Cell Cycle, Communication, Signal Transduction Flashcards

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1
Q

Why do cells divide

A

Wound healing and organ maintenance

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2
Q

How do cells divide

A

Cell growth and chromosome replication
Chromosome segregation
Cell division

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3
Q

Mitosis

A

Prophase, prometaphase, metaphase, anaphase, telophase

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4
Q

Prophase

A

Cytoskeletal structure is checked if it is ready for cell division

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5
Q

Prometaphase

A

Chromosomes are accessible for microtubules (nuclear envelope is fragmented)

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6
Q

Metaphase

A

All condensed chromosomes are aligned

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7
Q

Anaphase

A

Chromosomes are moving to the side

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8
Q

Telophase

A

Reformation of nulcear envelope, subdivide cytoplasm

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9
Q

Cytokinesis

A

2 daughter cells are separated

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10
Q

G1 phase

A

Cell growth, new organelles, transcription and translation

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11
Q

G0

A

Cell in rest

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12
Q

S-phase

A

DNA synthesis, duplication of chromosomes

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13
Q

G2-phase

A

Cell growth, cpndensate chromosomes, check internal/external factors

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14
Q

Interphase and M-phase

A

Interphase: G1, G2, S, G2

M-phase: Mitosis and cytokinesis

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15
Q

Cell cycle check points

A

Enter cell cycle and proceed to S-phase (environment favorable)
G2/M checkpoint (environment favorable)
Trigger anaphase and proceed to cytokinesis (are all chromosomes attached to the spindle)
Checkpoints regulated by cyclins and cyclin-dependent kinases

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16
Q

Cyclin activity

A

is ended up by ubiquitination and degradation of the cyclin

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17
Q

Survivin

A

critical to form the microtubule spindles

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18
Q

centrioles

A

precedes spindle formation, dubplicated during S-phase and migrate to opposite sides of the nucleus ( under control of M-cdk)

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19
Q

Anaphase A and B

A

A: shortening of kinetochore microtubules
B: Sliding force is generated between interpolar

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20
Q

Cytokinesis is triggered by

A

Dephosphorylation of Cdks and cyclin breakdown by APC/C ubiquitination

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21
Q

Midbody

A

Final contact between 2 daughter cells

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22
Q

Contractile ring

A

actin and myosin

23
Q

Mitotic spindle

A

Microtubules

24
Q

Mitogens

A

activate a new wave of G I/S-Cdk activity to drive the cell to the S-phase

25
Q

Cell apoptosis

A

Programmed cell death

26
Q

Extracellular apoptosis

A

Cell loses its shape and shrinks
The plasma membrane forms protrusions (blebs)
Cell debris is recognized by macrophages that clear the remnants

27
Q

Intracellular apoptosis

A

The nuclear envelope disintegrates and chromatin is degraded
Degradative vacuoles are formed
Irreversible

28
Q

Survival factors block apoptosis

A

Increased production of anti-apoptotic Bcl2 protein
Inactivation of pro-apoptotic BH2 only Bcl2 protein
Inactivation of anti-IAPs

29
Q

P21

A

produces a protein that inhibits Cdk

30
Q

p53

A

uncontrolled cell division (cells divide on the wrong location at the wrong time)

31
Q

3 types of microtubules involved in spindle formation

A

Aster microtubules
Kinetochore microtubules (separate chromosomes)
Interpolar microtubules (separate 2 poles of the cell)
Position in the cell is different

32
Q

Actin

A

Specific localization in the cell, important role in last part of cell division, molecules made of monomers that are stacked on top of each other, polymerization (requires ATP) and de-polymerization

33
Q

Different proteins involved in the regulation of actin filaments (6)

A
bundling proteins (in filopodia)
Motor proteins
Side-binding protein
Capping protein
Cross-linking protein (in cell cortex)
Severing protein
Actin monomer (nucleating protein and monomer-sequestering protein)
34
Q

Movement of actin

A

Cell is attached to the surface
Actin polymerization at plus end protrudes the plasma membrane, cortex under tension, movement of unpolymerized actin
Focal contacts (contain integrins, contraction)
Myosin I is involved in transport and movement in the cell

35
Q

Active network assemble and sis-assembly (4 proteins)

A

Nucleating protein
Depolymerizing protein
Actin monomer
Capping protein

36
Q

2 additional things about actin

A

Network of actin filamets just beneath cell membrane is really dense.
Microtubules don’t reach the membrane, cargo goes from microtubule to myosin

37
Q

Typical signal cascade

A

Extracellular signal molecule
Receptor protein
Intracellular signaling proteins
Target proteins (metabolic enzyme, gene regulatory protein, cytoskeletal protein)

38
Q

Structuring of signaling process

A

Relay, modulation, amplification, divergence

No amplification: signal can become lost

39
Q

Cell surface receptors (transmembrane receptors, hydrophilic signal molecule

A

Ion channel linked receptors: respond by conformational change, opens a channel in membrane
G-protein-linked/coupled receptor (GPCR): 7 transmembrane receptor

40
Q

GCPR

A

protein interacts with G protein, signal: conformational change, release G protein, GTP binds, protein dissociates, activation of target protein by subunit, hydrolysis of GTP, inactivation subunit, dissociation from target protein, inactive subunit reassembles with other complex to form G protein

41
Q

Synthesis and breakdown of cAMP second messenger

A

ATP –> cyclic AMP –> 5’ AMP (termination signal cause cell should not always be on, new signal)

42
Q

Example pathway 1

A

Signal molecules activates receptor, activates a subunit of G protein, ATP –> cyclic AMP, binds to inactive kinase, activates PKA, can enter through nuclear pore, Pi is added and can bind DNA, RNA transcription

43
Q

Example pathway 2

A

G protein comes to receptor, a protein, activated phospholipase S, inositol phospholipid is splitter, IP3 is active messenger molveule, can bind to Ca2+ channel, lets Ca2+ through, calcium binds to kinase, conformational change, activation PKC, can activate downstream targets

44
Q

Example 4

A

Photon activates G protein, signal makes neurotransmitter release

45
Q

Enzyme linked receptors

A

Membrane protein that form dimers as the molecule binds

46
Q

Receptor tyrosine kinase signaling

A

Receptor molecule can bind ligands, 2 monomers are brought together by external protein (dimer), kinases present in receptor protein can activate the receptor with Pi, different types of proteins can bind to receptor. Signal relayed by activated signaling proteins into the cell’s interior

47
Q

Ras-Map-kinase pathway:

A

Adaptor protein can bind to receptor, recruites ras-activating protein, allows inactive Ras protein coupled to membrane, activates GTP bound Ras protein (GDP), activates MAP-kinase-kinase-kinase, ATP, 1Pi MAP-kinase-kinase, ATP, 2Pi MAP-kinase, ATP, Protein X + protein Y (changes in protein activity), gene regulatory protein A + gene regulatory protein B (changes in gene expression) ALL PROTEINS ARE PHOSPHORYLATED. Mutation in ras protein can cause tumors, growth signal

48
Q

Cytokine receptor signaling

A

kinase is not present in receptor but attached to the protein, active kinase phosphorylate receptor, can recruite proteins, proteins are phosphorylated, fully phosphorylate: form a complex, move into nucleus, activate transcription

49
Q

Growth factor signaling

A

growth factor activated by ligand binding and dimerized, kinase (attached) phosphorylates second kinase, forms dimers

50
Q

Intracellular receptors

A

Respond to signal molecules that can pass through the membrane (hydrophobic)

51
Q

Cortisol

A

Cortisol goes through membrane, binds to intracellular receptor protein: conformational change, activates receptor cortisol complex moves into nucleus (needs conformational change!), binds to regulatory region of target gene and activates transcription.

52
Q

The role of phosphorylation as an activity switch

A
  • Protein OFF: signal comes in, kinase activates (can put phosphate on a group, phosphorylate), ATP, puts P on protein, conformational change due to negative charge, phosphatase inactivates, P is pulled off the protein
    • Protein OFF, molecule can bind GPD, Protein ON can bind GTP, Signal, GTP binding activates, GDP, protein ON, binds GTP, GTP hydrolysis inactivates, P disassociates
53
Q

Genomic and direct routes of signaling

A

Fast: movement, cell needs to respond
Slow: protein bound to alter gene expression