regulation of cell cycle (13) Flashcards

1
Q

when does the commitment to proceed into mitosis occur?

A

shortly before the beginning of S phase

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2
Q

where are the two other checkpoints in the cell cycle?

A

entry into mitosis (between G2 and M)

transition from metaphase to anaphase (during M)

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3
Q

what is the regulatory subunit that must be combined with the cdk to make it active?

A

a cyclin

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4
Q

describe the concentration flow of cyclin and the kinase subunits during the cell cycle

A

The concentration of the cyclin subunit of a mitotic cdk increases gradually during the cell cycle then decreases suddenly
-the kinase concentration stays constant

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5
Q

why is there a “lag” between the increase in cyclin activity and the activation of cdk? (3 factors/steps)

A
  1. The cyclin subunit must be synthesized and must bind to the kinase
  2. The catalytic subunit is phorphorylated. 1 phosphate is needed for CDK activity, the other inhibits the cdk activity
  3. A phosphatase removes the inhibitory phosphate, activating the cdk
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6
Q

what is the name of the cdk inhibitor kinsase?

A

wee1

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7
Q

what is the name of the cdk activating kinase?

A

Cak

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8
Q

what is the final step in cdk activation?

A

removal of the inhibitory phosphate by a protein phosphatase starts a positive feedback loop. Activity of a few molecules of the cdk as a protein kinase stimulates the phosphatase to make more active cdk molecules

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9
Q

how do you inactivate cdk?

A
  1. Cyclin subunit is ubiquitylated by an E3 ubiquitin ligase, targeting the cyclin subunit for the proteolytic destruction by the proteosome
  2. The activating phosphate is removed from the kinase subunit
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10
Q

how many kinetchores need to be attached for the E3 ligase activation?

A

all of them

will not occur if even one isn’t attached

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11
Q

what is the APC?

A

a ubiquitin E3 ligase, targeting proteins for desctruction

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12
Q

what activates the APC?

A

tension on all the kinetochores

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13
Q

what are the two main proteins that p53 activates transcription for?

A

p27 and p21

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14
Q

what is cisplatin? why and how does it work?

A

it is a DNA damaging agent
why it works in brca cancers:
-If you damage the dna enough, and you cant fix it—you can induce apoptosis

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15
Q

in addition to DNA damaging agents, what is another molecule that can be used in brca cancers?

A

dna repair inhibitors

ex. PARP inhibitors

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16
Q

what is the action of G1 CDK?

A

CDK inactivates the retinoblastoma protein (Rb) and triggers the synthesis of genes needed to progress into S phase