Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Molecules Exam 1b > Flashcards

Molecules Exam 1b Flashcards

1
Q

Protein targets: GPCRs

A

They control the opening of ion channels by stimulation or inhibition of effector enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The first and second messenger of GPCRs

A

First: Ligand
Second: Effector enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the second messenger of GCPRs do?

A

Activate protein kinases for protein phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain how different diseases can help us understand the processes of each of them

A

Cancer is the product of an abnormal cell surviving and replicating. In a patient with Alzheimer’s, these abnormal cell processes always fail. Therefore, patients with Alzheimer’s have an extremely low chance of getting cancer. Could a treatment for Alzheimer’s be located in the mechanisms of cancer?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Protein target: Enzyme-linked

A

Receptor on the cell surface bind with enzymes(ligands). This causes dimerization of the receptor. Dimerization causes phosphorylation of the target proteins which helps elicit a cellular response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the dominant forces in drug-target binding?

A

Noncovalent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the target in enzyme-linked receptors?

A

Growth factors like insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Protein target: Nuclear (intracellular) receptors

A

The ligands bind intracellular and transcription factors are ligand-activated. Has a slow effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Target of nuclear receptors

A

Sex hormones and other steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Protein target: Ion channels

A

Proteins that control the opening and closing of ion channels and, thus, the ions that pass through them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which protein target is important for neuronal and cardiovascular function?

A

Ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Proteins that transport molecules across cell membranes

A

Transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Biologic targets: Nucleic acids

A

These drugs usually work to inhibit or block replication, transcription, and/or translation by modifying nucleic acids (cancer drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Biologic targets: RNAi

A

Can target nucleic acids by binding to the complementary strand of RNA to stop replication. Double stranded RNA stops protein formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Biologic targets: Lipids

A

Drugs that bind to the cell membrane and change the permeability. This controls what can and cannot pass through the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Established target

A

The research has already been done on this target. Basically trying to make a drug that works on this target better than whatever is currently on the market by working better or having less side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Novel target

A

No research has been done on the target. The proposed targets must be validated. Is way more harder to develop a drug this way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Genotype effects on a drug response

A

Pharmacogenomics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the purpose and role of target validation?

A

When the target, after being modified pharmacologically, is proven to be effective and safe for human disease in a long-term clinical setting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Phenotype-based discovery

A

Find some compound first and then figure out how it works. You use initial drug screening to find a hit, and then optimize a target based on that. It is also unbiased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Target-based discovery

A

Choose a target first, and then find some active compound that will work on the target. Hypothesis-based

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does gene silencing help validate a target?

A

You knock out or knock down a gene in order to see if there is a change in function. If there is a change, then you know that that gene effects the disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does CCR5 work?

A

It is a receptor that helps replicate HIV. If you block it, then you stop the virus from replicating. If someone does not have this receptor, they will not get HIV even if they are exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4 steps of target validation

A
  1. Link gene to disease
  2. Determine expression pattern in normal vs. disease tissues
  3. Manipulate target
  4. Find mechanisms of action via in vitro and in vivo assays
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do antisense oligonucleotides work to silence genes?

A

They bind to complementary target mRNA in order to block the expression of any gene being studied. It kills the messenger. It is quick, rapid, and predictable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does RNAi work to silence genes?

A

A natural process to protect agains viruses and other elements that utilize dsRNA to self-replicate (their virus or disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are dsRNAs?

A

Double strand RNAs that lead to cell death and flu-like symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Negative control siRNA

A

An siRNA that has the same nucleotide composition but not homogenous to the genome (diverse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Positive control siRNA

A

All of the other reagents but NO siRNA

30
Q

When a gene from another species is inserted into its genome

A

Transgenic

31
Q

Gene replaced with non-functional mutant

A

Knock-in

32
Q

Constitutive gene knockout

A

Target gene is permanently disrupted

33
Q

Conditional gene knockout

A

Eliminated a specific gene in a certain tissue or time specific manner. Target is more precise, and the genes in the rest of the body are unaffected

34
Q

Reporter genes

A

Certain genes are chosen to be reporter genes because they affect the organism in a way that the characteristics expressed are easily identifiable and measured. They are indicators of whether the specific gene is taken up or expressed by the cell in the organism

35
Q

Cas9 role in CRISPR

A

Nuclease scissors cleave dsDNA which activates the double-strand break repair machinery (helps put it back together)

36
Q

CRISPR vs. RNAi

A

RNAi goes in and temporarily knocks down mRNA in the transcription stage. It also is naturally occurring. CRISPR is artificial and permanent

37
Q

What is the part of CRISPR that can act like an immune system if original gene comes back after editing?

A

TracrRNA/trRNA (trans-activating RNA)

38
Q

CRISPRi*

A

Targeted silencing of transcription and requires inactive Cas9 (dCas9) and sgRNA. These elements bind to DNA to halt transcription.

39
Q

Can bind to a receptor but produces less than max effect

A

Partial agonist

40
Q

Kd in relation to binding affinity

A

Koff/Kon, therefore a small Kd = a high binding affinity

41
Q

Indicator of potency

A

EC50

42
Q

The ability of a drug to produce a max response

A

Efficacy

43
Q

Tenacity with which a drug binds to its receptor

A

Affinity

44
Q

Competitive antagonist on a curve

A

Shifts curve to right; EC 50 changes, therefore potency changes. Emax remains the same

45
Q

Can competitive antagonists’ inhibitory effects be overcome?

A

Yes, by adding a higher concentration of agonist (binds reversibly)

46
Q

Non-competitive antagonist on a curve

A

EC 50 remains the same, but the Emax is decreased.

47
Q

Can noncompetitive antagonists’ inhibitory affects be overcome?

A

No, this is because they bind irreversibly. Primary effect of a noncompetitive antagonist is to reduce maximal effect

48
Q

Drug binds within the same site as the receptor’s ligand

A

Orthosteric binding (most common)

49
Q

Bind to a site different from that of the orthosteric agonist binding site

A

Allosteric binding

50
Q

Explain the concept of Spare Receptors

A

Non-liner occupancy response coupling. Don’t always have to occupy every receptor to get a max response. If there are 100 receptors available but only 10 are needed to reach max effect, the EC50 is 5

51
Q

TI equation

A

TI = TD50/ED50

52
Q

Drug is still binding but no effect is occurring

A

Desensitization

53
Q

RAPID decrease in drug response after a few doses of the drug. Increasing the dose CANNOT produce the same effect

A

Tachyphylaxis

54
Q

A gradual loss of response, person will acquire a resistance to the drug after prolonged use

A

Tolerance

55
Q

Down Regulation

A

Can lead to tolerance. Decrease in expression of a receptor in response to increased activation/drug. Meaning that even though you are taking more of the drug, the effect is decreasing (developing tolerance)

56
Q

Up Regulation

A

Increase in the number of receptors in the surface of the target cells, making them more sensitive

57
Q

Selectivity for different receptor subtypes

A

Receptor selectivity

58
Q

Selectivity for different signaling pathways coupled to the same receptor

A

Functional selectivity (biased agonism)

59
Q

Intrinsic toxicity (Type A)

A

Affects all individuals at the same dose, predictable, dose related

60
Q

Idiosyncratic toxicity (Type B)

A

Rare and unpredictable, unclear relation to dose, affects only susceptible individuals

61
Q

Basic assumptions made in safety testing

A

-Assume that animal toxicity will translate to that of humans
-Animals are bred essentially pure, but humans are diverse
-Even in a rigorous animal testing (1000-2000 animals testing) it is still nothing near millions of people
-Dosage given to animals is highly regulated, but humans sometimes miss a dose or take too much

62
Q

Any effect that could lead to cell death

A

Cytotoxicity

63
Q

The inability of a drug to induce a mutation in a cell can be indicative of possible carcinogenic activity. Test the ability of a molecule to produce changes in DNA of a modified salmonella

A

Mutagenicity

64
Q

Hepatic Toxicity

A

Liver damage, think of first pass effect, especially in toxic doses.

65
Q

3 “R”s in Assay Development

A

-Robustness(obviousness)
-Relaibility
-Relevance

66
Q

Is biochemical assay target or phenotype based?

A

Target-based

67
Q

Is cell-based assay target or phenotype based?

A

Phenotype-based

68
Q

Emission of light during a chemical reaction that does not produce a significant quantity of heat

A

Chemiluminescence

69
Q

Production and emission of light by living organism (Lightning bugs)

A

Bioluminescence

70
Q

Goal of assay

A

To develop a kind of assay that best encompasses the function of the target in the cell

Year 3 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions