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Biochemistry > Exam 2, Foundations > Flashcards

Exam 2, Foundations Flashcards

1
Q

Type I collagen is found

A

in bone, skin, tendon, ligaments, cornea, and internal organs

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2
Q

Type II collgen is found

A

Cartilage, IV discs, eye

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3
Q

Type III collagen is found in

A

skin, blood vessels, reticular fibers

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4
Q

Type IV collagen is found in the

A

basal lamina (sheetlike instead of fibrillar)

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5
Q

Ehler’s Danlos Type IV

A

mutations in collagen Type III

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6
Q

Marfan’s syndrome

A

mutations in the fibrillin gene

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7
Q

hyaluronic acid is different in that it

A

not bound to protein and does not form a preoteoglycan

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8
Q

Fibronectin

A

connects cells to the components of the ECM and collagen

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9
Q

Laminin

A

binds to membranes of epithelial and muscle cells

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10
Q

Mast Cells bind which type of receptors?

A

IgE receptors preent on the plasma membrane

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11
Q

allergic rxns are mediated by

A

mast cells and IgE

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12
Q

Alport’s syndrome:

A

Type IV defect

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13
Q

what is the enzyme and cofactor involved in the committedstep of purine synthesis?

A

APRT and glutamine

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14
Q

Lesh nyhan syndrome comes from a defect in

A

HGPRT

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15
Q

defect in HGPRT causes? (how)

A

HGPRT decreases salvage pathway and leads to increased levels of uric acid through increased purine catabolism and gout. IT is also thought that HGPRTis important in the briain which is why it causes lesch nyhan

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16
Q

orotic aciduria is due to

A

a defect in UMP synthase, the enzyme that converts orotic acid to OMP and OMP to UMP during pyrimidine synthesis.

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17
Q

orotic aciduria is characterized by

A

macrocytic anemia and delayed physical an dintellectual development

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18
Q

treat orotic aciduria using

A

UMP because UMP will then go on to make udp and utp and CTP, and will also inhibit the action of CPSII and CAD which are involved int ehf irst step of the pyrimidine synthesis

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19
Q

Ribonucelotide reductase is used to convert

A

ribonucleic acid to deoxyribonucelic acid

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20
Q

what stimulates and inhibits the activity of RNR

A

ATP stimulates and dATP inhibits

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21
Q

ATP binding to specificity site

A

makes RNR bind UDP or CDP t make dCTP or dUTP which is rapidly converted to dTTP

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22
Q

what stimulates the production of dGDP

A

dTTP

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23
Q

What is the result of ADA (adenosine deaminase deficiency)

A

SCID

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24
Q

Explain SKID

A

when ADA is broken, dAMP builds up. B and T cells rapidly phisphorylate this dAMP to dATP which negtively regulates ribonucelotide reductase. Now RNR is inhibited and you cannot make nucelotides and cell proliferation halts

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25
Q

hydroxyurea targets

A

ribonucleotide reductase by quenching the free radical on it and cell cannot divide

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26
Q

Fluorodeoxyuracil targets

A

thymidylate synthase by trapping the enzyme

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27
Q

methotrexate inhibits

A

Dihydrofolate reductase (DHFR) which allows the reduction cascade of thimydilate synthase, which is important in the production of dTTP from dUTP. PRevents the cycing of DHF back to THF to continue the production of dntps

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28
Q

why is dTTP rapidly made from dUTP

A

because high levels of Us are mutagenic

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29
Q

what is it important to measure before treating a patient with 5-fluorouracil and why?

A

It is importnt to measure dihydropyrimidine dehydrogenase activity because defects in this enzyme reduce pyrimidine catabolism and can lead to high circulating levels fo 5-fluorouracil

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30
Q

allopurinol blocks what and is used for what

A

xanthine oxidse which converts xanthine and hypoxanthine into uric acid. It decreases the aount of uric acid and also hypoxanthine can be used in salvage to make purine, and the production of these purines can inhibit APRT and decrease purine synthesis. It is used to treat gout.

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31
Q

genetic anticipation is worse when passed on from a

A

father

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32
Q

CAg codes for

A

glutamine

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33
Q

stretches of glutamine promote

A

aggregation

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34
Q

the DNA pol I has three functions. The 3’ –>5’ exonuclease is used for

A

editing out incorrectly added nucelotides which is stimulated by mismatches

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35
Q

DNA pol I makes DNa in the

A

5’ –> 3’ direction

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36
Q

the 5’ –> 3’ exonuclease activity og DNA pol I is used to

A

remove DNA or RNA primars. It binds to sinle strand nicks and excises DNA in front and behind it. Involved in nick translation.

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37
Q

What is MGMT and why do i care about it?

A

MGMT is methyl guanine methyl transferase. Alkylation of guanine leads to a loss of a base and problems in replication. When there is alot of this, p53 is active and the cell will die. Use temozolamide to alkylate guanine and lead to activaatioj of P53 and cell death. MGMT is responsbible for converting guanine that has been alkylated back to guanine and protecting the cell. If there is alot of MGMT that is active, the cell will be resistant to remozolomide. When MGMT is methylated, MGMT is inactive. So Test to see if MGMT is methylated/ inactive and if it is, then the patient will respond to temozolomide.

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38
Q

how does telomerase work?

A

telomerase adds repeat structures TTAGGG tot he 3’ end of each strand. It creates a G rich non-coding send. When telomere level falls, cell division ceases.

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39
Q

homologous recombination is done through

A

BRCA1 and BRCA2

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40
Q

nonhomologous end joining is good or bad?

A

BAD BAD BAD

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41
Q

Why are cancers with BRCA1 and BRCA2 mutations more sensitive to radiation?

A

radiation induced double stranded DNA breaks. BRCA1 and 2 are responsbiel for ds repair, so when there are mutations the cell is not repaired and undergoes cell death

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42
Q

what in the world is base excision repair and what disease does it relate to?

A

Base excision repair is used when a guinine is exposed to ROS and forms 8-oxoguanie. The 8 oxoguanine is removed a flap is created, and when it is rich in CAG repeats, the Cs and Gs are very stbale and pair together. They are resistant to cleavage by the flap endonucelase and the repeat can be expanded.

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43
Q

What does UV light do to DNA aand what kind of DNA repair does it incite?

A

UV light induces nucelotide excision repair where bulky pyrimidine dimers formed by UV light are repaired. UV light promites the formation of thymidine dimers

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44
Q

What happens in the nucelotide excision repair pathway?

A

cut the DNA on either side of the damage

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45
Q

BAse-Hunter

A

Base excision repair = huntingotn

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46
Q

problems with nucelotide excision repair result in

A

xeroderma pigmentosa

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47
Q

the signature of a translesion synthesis is a

A

CC –> TT change in bases

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48
Q

what is mismatch repair?

A

mismatch repair is the repair machinery working at replication forks -> cuased by polymerase making mistakes

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49
Q

problems in mismach repair lead to

A

lynch syndrome, a non-polpous colon cancer

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50
Q

BRCA1 and BRCA2 are genes that

A

produce tumor supressor proteins

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51
Q

myc is a

A

proto oncogene

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52
Q

Rb is a

A

tumor supressor that when phosphorylated by G1-CDK allows E2Fto stimulate the G1/S phase

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53
Q

tumor supressor have what type of mutations

A

loss of function

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54
Q

APC targets what for degredation?

A

M-phase cyclin and securin. which negatively regulates separase, which separates sister chromatids

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55
Q

what does wee 1 do?

A

wee1 puts a negative phosphorylation onto M-cdk and preventing the initiation of mitosis. When wee1 is gone, the cells enter mitosis too eaarly and are too small.

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56
Q

what does CDC25 do

A

CDC25 takes off the inhibitory phosphate added by wee1

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57
Q

what usually keeps P53 off?

A

MDM2, which ubiquitinates it

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58
Q

what does P53 do

A

It is a tumor supressor and a TF that induces the expression of p21 and other proteins that supress the cell cycle progression by inhibiting s-cdk

59
Q

symptoms of CML

A

inability to progress along the erythroid and megakaryocyte lineage. with increased white cells.

60
Q

whats up with BCR ABL

A

ABL codes for a tyrosine kinase in cell proliferation that has a catalytic and regulatory domain. When the translocation occurs between 9 and 22 the reguaotry domain is lost.

61
Q

what do you use to treat CML

A

imatinib which binds to the tyrosine kinase activity and inhibiting it

62
Q

test for CML using

A

fish or PCR

63
Q

major molecular response is

A

10000 fold reduction in bcr abl gene

64
Q

what are acetyl groups added to and what is the effect

A

lysines. When this happens the positive charge is lost and the packing on the histone gets looser allowing for DNA –> transcription of DNA

65
Q

what are transcripts capped by on the 5’ end

A

7-methyl gunaine structure

66
Q

start codon is

A

AUG methionine

67
Q

stop codon

A

UAG, UGA , UAA

68
Q

missense

A

when a single AA is changed thus changin the codon added

69
Q

frameshift

A

reading frame shift from addition or deletion

70
Q

nonesense

A

insertion of a stop codon

71
Q

silent

A

degenerate DNA code

72
Q

cytosine methylation is associated with

A

repression of gene expression due to steric hinderance and condensing chromatin

73
Q

promoter regions are rich in GC repeats called a CG island. when these are methylated

A

gene repression

74
Q

general overview of notch signalling

A

another cell with delta on it interacts with notch, notch is cleaved and the intracellular part goes into the nucleus, displaces acetyltransferases on hstones and gene expression!

75
Q

General WNT process

A

wnt is iportant in epidermal morphogenesis. B-catenin is usaully phosphorylated and thus ubiquiniated by APC. When wnt binds, APC falls off, b catenin goes to the nucelus as a TF -> proliferation

76
Q

hedgehog signalling general process

A

when hedgehog is off, protein ci is degraded and the degraded parts go to the nucelus as a reprssor. When hedgehog is active, CI is not cleaved and gos to the nucleus as an activtor that recruits histone acetyl transferases

77
Q

epimers

A

differ at a single carbon

78
Q

alpha is when

A

C1 group is down and in trans

79
Q

beta is

A

c1 group is up or in cis

80
Q

pattern of glucose

A

down up down up

81
Q

mannose is a

A

C2 epimer f glucose because the C2 carbon is up instead of down

82
Q

galactose is a

A

c4 epimer of glucose because the C4 carbon is up instead of down

83
Q

to distinguish D-glucuronic acid from l-iduronic acid

A

If C6 is up = D

if C6 is down = L

84
Q

default pathway in protein production

A

secretion

85
Q

glycosyltation occurs

A

co-translationally

86
Q

carbohydrates are linked through n-glycosidic bonds to proteins on

A

asparagine residues: ASN-X-SER

87
Q

What holds an oligosacharride in place waiting for a signal recognition sequence for glycosylation to come through?

A

dolichol : it is attached to to phosphates and an oligosacharide and when the asn-x-ser (or thr) comes through it is tranfereed onto the protein

88
Q

mislocation of lysosomal hydrolases results in i cell disease and is the result of a missing

A

mannose-6-phosphate. Cells are defective at targeting certain enzymes to lysosomes

89
Q

what defines the complex class?

A

the prescence of sialic acid

90
Q

what is the importance of glycosylation?

A

protection from degregation and molecular recognition

91
Q

Why would a new born baby get jaundice as a result of blood type incompatibility

A

If a mother is O she will make antigens to A and B, but the baby will not make antigen to her. So, mom’s serum is destroying the baby’s blood –> jaundice

92
Q

type B vs A where B has a ____ and A has a ____

A

A has a galnac o, B has a gal

93
Q

general structure of a GAG

A

disacharride repeats made of a carbohydrate acid (glcNac or GalNac) and an amino sugar (GlcA). They are VERY negatively charged and do not have a compact folded shape

94
Q

tell me about the flu

A

the flu virus has hemaglutanin which recognizes sialic acid in the respiratory tract. It will adhere and infect. Has an enzyme called neurominidase that cleaves off the sialic acid and allowed it to fall off and ifnect a new cell.

95
Q

what does tamiflu do?

A

tamiflu looks like sialic acid, so binds to neuromididase and inhibits it. slows down the flu.

96
Q

antibiotics are molecules that target

A

ribosomes of bacteria

97
Q

hyaluronic acid is differnt becauase

A

it is not covalently attached to a protein and is the only GAG also found in bacteria. It is also unsulfated

98
Q

Mucopolysachcharidoses are a result of

A

defects in degredation of GAGs since the undegraded or partially undegraded gags accumulate in lysosomes, they fall under the title of an LSD

99
Q

Hurler disease is a defect in

A

alpha-irunidase , autosomal recessive

100
Q

process of degredation of a mucopolysacharide

A

start from the non-reducing end, if there is a sulfur, remove with a sulfurtase, cleave off the iduronic acid

101
Q

scheie and hurler scheie are when

A

you have a defect in alpha 1 iduronisdase (dermatan sulfate and iduronidase affected)

102
Q

the repeat unit in collagen is

A

gly-x-y, where x is proline and y is hydroxyprline

103
Q

the glycine in collagn is required because

A

of the small size: it allows the 3 chains to come into close contact

104
Q

the hydroxyproline/hydroxylysine is important in collagen because

A

they confer thermodynamic stability on the triple helix structure. proline –> stabalization and lysine –> crosslinking and glycosylation

105
Q

type I collagen is found in

A

bone

106
Q

type III collagen is found in

A

blood vessels and skin

107
Q

the enzymes that hydrxylate collagen on the pri and lys residues require what to function?

A

alpha ketoglutarate, o2, Fe, and VITAMIN C

108
Q

scurvy is due to a

A

deficiency in vitamin C, so you dont have the hydroxylation on your collagen and you lose your thermo stability.

109
Q

what are collagen pro pieces, when are they cleaved and why are they important

A

they are sequences found at the amino and carboxy termini and are necessary for triple helix formation and prevent the collagen from accumulating. They are cleaved off after they are secreted

110
Q

Osteogenesis impoerfecta is a problem with

A

collagen type I, which is why it can be seen in the bone.

111
Q

ehlers danlos is a problem with

A

collagen type III which is why is it seen in the skin and blood vessels. Ehler’s danlos –> aortic dissection

112
Q

type IV collagen has propieces, why are they important

A

the basal lamina that does not have its proieces cleaved after secretion. the propieces help to layer them into a network

113
Q

wnt is said to be

A

autocrine / paracrine. aka acting in the same cell of a nearby cell

114
Q

lynch syndrome

A

a defect in the APC of wnt signalling, (where wnt binds to the cell and causes b-catenin to be active and go to the nucelusleading to cell growth) lynch syndrome is a problem with the APC o beta catenin is always on.

115
Q

big takeaway from hedgehod is that

A

cells have variable thresholds for response to the secreted shh signalling

116
Q

how to know spleen or lymph node

A

lympph nodes have a sinus lumen that is not empty

117
Q

the thymus

A

has no germinal centers and is lobulated

118
Q

macrphages are dervied from

A

blood monocytes

119
Q

mast cell derives from

A

immature mast cells

120
Q

prostaglandins are released from

A

mast cells

121
Q

mast cells are commonly located along

A

blood vessels

122
Q

plasma cells differentiate from

A

lymphocytes

123
Q

tensile strength refers to

A

collagen

124
Q

intramembraneous ossification important in the

A

mandible

125
Q

osteocytes are derived from

A

osteoblasts

126
Q

vertebrae are an example of

A

endochondral ossification

127
Q

periosteal bud formation in

A

endochondral

128
Q

thymus stroma is made up of

A

epithelioreticular cells

129
Q

humoral antibody response

A

B-lymphocytes

130
Q

hungtingtons disease is on chromosome

A

4: autosomal domnant

131
Q

NF1

A

chromosome 17 autosomal dominant

132
Q

Marfan

A

autosomal dominant fibillinopathy, chromosome 15

133
Q

disease that is an example of locus heterogeneity?

A

TSC: tuberous sclerosis complex where autosomal dominant mutations on chromosomes 9 and 16 –> the same disease.
involves the CNS, eye, heart, kidney and lung

134
Q

spinal muscular atrophy is autosomal recessive disorder

A

floppy infant

135
Q

type I osteoperosis

A

post emno pausal women, most severe

136
Q

type II osteoperosis

A

elderly due to osteoblastst aht dont work

137
Q

Type III osteoperosis

A

econdary to drug therapy

138
Q

rickets due to

A

lack of vitamin D ad calcium int eh diet

139
Q

cathepsin K is a

A

lysosomal enzyme

140
Q

Appositional growth:

A

growth occurs from outside borders; chondrocytes develop from the

perichondrium

141
Q

Interstitial growth:

A

cartilage develops inside existing cartilage; happens from formation of isogenous groups

142
Q

repair occursr through

A

endochondral ossicifation

143
Q

PTH increases

A

CA in the blood

Biochemistry (3 decks)

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