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MTC > MTC Exam III part IV > Flashcards

MTC Exam III part IV Flashcards

1
Q

What three proteins are super important in worm apoptosis?

A

ced 3 and 4 are positive apoptotic regulators

ced 9 is an apoptosis repressor

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2
Q

what is the human homolog of ced3? Of ced4?

A

ced3: caspases
ced4: APAF-1 adaptor that transduces death signals

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3
Q

what is the human homolog of ced9?

A

BCL-2

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4
Q

How do BCL2 and BCL2 related proteins work?

A

some BCL2 related proteins are pro-apototic, others are anti-apoptotic
BAX, BAD and BIM promote apoptosis
BCL2 and BCLX are anti-apoptotic
they form homo and heterodimeric complexes
these families play a role in determining whether cytochrome C is released from the mitochondria. BCL2 located on mitochondrial membrane.

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5
Q

describe basic caspase structure/secretion

A

present as inactive zymogens
cleaved caspases yield a large and small subunit. they associate to form a heterodimer. 2 heterodimers must come together to make an active tetramer

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6
Q

what are the two classes of caspases and what domains do they have?

A
  1. initiators, which have DED or CARD domains (death effector domain or caspase recruitment domain)
  2. effectors: prodomains activated by cleavage by upstream caspases
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7
Q

extrinsic cell death pathway

A

Fas death receptor binds a death ligand
leads to the recruitment and activation of initiator caspases
critical for T-cell deletion, but too much Fas seen in lupis and ALPS syndromes

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8
Q

intrinsic cell death pathway

A

bax increases at the mitochondrial outer membrane
cytochrome c is released
cytochrome C complexes with APAF-1 and procaspase 9 to form an apoptosome
apoptosome causes aggregation and activation of caspase 9
caspase 9 activates caspase effectors 3 and 7

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9
Q

Hutchinson-Gilford Progeria Syndrome

A

progressive aging syndrome due to problems with progerin aka nuclear lamin A protein (LMNA gene)
usually a C to T substitution that leads to activation of a cryptic splice site and the loss of 50 aas. normally, prelamin A wopuld have a C terminal CSIM sequence attached to a farnesy group by farnesyl transferase. This allows the CSIM to be cleaved.by ZMPSTE24. Then, the C terminal is capped and ZMPSTE cleaves 15 more aas. in progeria patients, ZMPSTE can’t do the second cleavage- too much is missing.

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10
Q

progeria treatment

A

statins and bisphosphonates and farnesyl transferase inhibitors

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11
Q

What is a cancer associated fibroblast/myofibroblast?

A

help induce tumor formation and are more mobile than normal fibroblasts

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12
Q

characteristics of tumor vasculature

A

dilated, thinwalled capillaries, tortuous vessels, chaotic archetecture, fewere pericytes,fewer lymphatics

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13
Q

PDGF

A

platelet-derived growth factor

important for pericyte recruitment and vascular maturation

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14
Q

Ang1

A

mediates interactions btw endothelial cells and smooth muscle cells. not upregulated by hypoxia

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15
Q

Ang2

A

needed for vascular remodeling and blocks Ang1. often overexpressed in tumors, so tumors don’t have a stable vasculature
leads to angiongenic response when combined with VEGF

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16
Q

thrombospondin 1 (TSP1)

A

target of p53 that interferes with FGF2 and VEGF and promotes apoptosis; anti-angiogenic

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17
Q

Endostatin

A

collagen cleavage fragments that inhbit VEGF and FGF2 and endothelial motility and induces apoptosis; anti-angiogenic

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18
Q

TIMPs (tissue inhibitors of metallow proeinases

A

prevent ECM breakdown. anti-angiogenic

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19
Q

HF-1alpha

A

controlled by von hippel lindau tumor suppressor (VHL)
under hypoxic or VHL-deficient conditions, HF-1alpha dimerizes with HF1-beta and translocates to the cell nucleus
there it binds to HRE genes that increase VEGF, PDGF and TGF expression

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20
Q

VEGF

A

stimulate migration, prolif, and permeability of arterial, venous and microvascular endothelium. VEGF tends to be sequestered in ECM but is released as the ECM is remodeled.

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21
Q

What kind of receptor is VEGFR?

A

tyrosine kinase

22
Q

FGFs

A

mitogen for fibroblasts and vascular endothelial cells, modulates VEGFs

23
Q

passenger mutations vs. driver mutations

A

passengers: mutations that don’t have an impact on cancer development
drivers: mutation that is of great significance in cancer development

24
Q

adjuvant therapy vs. neoadjuvant therapy

A

adjuvant therapy: combonation of systemic and localized therapy; neoadjuvant therapy: only systemic therapy used because localized therapies aren’t possible

25
Q

gompertzian growth model

A

describes growth of most solid tumors: growth rate is highest when the tumor is smallest.

26
Q

3 critical differences in DNA repair/synthesis btw normal and cancerous cells

A
  1. translesion DNA synthesis happens in tumors: errors are ignored
  2. lots and lots of breakage-fusion-bridge cycles
  3. telomerase activity
27
Q

What is the signficance of HSP90

A

this is a chaperone that is upregualed in cancer cells because it helps with protein folding and prevents the unfolded protein response and cell death

28
Q

Warburg effect: what is it?

A

observation that tumor cells have a higher glucose utilization rate and a higher lactate production rate than normal cells (glutamine uptake is increased and lipid and nucleic acid production goes up as well)

29
Q

How does the krebs cycle change in the cancer phenotype?

A

it goes down- pyruvate tends to go to lactate more than it normally would. Also, the Krebs cycle is mostly used as a way to get carbon skeletons for anabolism. So, some pyruvate will get to acetyl coA (enzyme is pyruvate dehydrogenase), it will combine with OAA to make citrate, which will be used for fatty acid and cholesterol synthesis. Krebs cycle continues by bringing in more glutamate, which can be converted to alpha-ketogluterate.

30
Q

PIK3 pathway

A

constitutively activated in cancer phenotype. PI is phosphorylated to make PIP. PIP promotes growth thru Akt/mTOR. HIF-1 expression upregulates glucose transporters and glycolytic enzymes

31
Q

PARP-1 inhibitor

A

used for triple negative breast cancer. inhibiting PARP-1 is bad for breast cancer because it leads to too much DNA damage for the breast cancer cells to survive- example of synthetic lethality.

32
Q

direct vs. indirect gene therapy

A

direct: direct transfer of genes to pt.
indirect: remove target cells from pt, modify them, return them to pt.

33
Q

GPCR family and senses

A

G protein coupled receptor family. receptors for secondary messengers (used in light, smell, pain, and some taste). 7 TM domains

34
Q

5 tastes

A

salty, sour, bitter, sweet, umami

35
Q

Which tastes uses ino channel taste receptors? which channels?

A

Salty: use an ENaC that causes depolarization when Na is around. upregulated by aldo.
Sour: multiple channels: ENaC, K, TRPP2.

36
Q

What receptors and biochem pathways are used to taste natural sweeteners?

A

T1R receptors: T1R2 and T1R3. form heterodimers to interact with the tastant. Gs pathway is activated. We see a cAMP increase, an inhibition of K channels and gating of the CNG channel: depolarization occurs.

37
Q

What receptors and pathways detect artificial sweetners?

A

same receptors: T1R2 and T1R3- but a Gq-phospholipase C-beta pathway. Gustducin mediates it and the channel used is called TRPM5.

38
Q

How do we detect umami?

A

heterodimers of T1R1 and T1R3 that trigger use of gustucin and TRPM5.

39
Q

What receptors and pathways are used to taste bitter?

A

T2R heterodimers serve as receptors. pathway involves gustducin and TRPM5 depolarization.

40
Q

What is the arrangement of cells for olfaction?

A

biopolar neurons with many dendrites line the nasal mucosa. the axon of these bipolar neurons synapses with cells of the ofactory bulb called mitral cells. the junctions btw olfactory neurons and mitral cells occur at glomeruli.

41
Q

What are the receptors and pathways for smell?

A

receptors are Golfs. Golfs activate a CNG channel using cAMP. Once the CNG channel is open, Ca++ enters the cell and the signal is further amplified. (though Ca++ also inhibits CNG channel)

42
Q

Kallman syndrome symptoms

A

hypogonadotropic hypogonadism and anosmia (can’t smell)

43
Q

what happens to the GPCR/opsin- 11-cis-retinal complex when light hits?

A

GPCR is released into its active form, called metarhodopsin and trans-retinal is produced.

44
Q

describe what happens to a vision cell when stimulated with light.

A
  1. trans-retinal produced and metarhodopsin is formed (dissociation btw opsin and 11-cis-retinal).
  2. metarhodopsin acts on transducin, a heterotrimeric molecule that normally carries GDP when not stimulated. A GTP replaces the GDP and the Talpha subunit is released.
  3. T-alpha transducin ssubuint removes the inhbitor from PDE.
  4. PDE decreases cGMP levels
  5. decreased cGMP levels close the CNG channel
  6. Ca can’t get into the cell and the cell becomes hyperpolarized
  7. glutamate secretion is prevented.
45
Q

words for red, green, and blue colorblind

A

red: protanopia; green: deuteranopia; blue: tritanopia

46
Q

retinosis pigmentosa

A

progressive vision loss; decreased night vision because of rod cell degeneration.

47
Q

how does hearing work, very briefly?

A

sound waves are created by stapes at the round window and cause vibrations in the basilar membrane. the vibrations in the basilar membrane cause the position of hair cells to change with respect to the tectorial membrane.

48
Q

connexin-26 defect

A

most common genetic cause of deafness. it is a gap junction protein

49
Q

What receptors are used to detect cold?

A

TRPM

50
Q

what receptors are used to detect heat?

A

TRPV (activated by trkA

51
Q

HSAN-4

A

lack of pain sensation- it’s a disorder. caused by trkA mutations.

52
Q

SCN9A

A

another channel important for mediating pain: mutations can either cause loss of pain sensation or extreme pain syndromes.

MTC (11 decks)

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