during development as a fetus, ova develop from oogonia cell in ovarian cortex that have decended from the primordial germ cells by a series of 20 mitoses

117
Q

before ovulation

A

oocyte rapidly completes meiosis I- one oocyte becomes a secondary oocytes, other becomes a polar body- meiosis II begins to metphase - halts, only completed after fertilizaiton

118
Q

fertilization

A

completion of metaphase II- formation of second polar body, chromo of fertilized sperm/egg form pronuclei

119
Q

most common mutational mechanism

A

meitoic nondisjunction, primarily in oogenesis

MCM Final (4 decks)

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