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MCM Final > Biochem > Flashcards

Biochem Flashcards

1
Q

Describe long range, hormone signaling via the blood

A

Endocrine signaling, it is long lasting (on the minutes scale)

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2
Q

Describe paracrine signaling

A

The signals are called paracrine factors
They diffuse to neighboring cell of a different cell type
They are short lived
Important in neurotransmission

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3
Q

Describe autocrine signaling

A

Common in growth factors for cancer

Cells self stimulate

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4
Q

Describe direct or juxtacrine signaling

A

Signal binds to cell that is is in contact with

Immune cells use this

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5
Q

Lipohillic signals are ______ lived and they have what 2 receptors

A

Long, cytoplasmic and nuclear

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6
Q

What are some common lipophilic and hydrophilic medications

A

Lipo-contraceptives

Hydro-epinephrine

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7
Q

Graves’ disease causes ____________ and presents with decreased _____ and increased _______

A

Hyperthyroidism, TSH, T3 and T4

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8
Q

What are the symptoms of Graves? Who does it affect? What are some treatments?

A

Weight loss, tachycardia, insomnia, thyroid goiter, “buggy eyes”
Women, presents by 40
Resection of the thyroid, radioactive iodine, and pharmacological intervention

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9
Q

The TMD of G-protein-coupled receptors have 7 _______ that are arranged in a _________ pattern. The ECD relies on _________ bonds

A

Alpha helices, circular, disulfide

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10
Q

________ activate G proteins while ___________ inactivate them

A

GEF, GAP

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11
Q

______________ proteins produce secondary messengers

A

Effector

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12
Q

Gs, Gi, Gt, and Gq are activated by or activate what?

A

Activates AC->cAMP activates PKA
Inhibits AC
Activated by light; activates cGMP PDE (cGMP->GMP)
Activates PLC; IP3 opens Ca channel on SR or ER

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13
Q

Caffeine affects what?

A

Inhibits cAMP PDE -> increased cAMP since breakdown is slowed

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14
Q

Albuterol is a ____________ which activates ________________ receptors. What is one side effect of its use for asthma?

A

Beta agonist, beta-adrenergic, increased HR

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15
Q

What is the MoA of cholera toxin?

A

Decreased GTPase activity
Gsa remains active and therefore AC keeps producing cAMP, this keeps intestinal Cl- channels open, Cl- leaves and water follows

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16
Q

What is the MoA of pertussis?

A

Gia prevents dissociation of alpha subunit from G protein complex -> less inhibition of AC ->too much cAMP->lots of fluid and excess mucous in airways

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17
Q

How are GLUT4 and G proteins similar?

A

They can both be sequestered in vesicles when not needed. GPCR can even be degraded

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18
Q

What is another mechanism to control GPCR response without sequestering them?

A

Phosphorylation of GPCR which causes arrestin to bind

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19
Q

Phopshotyrosine is recognized and bound by the adapter and docking protein _______________.

A

SH2 domain of Grb2

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20
Q

Binding of substrate to RTK causes a conformational change followed by ________________

A

Autophosphorylation

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21
Q

There are RAS dependent and RAS independent pathways associated with RTK. What do they do?

A

RAS dependent cause changes in gene transcription

RAS independent cause changes in protein and enzyme activity

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22
Q

JAK STAT receptors offer a more __________ route to altering __________

A

Direct, transcription

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23
Q

STAT goes to the _____________ after activated

A

Nucleus

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24
Q

What kind of molecules bind to JAK STAT receptors?

A

Cytokines

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25
Q

RAS mutations are linked to ___________

A

Cancer

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26
Q

_________ blotting uses DNA probes and targets DNA

A

Southern

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27
Q

_____________ blotting involves a ssDNA probe and targets mRNA

A

Northern

28
Q

Western blotting is used for early detection of _____

A

HIV

29
Q

Western blotting targets ____________

A

Protein

30
Q

What is the target of Eastern blotting?

A

Post-translational modifications of proteins (lipids, carbs, phos., etc.)

31
Q

One of the main purposes of PCR is early detection of micro organisms responsible for what diseases

A

HIV, bacterial and fungal infections that cause Lyme disease

32
Q

What does PCR allow us to do? What are the three main steps?

A

Amplify isolated DNA

  1. Heat
  2. anneal
  3. extend
33
Q

VNTR are used to detect what 3 diseases?

A

Huntington disease, Fragile X, Frederick Ataxia

34
Q

ELISA should be used to confirm HIV in what time period? What can be used to confirm? Why is confirmation needed?

A

4-6 weeks
Western blotting
ELISA can give both false-positives and false-negatives

35
Q

What does VNTR do in layman’s terms?

A

Shows how many copies of a repeated section are present

36
Q

What are the two types of ELISA and what are they used for?

A

Indirect - measures amount of Ab in a sample

Sandwich - measures the amount of antigen in sample

37
Q

ELSA can be used to detect ________________ commonly found post MI

A

Troponin

38
Q

What are the 3 general stages of the cell cycle? And what do they do?

A

Mitosis - nuclear division at beginning and cytokinesis at the end
Interphase - G1 -RNA and protein synthesis needed for DNA replication
S - DNA synthesis
G2 - DNA stability is checked
G0 - poor nutrient/environmental conditions (brain, cardiac muscle, RBC)

39
Q

What happens during G1 phase?

A

RNA and protein synthesis

Cell growth

40
Q

What happens during S phase?

A

DNA replication
Histone synthesis
Centrosome formed
Chromosomes duplicate

41
Q

What happens during G2 phase?

A

preparation for mitosis

42
Q

What happens during M phase?

A

Mitosis (PMAT) and cytokinesis

43
Q

Where is the restriction point? What is it dependent on?

A

Before G1 checkpoint towards the end of G1

Growth factors

44
Q

What is the checkpoint at the end of G1?

A

DNA damage check

45
Q

What is checked at the end of G2?

A

Verify complete genomic duplication

46
Q

What happens during the metaphase checkpoint?

A

Checks to make sure chromosomes are attached to the mitotic spindle

47
Q

What activates cyclin-CDK?

A

CAK phosphorylates the cave site

CDC25 phosphatase removes an inhibitory phosphate from the roof site

48
Q

What inhibits cyclin-CDK complex?

A

P27 binds to it

WEE1 kinase adds an inhibitory phosphate to the roof site

49
Q

What is the function of the T-loop?

A

It serves as a regulation mechanism and only moves out of the active site after cyclin binds
This site is then phosphorylated by CAK (the cave site)

50
Q

What cyclins are linked to what stage?

A

G1 - D
G1/S - E
S - A
M - A/B

51
Q

Besides levels of phosphate, how else can you inhibit cyclin-CDK?

A

binding of P27

52
Q

What is one way the M cyclins are regulated?

A

Ubiquitinylation –> degradation by proteosomes

53
Q

How does P53 protect the cell? What is it normally inhibited by?

A

It leads to increased transcription of p21 which then binds to CDK-complexes and causes cell cycle arrest
P53 is normally inhibited by MDM2 which is a ubiquitin ligase

54
Q

P53 activity can lead to what two outcomes

A
  1. Reparable damage leads to cell cycle arrest and DNA repair
  2. Irreparable damage leads to apoptosis pathway
55
Q

What are the general apoptosis pathways? What causes them?

A
  1. Extrinsic binding (TNFalpha and Fas)

2. Intrinsic (leakage of Cyt C from mito)

56
Q

What caspase does the extrinsic pathway activate?

A

Caspase 8 (it starts in the pro-caspase form)

57
Q

What are the two major classes of caspases? What caspases are involved?

A

Initiatiors (caspase-8 and caspase-9)

Executioners (caspase-3)

58
Q

Is BAX pro or anti-apoptotic? How does it work?

A

Pro-apoptosis

Active BAX proteins aggregate in the mito membrane and form a pore for proteins to be released through into the cytosol

59
Q

What activates Apaf1?

A

The binding of mitochondrial Cyt C

It then forms an apoptosome which activates Caspase-9

60
Q

What is the difference between a proto-oncogene and an oncogene?

A

Proto-oncogenes have the potential to cause cancer if they undergo gain of function mutations
These genes are generally responsible for normal cell growth and division

61
Q

What mutation in HER2 causes cancer? What cancer does it cause?

A

Change in TMD from a Val to Gln, this causes dimerization and ultimately RTK activity
Breast

62
Q

Heterozygosity for the RB protein causes what?

A

Cells to be predisposed to cancer (requires another hit)

63
Q

What are some cancer associated viruses?

A

Epstein Barr, HepB, HPV, Kaposi Sarcoma

64
Q

What anticancer inhibits BCR-ABL fusion protein?

A

Gleevec

65
Q

What is the MoA of herceptin?

A

Ab (the drug) binds to disallow dimerization, assists immune cells in recognizing cancer cells, and can lead to endocytosis and degradation

66
Q

What is the MoA of gleevec?

A

It doesn’t allow ATP to bind to BCR-ABL fusion protein

67
Q

Lipophilic signals are carried in the blood by ____________________

A

Carrier proteins

MCM Final (10 decks)

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