Brainscape's Knowledge GenomeTM

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


See full index

SFM > Cell Cycle, CA and Death > Flashcards

Cell Cycle, CA and Death Flashcards

1
Q

Prophase

A

The cell begins to assemble the mitotic spindle, a set of microtubules extending from the centromeres which will later attach to the chromosomes

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

Prometaphase

A

The nuclear envelope disintegrates, and the microtubules of the mitotic spindle attach to the chromosomes

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

Metaphase

A

The chromosomes are aligned on the mitotic spindle. There is a pause here to allow all chromosomes to become attached

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

Anaphase

A

The cohesion proteins which bind the sister chromatids together are cleaved and the chromosomes are pulled apart by the mitotic spindle

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

Telophase

A

The nuclear membrane reconstitutes around each set of chromosomes.

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

G0 -phase

A

quiescent, intact proliferation capacity, non-cycling

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

G1 -phase (Gap 1):

A

duration between completion of cell division and initiation of DNA replication where cells start building cell mass

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

S-phase (Synthesis)

A

DNA replication

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

G2 -phase (Gap 2)

A

duration between completion of DNA replication and initiation of cell division

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

M phase

A

Mitosis

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

Progression vs Transition of cell cycle

A

“Progression” going through the cell cycle phase

“Transition” from on phase to another

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

Cyclins with CDK’s

A

CDK4/6 bind with cyclind D

CDK2: binds with cyclin E and A

CDK 1: Binds with B

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

Which Cyclin is found in Mitosis

A

B

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

Which cyclin is found in G1

A

D1, E

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

Which cyclin is found in S

A

Cyclin A

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

What are positive cell cycle regulators and what are negative cell cycle regulators?

A
  • cyclins and CDK
  • cyclin dependent kinase ihibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe how to activate Cyclin CDK complexes.

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

Cell cycle negative regulators:

A
  • They block the action of CDKs
  • Ensure tight control of the cell cycle (Balance)
  • Activated upon cell cycle checkpoint activation
  • ink ihibits D-CDK4/6
  • kips inhibit the rest in the cell cycle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ink4 can bind to a CDK in what ways

A
  • bind when cyclin isnt bound so it rpevents it from binding
  • or it can bind after cyclin binds preventing ATPase use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

p27kip binds in what way?

A

Bind after cyclin binds to CDK to block ATP binding

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

CKI: p21 cip1/waf1

A

induced by p53 tumor supressor

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

p27 kip1

A

cell cycle arrest in response to growth supressers like TGF beta

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

ink4: p16 ink4a

A

cell cycle arrest in senescence

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

Cell cycle entry and progression

A

1) mitogen binds to mitogen receptor and activates RAS
2) RAS then activates map kinase
3) map kinase activates gene regulatory protein
4) goes into nucleus which then acts as a TF and makes MYC
5) MYC will then increase Cyclin D and s-CDK to phosporylate RB
5) E2F is made which will help entry to s phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Restriction point

A

One way site, not coming back

point where cells comit to devide

happens between d-ckd 4/6 and e cdk 2

26
Q

G1/S transition

A

When E–CDK2 complexes drive pRb hyperphosphorylation, this liberates E2F transcription factors from pRb control, enabling the E2Fs to trigger increased transcription of the cyclin E and E2F1 genes; this leads to the synthesis of more cyclin E protein and the formation of more E–CDK2 complexes, which function, in turn, to drive additional pRb phosphorylation. At the same time, the newly synthesized E2F1 protein drives its own expression, further amplifying its activity.

27
Q

During S phase what does its cyclin do?

A

just stablizes the pre replication complex making sure that DNA rep will happe and will be sustanined at S phase.

28
Q

G 2 to M transtition

A

Activation of CDK1/cyclin B at the G 2 /M boundary

  • Activation of CDK1/cyclin B at the G 2 /M boundary maintained by Cdc25
  • CDK1/cyclin B translocate to the nucleus

CDK1/cyclin B initiate spindle assembly

• Activated anaphasepromoting complex (APC) destroy cdk1 freeing cyclin B for degradation

29
Q

Check points of cell cycle: whats the point?

A

Checkpoints are biochemical circuits that detect external or internal stimuli and send appropriate signals to the cell-cycle system.

• Checkpoints mostly activated by genotoxic stress mainly DNA damage.

30
Q

G1 checkpoint

A

ATM is a sensor that is also a kinase to check on DNA damage:

2 pthways: The faster pathway acts via the activation of Chk2 and the inactivation of Cdc25. Thus, inhibitory phosphates of the CyclinE/Cdk2 complex can no longer be removed.

Slow pathway: The slower pathway involves the stabilization of p53 and transcriptional upregulation of p21 which binds and inhibits the Cyclin/Cdk complexes (d/ cdk46 and E/cdk2)

31
Q

G1 Checkpoint: p16

A

Another pathway that if activated cells will never replicate

32
Q

G2 checkpoint

A

2 pathways again:

  • slower pathway will inhibit cycB1 CDK1 through activated p53 pathway
  • fast pathway is that chk1 and chk 2 will phosporylate and inactivating it thus inactiviating the cyclin cdk complex
33
Q

Tumors

A

Space occupying lesions that may or may not be neoplasms

34
Q

Neoplasm

A

relatively autonomous abnormal growth with abnormal gene regulation, 2 types: benign and malignant (→ cancer)

35
Q

Cancer

A

Malignant neoplasm (can produce metastasis)

36
Q

Metastasis

A

Secondary growth of cancer at different - location from primary neoplasm

37
Q

Stages of Carcinogenesis

A

Initiation • Simple mutation in one or more genes that control key regulatory pathways of the cell (change in DNA sequence)

Promotion • Selective functional enhancement of signal transduction pathways that were induced by initiator by continuous exposure (involving changes in gene regulation)

Progression • Continuing change of the basically unstable karyotype (further changes in karyotype)

38
Q

Initiation

A
  • rreversible
  • no threshold
  • Genotoxic agents include chemicals, radiation, reactive oxygen species, and viruses
  • Involves sequence change in cellular DNA
  • Single gene mutation, chromosomal translocation, and gene amplification
  • Can be a result of the activation of oncogenes or the inactivation of tumor suppressor genes
39
Q

Promotion

A
  • Promotion occurs over a long period of time
  • Reversible in its early stages
  • Involves gene activation or repression such that the latent phenotype of the initiated cell becomes expressed through cellular selection and clonal expansion. -Threshold exists (time and dose)
40
Q

progression

A
  • involves further complex gene changes and irreversible changes to gene experssion which will cause karyotypic instability
  • benign tumors start turning into malignant neoplasms
41
Q

Oncogenes

A

Expression of these genes is tightly control under normal circumstances. Loss of regulation of gene expression can lead to enhanced expression of these proteins which leads to unregulated cell division and growth.

42
Q

Tumor suppressors

A

These are cellular genes that serve to check or inhibit cell division. Loss of expression of these proteins leads to cell growth or cell division.

43
Q

What are the 3 ways you can find an oncogene

A

Cellular proto-oncogenes that have been captured by retroviruses,

Virus-specific genes that behave like cellular proto-oncogenes that have been mutated.

Cellular proto-oncogenes that have been mutated,

44
Q

Type 1 transducing virus

A

Cellular Oncogene is carried in Retro virus

45
Q

Type 2

A

NON Transducing virus:

cellular oncogene activated by proviral insertion and intergration

46
Q

Type 3 retroviral oncogene

A

retroviral transactivating protien disrupts the normal regulation of the cellular transcripton

47
Q

type 4 oncogenic retrovirus

A

inpropreate cellular signaling resulting from viral envolope/ cell receptor interactions

48
Q

Name 2 oncogenes

A

Ras and Myc

49
Q

Tumor suppressor genes

A

Recessive

Normal activity: repress growth

no known analogus in oncogenic viruses

examples are: Major examples are: p53, Rb, p14ARF, p16INK4A

50
Q

Tumor supressor gene: P16INK4A

A

showed inactivation of the INK4a locus on human chromosome 9p21 in human cancers (2nd most commonly inactivated gene)

• Gene mutation • Gene deletion • CpG island methylation in promoter

normally when you have its it regulates G1 check point

51
Q

Rb (Retinoblastoma)

A

-if mutated restriction check point is ungregulated

52
Q

Tumor microenevrioments

A
  • is the tissue environment in which cancer cells exists, that include normal cells, secretory factors, and the extracellular matrix.
  • there are barriers for therapy beacuse so much is in the way
  • desmoplastic rxn: to much tissue that isnt the cancer but is around the cancer thus you cant access et
  • microenviroment can promote tumor progression, therapy resistance and recurrence: the cell arounds the ca cell can have mutation that produces paracince signals for other cells to devide
53
Q

Radiation

A

effective on cells which have: repoductive activity, cells that have longer diviving future ahead and cells that are least differentated

-you break dna bonds or you use hydrolysis of water to produce powerful damaging free radicals

54
Q

chemo aklylating agents

A

capable of denaturing certain macromolecules such as DNA macromolecules

55
Q

intercalating agents

A

which interact with DNA and are intercalated between two bases, inducing a structural change and a functioning of this molecule– cleaving agents, capable of breaking DNA molecules.

56
Q

antimetabolites

A

that can be structural analogues of purines or pyrimidines; they block the synthesis of the corresponding bases (5 FU), or folate analogues

57
Q

mitostatic agents

A

s that inhibit tubulin synthesis, these being cell spindle poisons

58
Q

plat derivates

A

which plays a role by DNA binding

59
Q

Necrosis:

morphological changes

cells involved

inflammatory outcome

major biochemical features

» Describe the basic regulatory mechanisms

A

Morphologically characterized:

Cell membrane: Swelling and rupture. 2. Cytoplasm: Increased vacuolation, organelle degeneration, and mitochondrial swelling. 3. Nucleus : Clumping and random degradation of nuclear chromatin and DNA (karyolysis)

Cells involved: all

inflamation: yes

biological features: Extensive failure of normal physiological pathways that are essential for maintaining cellular homeostasis, such as regulation of ion transport, energy production (ATP Depletion) and pH balance.

You target: Two players are involved and target the mitochondria: 1. Receptor-interacting protein 1 (RIP1) 2. Poly [ADP-ribose] polymerase 1 (PARP-1)

60
Q

Apoptosis

morphological changes

cells involved

inflammatory outcome

major biochemical features

» Describe the basic regulatory mechanisms

A

Also called programed cell death

• Morphologically characterized by: 1. Cell membrane: membrane blebbing and eventually fragmentation into membrane bound apoptotic bodies. 2. Cytoplasm: Fragmentation and shrinkage 3. Nucleus : Chromatin condensation and degradation via specific DNA cleavage leading to nuclear fragmentation.

Cells involved: hematopoietic cells and their malignant counterparts (liquid tumors). Apoptosis only plays a modest role in the treatment response of most solid tumors, which constitute the major part of human malignancies.

No infalmation

biochem feature: cell membrane looses assyemerty, phospatilserine is exposed, caspase and mitochodria dependent

Triggers are: DNA damage, death receptor singaling cell membrane or mitochodria dalamge

61
Q

Autophagy

A

self eating of cell and recycling

Morphologically characterized by: 1. Cell membrane: membrane blebbing. 2. Cytoplasm: accumulation of two-membrane autophagic vacuoles. 3. Nucleus : Partial chromatin condensation No nuclear and DNA fragmentation.

  • Cells involved: All cell types
  • Inflammation: No.
  • Biochemical features: Caspase-independent and increased lysosomal activity.
62
Q
A

SFM (31 decks)

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