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MCM Final > Correlation Boxs > Flashcards

Correlation Boxs Flashcards

1
Q

Describe the process of making insulin out of preproinsulin

A

B cells produce preproinsulin (104 AAs)
20-residue signal peptide is cleaved in ER lumen to produce proinsulin
Proinsulin passes through Golgi into B granules where it’s cleaved twice to release 33-residue C peptide leaving behind mature insulin which contains two peptides linked by two disulfide linkages

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2
Q

What cofactor is required for mature insulin storage? Where is it stored?

A

stored in B granules as a Zn-bound hexameter until secretion from pancreas

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3
Q

What is an useful assay for the assessment of pancreatic B-cell function? What else are these assays useful for?

A

C peptide
distinguishing between hypoglycemic disorders due to islet cell tumors (overproduction of insulin) and the infusion of exogenous insulin (facetious hypoglycemia)

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4
Q

What are some intracellular post translational modifications that can occur on the lysines and prolines of pro collagen? What about extracellular?

A

Intracellular
Lysines- generate 5-hydroxylysines some of which are glycosylated with galactose and glucose
Pralines- hydroxylated to produce 4-hydroxy- and 3-hydroxyprolines
Extracellular
Lysines- lysine and hydroxylysines can be oxidatively deaminated to aldehydic residues

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5
Q

Why are post-translational modifications of lysine and proline by hydroxylases in procollagen so crucial?

A

they are essential to proper assembly and cross-linking of collagen helices

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6
Q

How do nucleoside analog inhibitors work

A

Nucleoside analogues that lack the 3’-OH group that the DNA polymerase requires

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7
Q

What step must be completed before nucleotide analog inhibitors can work?

A

they must be converted to dNTPs

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8
Q

What are the three different nucleotide inhibitors and what do they treat?

A

ara-C (cytarabine): leukemia
acyclovir: viral infections
AZT: HIV

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9
Q

What does a mutation in MSHS or MLH1 result in?

A

NOTHING! You need a mutation in second copy

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10
Q

What does an acquired mutation in MSHS or MLH1 in already susceptible to hereditary nonpolyposis colorectal cancers result in?

A

MER system is nonfunctional and tumor develops

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11
Q

Why are people with xeroderma pigmentosum sensitive to direct sunlight?

A

UV component of sunlight causes cyclobutane thymine dimers to form in their DNA
their NER complex doesn’t work so it can’t repair it

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12
Q

glucagon, epinephrine, cortisol and insulin all affect the blood glucose pathways by what type of signaling mechanism?

A

endocrine

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13
Q

Mutations in what two genes result in Cockayne Syndrome? What are these resulting proteins involved in in normal individuals?

A

ERCC-6 and ERCC-8

Involved in transcription coupled repair

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14
Q

explain the symptoms of cholera and how it relates to GPCRs

A

cholera causes the infected person to die due to excess water loss
cholera ADP-ribosylates the Gαs, decreasing its inherent GTPase activity and causing it to remain in the GTP-bound active state. Also ADP ribosylates the Gαi, inhibiting it. This causes chloride ion channels to remain open and water to be lost

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15
Q

Signals from hydrophilic molecules act at the surface of the cell to often do what? What kind of receptors can these molecules bind?

A

control transcription factors to regulate gene expression

GPCRS, receptor tyrosine kinases

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16
Q

explain why lipophilic signal molecules in drug form can be taken daily while other hydrophilic signal molecule drugs must be taken within minutes of when they are needed

A

lipophilic drugs that have longer half lives can be taken daily
hydrophilic drugs with shorter half lives do not hang around in the blood as long and must be taken when needed. for example, epinephrine in auto-injectors

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17
Q

explain the symptoms of cholera and how it relates to GPCRs

A

cholera causes the infected person to die due to excess water loss
cholera ADP-ribosylates the Gαs, causing it to remain in the GTP-bound active state, causing chloride ion channels to remain open and water to be lost

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18
Q 
what is the name of the class of enzymes that modifies cAMPs to their non cyclic isomers?
name a few drugs that block these enzymes and explain how they achieve their desired effect
A

phosphodiesterase
boner pills
caffeine
they block phosphodiesterases (PD5 in the specific case of viagra)
and cause the build up of cAMP in the cell, prolonging the signal and causing vasodilation and boners, or in caffeines case, increased heart rate

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19
Q

1) what effect does epinephrine have on Beta-adrenergic receptors in the bronchial and intestinal smooth muscle?
2) what about in the heart?
3) how can the same hormone elicit different responses in different tissues!?

A

1) relaxation
2) contraction
3) although the same second messenger(s) are produced, physiologic pathways diverge, eliciting different downstream responses

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20
Q

what is albuterol
explain why a patient that is resistant to albuterol could be given epinephrine to achieve the same result. what would be a side effect

A

beta-agonist in the lungs; causes bronchodilation (is that a word?)
epinephrine affects the beta adrenergic receptors in the same way; also affects cardiac tissue although in opposite way so side effect would be tachycardia

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21
Q

1) what amino acid is a precursor to nitric oxide?
2) what ion promotes this transition?
3) explain how NO causes vasodilation
4) how does nitroglycerin work?

A

1) arginine
2) calcium
3) NO diffuses into neighboring cells, activates guanylate cyclase, leading to production of cGMP. cGMP activates PK-G, resulting in smooth muscle relaxation and vasodilation
4) nitroglycerin degrades into NO and causes above mechanism

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22
Q

what is the function of histamine?
how do anit-histamines work?
what amino acid is a precursor of histamine?

A

histamine binds to histamine GPCR (H1-H4) and induces sneezing, runny nose, itchy watery eyes
anti-histamines are lipophilic compounds that block the association of histamines to H1 GPCR
histidine, duh :)

23
Q

explain how Ras can be involved in a bunch of cancer

explain the function of NF-1 and how it relates to neurofibromatosis

A

overactivation of Ras due to mutation can cause Ras to remain in active state, leading to increased proliferation
NF-1 encodes a GTPase activating (GAP) protein. absence of NF-1 allows Ras to uncontrollably activate pathways that promote tissue growth

24
Q

SH2 domains recognize motifs on receptors that contain what residues

A

phosphorylated tyrosine residues

25
Q

A gene for transcription factors is mutated and leads to cancer. What do you call this type of gene?

A

oncogene

26
Q

How can misregulations of transcription factors that lead to cancer occur

A

increase in level of expression (e.g. increase in gene copy number) or by mutations in the coding sequence that alter the activity of a transcription factor (e.g. loss of a phosphorylation site that is required for the regulated shutdown of its activity)

27
Q

Why can the abnormal expansion of CG repeats in a DNA sequence lead to fragile X mental retardation?

A

expansion of CGG repeats leads to methylation of the cytosine
as methylation repeat region extends into the promoter area, transcription of FMR1 gene is turned off

28
Q

What are cells that never enter G0?

A

cells that are constantly dividing to replace cell population that are continuously lost
gut epithelium, skin, hair follicles, bone marrow

29
Q

How do you determine if someone is a mosaic? If they have a high percentage of mosaicism for trisomy in chromosome 21 how will they present?

A

chromosomal or microarray analysis

high percentage of mosaicism will present like a non mosaic form of the disease

30
Q

Prader-Willi (involves imprinting gene on the long arm of chromosome 15) is an example of what?

A

uniparental disomy

31
Q

Heterodisomy indicates what type of error

A

Meiosis I error

32
Q

Since somatic cells lack telomerase, what else are they susceptible to? How does this lead to the cell cycle being shut down?

A

telomerase protects cells from damage by promoting end cap structures
DNA damage leads to p53-mediated cell cycle arrest at G1 checkpoint

33
Q

a patient manifests a recessive disorder when only one parent is a carrier. how could this happen???

A

uniparental disomy

34
Q

What is the DNA content (in Ns) during

1) S phase
2) G2 phase
3) M phase
4) post-cytokinesis

A

1) 2n -> 4n
2) 4n
3) 4n
4) 2n

35
Q

Cardiac cells, neurons, and RBCs are examples of what type of cell class? (based on cell cycle) What is special about this class?

A

permanent cells

remain in G0 phase and thus cannot be regenerated

36
Q

What are types of stable cells and what do they require to enter G1?

A

hepatocytes, kidney tubule epithelial cells
require growth factors stimulation
allows for regeneration of damaged tissue

37
Q

What are cells that never enter G0?

A

cells that are constantly dividing to replace cell population that are continuously lost
gut epithelium, skin, hair follicles, bone marrow

38
Q

1) Ras is what type of protein?
2) how many subunits are in Ras proteins
3) mutations lead to what?
4) list some subfamilies

A

1) small G proteins (GTPase)
2) 1, monomer
3) cancer
4) ras, rab, rho, arf, ran

39
Q

1) what is the primary protein responsible for insulin resistance?
2) what are the likely upstream effectors that are ultimately leading to this protein’s malfunction?
3) how is this happening?
4) what triggers the kinase activity that leads to the insensitivity?

A

1) PKB
2) IRS-1/IRS-2
3) while tyrosine phosphorylation of IRS is necessary for recruitment of PI3K, serine/threonine phosphorylation inactivates IRSs, lead to their degradation. so multiple kinases could be responsible for this incorrect phosphorylation.
4) cytokines, free fatty acids, hyperinsulinemia

40
Q

list the active genes for transcription factors that can be used to induce adult human cells to exhibit many of the properties of embryonic stem cells

A

oct4
sox2
nanog
lin28

41
Q

1) what is the reagent used to measure indirect vs. direct bilirubin present in serum?
2) what are normal serum bilirubin values?

A

1) diazo reagent
2) adults - total bilirubin = 0.2-1.2 mg/dL and 0.1-0.3 mg/dL conjugated bilirubin
infants - 1-12mg/dL with negligible amounts of direct bilirubin

42
Q

1) congenital erythropoietic porphyria results form a deficiency in what enzyme?
2) what happens to intermediates in the pathway due to this deficiency?
3) what symptoms are a result of this diversion?

A

1) uroporphyrinogen III synthase
2) diverted to uroporphyrinogen I
3) red color in the urine, red teeth, premature destruction of erythrocytes and skin photosensitivity

43
Q

What is an example of something that ubiquinates cyclins?

A

APC/CDC20

44
Q

Where can you find activated benzopyrene? What does it cause?
What can cause the same mutation?

A

cigarette smoke
mutates genes like p53 (G->T)
aflatoxin a fungal metabolite in moldy grain and peanuts

45
Q

What causes replicative cell senescence? What enzyme would somatic cells need to have to prevent this?

A

progressive shortening of telomeres of chromosomes with each cell division
telomerase

46
Q

Since somatic cells lack telomerase, what else are they susceptible to? How does this lead to the cell cycle being shut down?

A

telomerase protects cells from damage by promoting end cap structures
DNA damage leads to p53-mediated cell cycle arrest at G1 checkpoint

47
Q

explain the changing color of bruises and how it relates to heme breakdown

A 
unoxygenated hemoglobin - blue
heme - red
biliverdin - green
bilirubin - reddish yellow
hemosiderin - reddish brown
bruise is pooling of blood, macrophage degrades hemoglobin --> heme --> biliverdin --> bilirubin --> released iron trapped as hemosiderin,
48
Q

1) what is the primary cause of neonatal jaundice?
2) explain how neonatal jaundice can affect brain
3) what are treatment options?

A

1) lack of conjugating enzyme
2) kernicturus
3)
a. phototherapy –> conversion to more soluble form
b. IM tin-mesoporphyrin (inhibitor of heme oxygenase)

49
Q

how can we treat acute intermittent porphyria?

A

hemin, blocks ALA synthase

50
Q

why was homeboy king george found to have arsenic in his hair?

A

arsenic was common in medicines that were given to the king. he was being treated for his variegate porphyria.

51
Q

What domains do adaptor proteins such as GRB2 and IRS-1 need to bind to motifs on the receptor that contain phosphorylated tyrosine residues?

A

SH2 or PTB domains

52
Q

What do small G proteins do? What are examples of small G proteins?

A

play roles in transduction of signals from plasma membrane receptors to the effect proteins such as kinases
control such diverse processes as cell proliferation, intracellular vesicular traffic, survival and apoptosis, cell shape and polarity, membrane transport and diffusion
RAS, RAB, RHO, ARF, RAN

53
Q

a mutation in VHL causes what? how?

A

adult T cell leukemia/lymphoma
it’s a tumor suppressor gene whose protein plays a role in ubiquination and degradation of the transcription factor hypoxia-inducible factor (HIF)

54
Q

v-src vs c-SRC
which one is the oncogene
which one is the proto-oncogene

A

v-src is the oncogenic form of the normal host proto-oncogene c-SRC

MCM Final (2 decks)

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