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Flashcards in extra info from Review Sessions Deck (187):
1

what do CDC6 and CDT1 do?

both essential for DNA replication and formation of pre-RC. they act as vehicles to assemble the pre-rc. Once loaded, you can assembly primase, helicase, etc..

cdc6 - loads MCM (helicase) proteins onto the DNA. regulates cell cycle checkpoints. activity regulated by cyclinA

cdt1 - knockouts for cdt1 are lethal - cells undergo mitosis but not dna replciation

2

what enzymes are needed to unite the lagging strand?

Fen-1, DNA pol delta, ligase

3

error in helicase?

meier-garlin

4

error in clamp loader (r-27)

autoimmune disease, chronic inflammation, cancer

5

why does replicative DNA poly have high fidelity

it's 3-5 exonuclease activity

enzyme has low kM for strand when mismatch occurs. it slows down rate that DNA unravels, allows the mismatch to be sequestered far away and be repaired

6

what encourages tight binding of DNA polymerase?

the narrow channel. More error prone DNA polymerases have larger crevice

7

describe nucleotide pool imbalance

as a result of accumulation of a particular nucleotide, a mistake if quickly skipped over because of the annealing of high concentration nucleotides occurs so quickly

8

what can stall the fork?

anything that gets in the way
centromeres - lots of protein
telomeres - lots of capping proteins
dna lesions or bulky adducts

9

premature activation/misregulation of the pre-RC can lead to

nucleotide pool stress

10

environmental factors that can mess up replication

sunlight casuing DNA damage (TT dimers)

massive amounts of damage - cell undergoes apoptosis. triggered by ATM stimulating p53 via the DDR

11

describe the error prone response

trasnlesion DNA polymerase uses non-template double strand.

when you have massive damage, sometimes you can't repair it. translesion polymerases skip the damage by including any random nucleotide. If it can keep the replication fork from moving without being stalled, that is one way to deal with massive DNA damage

12

repetitive elements can cause..

loops out of DNA sequences. another type of error in DNA replication.

-Error that occurs when Polymerase slips

once the stable hairpin structure forms, it becomes an impediemnt to replication

13

errors in XPA-G? what pathway?

errors in the NER pathway. Xeroderma pigmentosum

14

what is the common set of steps of repairing DNA damage

1. damage recognition by an enzyme specific to that damage type
2. enzyme will remove damage (just base, entire nucleotide, large segment) and leave a gap
3. DNA poly syntehsizes DNA to fill in
4. Ligase ligates

15

what causes HNPCC?

mismatch repair errors

16

what causes aicardi gouteries?

error in RER Excision repair, RNAse

17

in BER, the lesion is removed by?

DNA glycosylase = cuts sugar/ cuts base/ cuts bond between sugar and base, cuts glyosidic bond

18

In NER, gap is filled by?

DNA polymerase. Dna poly does make the phosphodiester bond with previous nucleotide, but need ligase for next one to seal

19

what is the biochemical mechanism that can be used to regulate actin assembly into microfilaments?

energy output and input involved. By using ATP as energy, can control rates of assembly.

fast growing end can do work through the assembly process

20

fillapodia

fast gorwing ends towards the membrane

21

stress fibers

bundles where each + end is against membrane. in middle you get overlapping - filaments

22

lammelapodia

broad edge of cell being pushed out. You have branched filaments. ART binds to ends to existing filaments and creatse a place to nucleate and assemble

23

contractile ring

similar to stress fibers - lots of filaments go around cell and overlap with each other. Can have myosin between filaments pulling them, involved in cytokinesis.

24

myosin I

Myosin 1- monomeric, standalone vesicular motor. Sngle ATP binding site. Tail associates with membrane, does not have long tail, has short tail. Vesicular transport if free, or binding of mysoin to plasma membrane to move the filaments relative to the PM.

25

myosin II

where in non-muscle?


Myson I I - contracile arrays. In muscle and non muscle.
-where in non muscle? Epithelial sheet that has to change shape during a process.
-bipolar arrays cause contraction

26

assembly of microtubules is...

rate limiting step?

more complicated than filaments, Uses GTP not ATP.

the slow GTPase activity of bound subunits

27

meier garlin syndrome

helicase error

28

clamp loader mutation

autoimmune, chronic inflammation, cancer

29

mechanism that controls DNA replication to once oer cycle

cyclinA/CDK kinase - degrade CDC6 and CDt1 by phosphorylation and removing

30

microfilaments can form

microvilli
filipodium/lammelapodium - fast growing ends push membrane out

stress fibers - each + end against membrane, overlapping filaments in center to get contraction

lamellapodium - broad edge fo cell fushed out, branched filaments, actin related protein (ART) binds to ends, allows nucleation.

contractile ring - lots of filaments go around cell and overlap. can have myson between filaments pulling, involved in cytokinesis

31

extending nerve terminus

assembly of actin. get actin subunits to the end, vesciles get transportered to end and "hop off"

32

secretory and actin

vesicles get close to membrane, actin filamnets bring them up to membrane, allow secretion

33

mysosin walking across actin filaments

same cycle of ATP bidning, myosin release, ATP hydrolysis, change in confirmation, reattatch, release energy and pull along filament

34

how is mysoin regulated?

depends where you are

in skeletal/cardiac muscle - directly involves calcium assocation with proteins on thin filament

or phosphorylation of proteins associated with myosin like chains

35

general contraction/relaxation cycle

Thin filament (actin), mysoin tries to move toward plus ends at Z disk, trying to move in 2 direction at once. The contractile unit (Sarcomere) shortens. This happens when calcium bins to the proteins on actin filaments, moving the tropomysin out of way so myosin can interact with actin. Regulated through sequestration of CA in membrane vesicles of SR that get released and pumped back in.

36

intermediate filaments

family of proteins that provide structural support, NOT tracks for motility

keratins, vimentin/related, neurofilaments, nuclear lamins (all cells)

37

microtubules vs microfilaments

microtubules - hollow, more complicated assembly, uses GTP and slow GTPase of beta subunits

microfilaments - use ATP and actin

38

microtubules involved in

nucleic and cell division, organization of intracellular structure, and intracellular transport, as well as ciliary and flagellar motility

39

where are microtubules found in cells?

nucleating sites (where - are togheter and cant assemble) associated with gamma tubulin rings to rapid assembly

40

what moves along microtubules?

membrane associated things

ER and golgi comparments move to different parts of cell

Dynein - pulls things closer to centrosome (-). keeps golgi next to nucleus. nuclear membrane and golgi have dynein associated

ER - spreads throughout microtubule network using kinesin

41

motile vs non motile cilia

motile - have dyneins

non-motile - lots of sensory receptors on membrane, no dynein

42

primary places where you see defects with cilia?

not having receptors on non motil cilia - causes polycistic kidney disease where the kidney cilia dont assemble or receptors are mutated

43

ramachandran plot

glycine?

certain regions are compatible with secondary structures due to bonding angles


glycine has large area in plot suggsting flexibility

44

can the C-N bond rotate?

no, all four atoms connected are in a plane and rotate together, C-N bond has partial double bond character

45

Phi Angle?

PSi angle?

Phi - Con

Psi - CC

46

phi and psi in beta sheets?

alpha helicies?

beta sheets - close to 180

minus 60 - alpha helix

47

if NH3+? pH must be..

if histidine is protonated?

if carboxyl is deprotonated?

below 8

must be below 6.5

must be above 4

48

Alpha-1-antitrypsin

serine protease, example of disease cuased by protein misfolding

leading to aggregation or loss of function

49

Correct function of alpha1-antitrysin

reactive center loop where neutrophil elastasce likes to cleave (cheese in mousetrap).

Bites the loop, forms covalent bond to loop. Loop cleaves and now inserts into central beta sheet (it is complementary)

-Loop drags neutrophil elastase down to lower section of alpha-1-at, and the interaction cuases neutorphil elastase to misfold

-other proteases now degrade neutrophil elastase

50

what can do wrong with alpha-1-antitrypsin?

2 things

-suggested by lock of similar antithrombin enzyme


when reactive loop inserted into beta sheet, it sprung all by itself (more stable, cant go back). Can no longer inhibit. Happens too much due to mutation - can no longer inhibit neutrophil elastase

second thing that can go wrong - insertion happens without cleavage, it mis inserts into neighboring molecule. Abundant in liver, causes a cascade of polymerization that builds up in liver

51

alpha helix amino acids

helix formers - mainly alanine, but also arginine and leucine

52

if the N-terminal is in the internal lumen of the ER...

, then when it is sent to the plasma membrane, the N-term will be on the external face.

53

Biosynthesis of glycosaminoglycan chains on proteoglycans occurs primarily in

golgi

54

When a protein destined for the plasma membrane is synthesized, it is inserted into the ER membrane with its extracellular domain on

the lumenal side of the ER membrane.

to be facing out of the cell, must be facing inside of the ER

55

lyosome, endosome, peroxisome

lyososome - degradation/recycling

endosome - sorting from endocytosis

peroxisomes - creates h202

56

2 organelles that do not communicate with other organelles via vesicles

mitochondria and peroxisomes are not a part of the vesicular trafficking pathways

57

when LDL receptor iis synthesized in the ER..

the LDL binding domain faces the ER lumin, but will face the cytosol once it reaches the PM

the adaptin domain starts off facing the cyotosol, will end up pointing inward

When we put proteins into the ER, we put them in the same way in correct orientation every time. Something that needs to face outward and inward
-something initially faces lumen then faces outside

58

mitochondrial receptor VS ER receptor

the receptor for the mito signal sequence is on the mito membrane

the receptor for the ER directing signal is in the lumen (Soluble)

59

scanning EM of golgi vs rough ER

rough ER will have visible studded ribosomes

60

golgi Vs SMOOTH ER?

golgi- tight pancake stack

61

lysosome scanning image

very dark, black

62

peroxisome scan

uniform gray, smooth, very dark spot in center (Crystallization of enzymes)

63

Phospholipids and Sphingolipids

Phospholipid
ex) phosphoglyeride - 2 fa, glycerol backbone, phosphate alcohol head

Sphingolipid
ex) Glycolipid- sphingosine backbone/fa, carbohydrate

shingomyelin -is a sphingolipid and a phospholipid (sphingosine, fatty, acid, phosphate choline

64

mito genome is in the

mito matrix

65

proteins required for Mito genome (RNA poly, DNA poly) come from the...encoded where?

cytosol, in the nucleus

transcribed in nucleus, translated in cytosol, transported into mitochondria

66

x-linked adenoleukodystrophy

cant import long fatty acids, beta oxidation doesnt occur, they accumulate

67

familial hypercholesterolemia

LDL can't get taken up by endocytosis. LDL receptor suffers a loss of function mutation, accumulated in blood

68

where are the ABO antigens synthesized?

in golgi

69

3 functions of golgi

n-linked sugars modified

o-linked sugars added to proteins and lipids

GAGS built on proteoglycan core proteins

ABO blood group antigens

degrade glycoproteins and proteoglycans

70

mucopolysaccharidoses

-defects in the degradtion of GAGS

71

oligosaccharidosis

defend in degredation of oligosaccharides

72

sphingolipidosis

defects in degredation of sphingolipids

73

inclusion-cell disease

defect in generating M6P tag on lyososomal enzymes. lysosomes fill with substrate with nothing to degrade them. the enzymes are sent throguh default pathway which is harmless because they only act at low pH

74

why don't the proteases in lysosomes self digest the other enzymes?

the other enzymes are protected by sugars, proteins are heavily glycosylated

75

all nuclear pores are ______, what determines the direction taken?

equivalent, direction is based on the carrier intermediate

76

there are vanishing amounts of GTP in the

cytoplasm

77

Role of Ran GTPase?

provides energy for transport in form of energy stored as chemical gradient

helps form export compleex and accompanies these complexes out of nucleus

78

homologous recombination mixes up...

parent and grandparent alleles by exhanging arms of chromosomes

79

we all inheret ______ loss of function alleles

250-300

80

half of our genome are ________

transposable element sequences

81

retrotranspons

in humans, move via RNA intermediate with RNA reverse transcriptase

82

retrotranspons and exon shuffling

Rretrotranspons have unique transposon ends. The enzymes recongize these tranposable ends. Make RNA out of this, reverse transcriptase can recognize the other two, and move entire
Normally the RT would transcribe and transport the small pink, instead it mistakenly cuts out and tranports the larger green gene between the two similar transposons

-this can cause misalignment

83

creation of unequal gene families by crossing over

an entire gene can get duplicated, or the same thing can occur WITHIN a gene causing a single exon duplication or deletion

84

multiplex PCR

many PCR in single tube, get multiple products. You've got 9 reactions at same time, done diagnostically, how you look for deletions in dystropin

85

RT-PCR

You can PCR and amplify when template is RNA - use RT enzyme to do first early rounds to turn RNA into DNA, then it’s a normal PCR. It’s a PCR where the first round is

86

Microarrays

lung cancer example but lots of things. Different kinds of tumors in cancers, how they might respond to different chemo treatments. Microarrays give you a readout of all the genes being expressed in that tumor. Gives you a very detailed view of what that cell is doing and how its doing it. Much more so then under a microscope (Stain, shape) very high res.
-tells subtype of cancer
-what mutations might be present
-what pathways elevated - will tell you what chemo will or wont work

87

FISH vs Microarray

fish - looking at whole chromosome, you see large changes in chrosomomes. Cancer cell karyotype. Shows approximate lesions of chromosome and how its been moved

typical microarray - analyzes mrna to determine expression (what and how much) of a gene. Tells more than fish, lets you get to see exactly where translocation is

88

spirochetes under a microscope can appear

either spiral or invisible (pallidum). need darkfield

89

What do we do antibiotics resistance testing on?

the enterobacteriaecae - they are so abx resistant due to horizontal gene transfers that we need to do agar plate + abx disks

90

what would a culture of rickettsia on agar look like?

rickettsia is intracellular, plane of agar would be blank. must culture in tissue

91

we do not do antibiotic resistance testing on...

environmental microbes, such as clostridium

92

to establish intracellular infection (4)

need type 3SS - important for host cell takeover/living inside of them

93

why don't we use the TB vaccine (bcg)?

our incidence of TB is low, and we primarily screen people as necessary with PPD. Giving people the vaccine would cause all PPD to come back positive, new way to screen would require chest xray

94

Childhood infection due to bacteriophage, has been declining ever since

scarlet fever

95

N.meningitidis

gram negative diplococcus that oxidizes maltose and has a a capsule

96

N.Gonorrhea

gram - diplococcus that does not oxidize maltose, has pili

97

most common disinfectant used for living tissue?

alcohol, is also a crossover agent used for countertops/objects

98

quaternary ammonium compounds

most common use of sterilization and disinfecting and detergent in hospital of surfaces. Quats have residual activity even after wiped off.

99

Augmentin, ceft, vancomycin all...

inhibit peptidoglycan synthesis

the beta lactams act as PBP substrate analog

vancomycin (glycoproteins) - bind to the terminal d-ala strands to block PBP

100

penicillinase/beta lactamase resistant penicillins

used against organisms that product beta lactamase

101

MRSA

has found a way to become resistant to all beta lactams and beta lactamse inhibitors

MRSA changed its PBP2 to PBP2a

102

cephalosporin generations

move up food chain, become more and more resistant to beta lactamase

103

carbepenams

the most powerful beta lactams, resistant to ALL beta lactamases, sensitive to carbepenemases

104

CRE

carbepenam resistant enterobacteriaca - stared off as just kleb, produces carbepenamases

105

why might a patient not respond to cephalosprin treatment?

the organism is producing beta lactamase to "break the floor of the garage"

106

treatment of simple betalactamases expressing organisms?

can use antibiotic + b lactam inhibitor (augmentin_

107

treatment of sophisticated beta lactamase expressing organisms?

produced by the ESBLS, can no longer use 3rd and 4th gen cephalosporins. use carbepenam

108

CRE's are ____

plasma encoded superbugs. plasmids contain genes for all mechanisms of resistance. we only have colistin left

109

treatment of CRE's?

colistin

110

most common immunodeficiency?

lack of IgA - get more colds and gi infections

111

why doesnt cholera have a high infant death rate?

IgA are present in breast milk

112

why is IL1B in a prophase?

so it is already made, and can quickly be cleaved by the inflammasome to be realeased to begin inflammation

113

enzyme for immunoglobulin class witching and somatic hypermutation?

AID

114

RAG1 and RAG 2 are needed to

recombine the b cell chain DNA

115

TDT

adds n-regions during splicing to give random diversity

116

N regions exist primarily in

heavy chains, leading to more diversity

117

someone without TDT

has antibody and t-cell receptors, but doesnt make as high affinity antibody because they dont have the same amount of diversity to start with

118

_______ is never present in T-CElls

AID

119

what stimulates AID in b-cells?

t-cells

120

t-independant antigen wil not

class switch or do hypermutation

121

western blot and elisa both show....

difference?

how much antigen there is

western blot takes longer and limits how much can be run at once

Western blot does let us know the molecular weight of the antigen

122

advantage of western blot?

lets us know molecular weigth of the antigen

-sometimes there is a mixture of things that are reactive, but we want to know the particular protein that is causing the reaction

123

_____ provides better info about size

______ is much more quantitative

western blot - size

elisa - quantitiative, shows amount

124

which can tell concentration of antibody, western of elisa?

both can, simply titrate until you don't have reaction anymore

125

Fc receptor on macrophage binds the

IgG constant region

126

what is an allergen?

an antigen that binds IgE

127

epitope

part of antigen that single monoclonal antibody binds to

128

the is no Fc receptor for...

IgM

129

complement can enhance phagocytosis due to

prescence of receptors for c3b on macrophages and neutrophils

130

____ is the main target of major complement receptors

c3b, used to opsonize a target to be cleared out of the body

131

b-cell differentiation timeline

heavy chain, then light chain. Heavy chain gets made first and each chromsome gets only one chance to rearrange its VDJ successfully.

Light chains get multiple cahnces to rearrange their DJ regions.

132

hapten experiment

carrier coated with hapens

t-cells respond to carrier
b-cells respond to hapten and carrier

switching the carrier - no secondary response by the B cells against the hapten

-B cells and T-cells need to be on the same page to have a secondary response

133

toxoids are similar to hapten molecules. TF

True

134

we get less crossreactivity with a monoclonal because

this is a laboratory artifact, we screen for crossreactives and they are not used

135

mito matrix contains

mito genome, beta-oxidation enzymes, TCA cycle enzymes

136

mito inner membrane contains

components of oxidative phosphorylation, ETC proteins

137

mito outer membrane contains

porin molecules

138

intermembrane space contains

cytochrome c - important for cell death signaling

139

all bacteria have...

internal plasma membrane

140

describe exotoxins

polypeptides secreted from pathogen or injected into host cell via t3ss

-superantigenicity
-actin depolarization
-interference with signal transduction

141

unknown anaerobes can be identified by

gram stain, biochemical tests, gas chromatography analysis of waste products

142

major pathogenic anaerobes

Clostridium, GNAB, and actinomyces

Gnab are gram -
clostridum and actinomyces are gram +

GNAB, actinomyces, and C.diff are normal flora

remainer of clostridum are soil organsism (tetani, botulinum) that depend on spore forming ability

143

anaerobic virulence depends on

exotoxin expression and tissue degrading enzymes to create abscesses

144

metabolism of staph?

facultative anaerobes - wall themselves off

145

treatment of anearobic infections?

antibiotics against the bacteria, antitoxin against the toxin, and wound draining/debridement

146

spirochetal trasmission

sexual, vector, environmental

147

common spirochete themes

cross into bloodstream quickly/easily

virulence primarily due to immune evasion (not antigenic but also immunomodule the host) - no vaccines

diagnosis challening - treponema are too small to see, cause various odd symptoms. Lyme tests are difficult

treatment easy

often get herx reaction

148

vaccines against spirochetes effective?

no vaccine, spirochetes are not immunogenic enough

149

syphilis

3 stages
painless chancre to variable rash/flu

to either early or late latency

to dangerous cardiac or CNS involvment. "Gummas"

150

lyme stages

early localized - rash
early disseminated - meningitis, facial paralysis, rashes, cardiac symtpoms

late disseminated - arthritis, encephalitis

151

treatment of lyme

doxycycline

152

appearance of vibrios

reservoir?

curved, gram - rods.

ocean dwelling, infected humans, halophiles (thrive in high salt concentrations)

153

most vibrios can cause

fecal oral gastroenteris primarily

may infect wounds exposed to ocean water

H.pylori causes peptic ulcurs

154

v.cholera

complex planktonic lifecyle outside of human host

pathogenic strains have O1 antigenic marker of colonization by lyosgenic phage that carries virulence factors

trasmission is fecal oral, usually killed in stomach via acid

155

virulence of v.cholera

encoded by lysogenic phage (has O1 marker)

-secretes mucinase to attatch/colonize intestine

-secretes choleragen - AB enterotoxin that interferes with signal transduction = massive watery diarreah

156

treatment of v.cholera

antibiotics may not be necessary, self limiting in otherwise healthy host

provide hydration and electrolytes

157

intracellular bacteria may be facultative-

facultative - enter has part of life cycle, can replicate outside on agar
-neisseria, enterics, mycobacter, bacilli, legionalla

or obligate, must be grown on tissue
-rickettsial, chlamydia

158

how do they get around?

pathogens use infected macrophages for transport around body, avoid humoral

159

treatment of intracellular bacteria?

tetracyclines except pregnant

160

Reactive arthritis may be caused by

chlamidia, shigella, or eneterohemmogenic e.coli

161

listeria

causes gentroententeritis, escapes endosome after endocytosis and uses actin based motility to spread between cells (ActA)

162

chlamyida

use t3ss to enter and create paranuclear inclusion body for the larger reticulate bodies to multiple in

163

enterobacteriaca

two groups

foodborne - shigella, e.coli, salmnella, yersinia

oppotunistic ICU bugs - kleb, enterobacter, proteus, providencia, serrata, morganella

164

describe the testing results of enterbacteraicace

gram -, non spore forming, straight rods, facultative anaerobes

catalase +, oxidase -, glucose fermenters

165

problem with the enterobacteriaceae

promiscuous with DNA, extreme abx resisitance is common. must do sensitivity testing

166

virulence factors of enterbacteriaceae?

pili for attatchment, t3ss for injecting enterotoxins and subverting gut macrophage.

allow themselves to be sampled by M-cells in peyers patches

167

Y.enterocolicita and macrophages

use subverted macrophages as trojan horse to local lyph nodes (false apendicitis)

168

s.typhi

system wide entry using macrophages

169

HUS

hemolytic uremic syndrome - pediatric complication caused by release of shiga toxin into bloodstream by either shigella or eneterhemmogenic e.coli

170

patients with human antigen b27 infected with enterobacteriaceae

may develope reactive arthritis (conjunctivitis, urethritis, and arthritis) after infection from Shigella, salmonella, yersinia, campylobacter, or chalomydia

171

the 6 ICU bugs

defense?

kleb, enterobacter, morganella, proteus, serratus, providencia

frequent catheter change and patient scrubdowns
-

172

growth rate of M.tuberculosis

slow, difficult to culture and defeats some antibiotics

173

gram stain of M.Tuberculosis?

poorly due to mycolic cell wall

174

spread of M.Tuberculosis

inhalation of infectious particles, spreads to lymph nodes, long bones, kindney, and CNS by hematogenous spread (trojan horse macrophages)

175

immunocompetent reaction to TB?

creates strong CMI, can hold latent

176

cd8 cells respond to tb by

killing infected macrophages and forming granulomas to wall off infection

177

classic TB

cough, weight loss, fever, bright pink chains of rods in sputum

178

extrapulmonary TB

ussually reactivations - scrofulas, genitourinary, CNA, skeletal

179

in pediatrics, TB can cause

miliary and meningitis

180

main treatment of TB

4 drug coctail with isoniazid, 2 week isolation

181

aytipical mycobacteria?

infection symptoms?

environmentally acquired, don't cause TB or leprosy

ussually cutaneous - scrofulas.
in compromised - may mimic TB, especially M.Kansasii

182

two forms of leprosy

treatmetn?

tuberculoid - strong cmi that causes nerve damage, paucibacillary, ppd +

leproid - weak CMI, causes extreme cutaneous damage, multibaccilarry, PPD -


2 years dapsone/rifampin

183

TF can be a...

an activator, repressor, or recuitor of chromatin modifier

184

what can result from enhancer translocation?

t-cell acute lymphocytic ademia - make tons of T-cells, way more than needed

185

Transcription factors use different motifs to..

contact DNA and provide specificity

typically have an alpha helix that inserts into major groove. multiple contacts gives specificity, does not need to unwind DNA helix

186

Transcription factors stimulate the general transcription machinery via a

mediator
-bridges RNA pol activators to RNA pol II and general factors

-required for transcription activation

187

what do chromatin modifiers do?

adds covalent modifications to histone N-terminal tails

acetylation - activation
deacteylation - deactivation
methylation - activation or repression
phsophorlyation - coupold to acetylation

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