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M2M Unit 1 > Random shit to memorize week 1 > Flashcards

Random shit to memorize week 1 Flashcards

1
Q

AZT inhibits…? and treats?

A
  • AZT inhibits reverse transcriptase - nucleoside analog that terminates the chain
  • Treats HIV
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2
Q

Cisplatin

A

alkylating agent used as a chemotheraputic

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3
Q

Actinomycin D

A

Intercalates with DNA, interferes with normal base pair stacking

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4
Q

Doxorubicin

A

Intercalates with DNA

Blocks DNA replication

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5
Q

Puromycin

A

-mimics amino-acyl tRNA to terminate translation

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6
Q

Dysteratosis congenita

A

telomere deficiency syndrome

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7
Q

Acyclovir targets…

A

viral DNA polymerase

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8
Q

Quinolones target…

A

bacterial DNA gyrase

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9
Q

Herditary non-polyposis colorectal cancer (Lynch Syndrome) caused by a mutation in ________

A

MMR

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10
Q

hMSH and hMLH proteins used in _________ and act to __________

A
  • MMR

- recognize new strand damage (via methylation and knicks) leading to cut in front of and behind damage

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11
Q

Specific DNA glycolases

A

used in BER to recognize damaged base in DNA sequence and excise it, thus exposing the AP site

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12
Q

Global Genome NER uses ________ protein to recognize damaged DNA and recognizes DNA _____________

A

XPC protein

recognizes damage anywhere in the genome

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13
Q

Mutations on Global Genome NER can result in ____________ and ____________

A

Cancer, Xeroderma Pigmentosum (XP)

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14
Q

TFIIH is involved in which kind of DNA repair

A

NER - XPB and XPD subunits unwind DNA

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15
Q

Transcription coupled NER uses _____ and ______ proteins to recognize damaged DNA and repairs DNA in ____________ regions

A

CSA and CSB to recognize damaged DNA

repairs DNA in transcribed region

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16
Q

Mutations on Transcription coupled NER can result in __________ and __________

A

CNS disorder, Cockayne syndrome (CS)

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17
Q

PARP is activated in what repair pathway?

A

single-strand break repair

amplifies damage singnal

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18
Q

RNA polymerase I makes…

A

makes rRNA

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19
Q

RNA pol II makes…

A

makes mRNA, small nuclear RNA, and micro RNA

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20
Q

RNA pol III…

A

makes tRNA

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21
Q

C-terminal Domain (CTD)

A
  • acts as a landing pad for proteins that effect elongation/processing during transcription
  • Present in RNA pol II
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22
Q

CTD is phosphorylated by ______ to allow RNA pol II to elongate RNA chain

A

CDK7 subunit of TFIIH

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23
Q

a-amanitin is a _________ that acts on/binds __________ to block __________

A
  • non-competitive inhibitor
  • RNA pol II (bridge helix)
  • RNA pol II translocation and thus transcription
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24
Q

Rifampicin blocks _________ by ________

A
  • blocks growth of RNA chain in transcription

- by binding to the exit channel in RNA pol II

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25
Q

TFIID

A

aka TATA Binding Protein

  • general transcription factor
  • Binds TATA box on the DNA sequence
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26
Q

TFIIH (3 subunits)

A
  • general transcription factor
  • functions in transcription and DNA repair (NER)
  • CDK7, XPB, XPD
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27
Q

XPB and XPD subunits of TFIIH act to ______

A

act as helicases that open up DNA strands (closed –> open complex in transcription)

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28
Q

Syndromes associated with mutations in TFIIH (3)

A

Xeroderma pigmentosum (XP)
Cockayne’s Syndrome (CS)
Trichothiodystrophy (TTD)

29
Q

3 reactions to add 5’ cap to pre-mRNA

A

1) Triphosphatase: removal of phosphate group
2) Guanylytransferase: adds guanine and synthesizes 5’–>5’ bond
3) Guanine 7-methyltransferase: adds methyl group at 7 position of guanine

30
Q

4 Functions of mRNA cap

A

1) Protects the 5’ end from exonucleases
2) Recognized by cap-binding complex, which helps with splicing and processing
3) Recognized by translation factor eIF4E (eukaryotic initiation factor 4E) for nuclear export into cytoplasm
4) Removal of cap signals mRNA degradation

31
Q

Abnormal _______ of CD44 contributes to _________

A

splicing

tumor metastasis

32
Q

Spinal muscular atrophy results from a defective ________ gene, but can be possible treated by ________ in order to activate the _______ gene in its place

A
  • defective SMN1

- alternative splicing –> SMN2 can take its place

33
Q

Two functions of the mRNA polyA tail

A

1) protection from degredation

2) export from the nucleus

34
Q

Two types of thalassemias, what is thalassemia, which one is worse

A

Thalassemia is anemia

1) Beta-Thalassemia
2) Gamma-Delta-Beta Thalassemia (worse)

35
Q

Beta Thalassemia is caused by a mutation in the ________ of the b-globin gene and results in _________

A
  • Mutation in the promoter region

- results in less promotion and thus less transcription

36
Q

Gamma-Delta-Beta Thalassemia is caused by a _________ in the b-globin gene and results in ________

A
  • mutation in splice site
  • results in NO globin transcription
  • very severe anemia
37
Q

Hemophilia B-leyden results from a mutation in the _________ of the clotting protein gene, but can be partially recovered why?

A
  • promoter region

- Partially better at puberty due to some overlap of TFs of androgen receptors

38
Q

Fragile X-syndrome results from a mutation in __________ to increase _________ upstream of FMR1 gene causing ________

A
  • mutations in DNA control elements
  • CG repeats
  • abnormally high methylation and transcriptional silencing
39
Q

What are the 4 families of sequence specific DNA binding proteins?

A

1) Hemeodomain (helix-turn-helix)
2) Zinc-finger
3) Basic Leucine Zipper
4) Helix-loop-Helix

40
Q

Homeodomain sequence specific DNA binding proteins are typically used for ___________

A

regulation of development

41
Q

the _______ family of SSDBP tend to form dimers

A

Basic leucine zipper

42
Q

Craniosynostosis results due to a mutation of the MsX2 protein at the __________ that causes MsX2 to ________ and results in ___________

A
  • at the DNA binding homeodomain
  • bind the DNA more tightly
  • gain of function, protein transcribed at higher level
43
Q

Androgen insensitivity syndrome is caused by a mutation in the ____________ resulting in _________

A
  • androgen receptor (zinc-finger protein) DNA binding domain OR ligand binding domain
  • decreased response to androgens
44
Q

Waardenburg Syndrome is caused by a mutation in the MITF gene that encodes a ____________ that regulates melanocyte development

A

basic helix-loop helix binding domain

45
Q

Two classes of chromatin remodeling factors

A

1) ATP-dependent chromatin remodelers

2) Histone Modifying enzymes

46
Q

ATP-dependent chromatin remodelers

A

Use ATP hydrolysis to break histon-DNA contacts to move histone octomer along DNA in order to allow TFs access to sites on DNA
(SWI/SNF)

47
Q

Histone Acetyltransferase (HAT)

A
  • acetylates histone tails
  • neutralizes + charge on lysine
  • allows DNA to be less tightly wound
  • transcriptional activator
48
Q

Histone deacetyltransferase (HDAC)

A
  • removes acetyl group

- transcriptional repressor

49
Q

Rubinstein Taybi Syndrome results from a CBP haploinsufficiency. This effects ________

A

HAT activity –> effects transcription of multiple gene targets

50
Q

Fragile X syndrome results from methylated DNA that recruits in ________ that ________

A

HDACs

silence transcription in that area

51
Q

Euchromatin

A

where genes reside that are actively transcribed (accessible area of chromatin)

52
Q

Heterochromatin

A

always repressed because DNA is inaccessible (at centromeres, telomeres, and some internal chromosomal positions

53
Q

Constitutive Heterochromatin

A

always heterochromatin

54
Q

Facultative Heterochromatin

A

can change to euchromatin depending on cell type or developmental stage

55
Q

Ways to regulate sequence specific DNA binding proteins (5)

A

1) Control protein conformation by binding a ligand
2) regulate entry into the nucleus
3) Regulate amount
4) Regulate binding to DNA
5) Phosphorylate SSDBP to alter properties

56
Q

Estrogen hormone binds to ________, inducing _______ and activating __________

A

Estrogen receptor
dimerization of ER
transcription by binding to the DNA

57
Q

Tamoxifen is a drug that binds to _______ preventing _________

A
  • the estrogen receptor

- prevents recruitment of HATs, inhibits transcription

58
Q

MDM2 protein acts on p53 to… (2 mechanisms for this)

A

Inhibit transcription of p53 genes

  • via ubiquination that marks p53 for degredation
  • by binding activation domain of p53
59
Q

Over-expression of MDM2 protein can cause _________

A

low levels of p53 and thus cancer/tumor growth

60
Q

Cyclosporin is an immunosuppressant that ____________ by ______________

A

inhibits transcription by sequestering the sequence specific DNA binding protein in the cytoplasm

61
Q

Id protein prevents _________ of _______ proteins, thus ___________

A

heterodimerization of helix-loop-helix proteins, thus inhibiting binding to the DNA

62
Q

_______ of the CREB binding protein allows CREB to ________

A

phosphorylation

recruit pol II transcription machinery

63
Q

NF-kappa-B

A
  • Sequence specific DNA binding protein

- involved in inflammation

64
Q

When I-kappa-B protein is bound to NF-kappa-B, NF-kappa-B is ___________. During inflammation conditions, I-K-B protein is ________, allowing NF-K-B to ____________

A
  • sequestered in cytoplasm
  • Phosphorylated and degraded

-allowing NF-K-B to bind and enhance transcription of inflammatory response genes.

65
Q

Aspirin

A

inhibits degredation of I-K-B protein, so it remains bound to NF-K-B, and sequestered in the cytoplasm

66
Q

NF-ATc

A
  • Sequence Specific DNA binding protein

- involved in immune response

67
Q

Calcineurin acts on NF-ATc to ___________, allowing NF-ATc to _____________

A

remove phosphate group from NF-ATc

enter into the nucleus and activate transcription

68
Q

Cyclsporin

A
  • immunosuppressant drug

- inhibits calcineurin activation, so NF-ATc remains phosphorylated in the cytoplasm

69
Q

B-Catenin is ____________ by APC. If APC is mutated then there is ___________ B-Catenin resulting in abnormal cell growth/cancer

A

phosphorylated/degreaded

a surplus of B-Catenin that can then get into the nucleus

M2M Unit 1 (9 decks)

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