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Cell Bio (BIOL 4004) > Exam 3 pt 3 > Flashcards

Exam 3 pt 3 Flashcards

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1
Q

RhoA

A

Monomeric GTPase which controls the assembly and contraction of the contractile ring

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2
Q

RhoA is turned on by

A

RhoGef, localized in the cell cortex at the future site of cell division

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3
Q

RhoA - GTP activates

A

formins which nucleat the growth of straight unbranched actin that can form parallel bundles

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4
Q

Phosphorylation of the _ by Rho-GTP kinases triggers

A

myosin regulatory light chain, triggers activation of myoson 2 whic assembles the contractile ring and contracts it

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5
Q

midbody

A

A narrow structure connecting daughter cells near the end of cytokinesis, it contains tightly packed microtubules derived from the antiparallel interpolar microtubules of the spindle midzone surrounded by a dense matrix material

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6
Q

_ initiates cytokinesis

A

dephosphorylation of Cdk substrates (due to APC/C mediated destruction of cyclins)

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7
Q

location of the cleavage in cytokinesis is determined by

A

mitotic spindle

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8
Q

astral microtubles

A

carry signal to the cell cortex which specify the site of furrow formation

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9
Q

spindle midzome

A

generates signals that specify the site of cleavage furrow formation

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10
Q

astral microtubles

A

promote the relaxation of actin myosin bundles except at site encircling the midzone of the spindle

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11
Q

for asymmetric division to occur

A

the spindle poles must be located assymetrically in the mother

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12
Q

syncytium

A

A large mass of cytoplasm, surrounded by a plasma membrane and containing multiple nuclei. It is formed when nuclear division occur in the absence of cytoplasmic division

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13
Q

cellularization

A

A coordinated round of cytokinesis during which membranes form around each nucleus of a syncytium, resulting in a multicellular structure

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14
Q

inactivation of _ occurs in late mitosis

A

Cdks

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15
Q

G1 phase in rapidly dividing cells

A
  • APC/C activated by Cdc20
  • activation depend on M-Cdk
  • as M-cyclin levels fall, Cdc20-APC/C activity decreases
  • Cdks reactivated immediately after mitosis

embryonic cells with no G1 phase

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16
Q

slower diving cells G1 phase

A
  • APC/C activation prolonged by Cdh2
  • activation inhibited by M-Cdk
  • as M-cyclin levels fall, Cdh1-APC/C takes over for Cdc20-APC/C
  • Cdks remain inactive through late mitosis until early G1

cells with G1 phase

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17
Q

Cdk activity low after mitosis due to

A

CKIs

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18
Q

p21

A

A CKI (Cdk inhibitor) whose transcription is stimulated by the gene regulatory protein p53. It binds to and inactivates G1/S-Cdk and S-Cdk, causing cells to arrest in G1.

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19
Q

p53

A

Gene regulatory protein activated by DNA damage, it functions to block progression through the cell cycle. Mutated forms of this protein are found in half of all human cancers.

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20
Q

Mitogens

A

Class of extracellular signal molecules which promote cell proliferation

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21
Q

Growth factors

A

Class of extracellular signal molecules which promote cell growth by triggering increased synthesis and decreased degradation of cellular molecules

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22
Q

Survival factors

A

Class of extracellular signal molecules which suppress apoptosis

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23
Q

platelet-derived growth factor (PDGF)

A

A mitogen which stimulates the proliferation (as well as growth, survival, differentiation and migration) of a large number of cell types; it is released from blood clots to help stimulate cell proliferation during wound healing

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24
Q

epidermal growth factor

A

stimulates proliferation on a wide variety of cell types

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25
Q

erythropoietin (EPO)

A

stimulates proliferation of RBC precursors

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26
Q

transforming growth factor beta

A

inhibits cell division by blocking progression through cell cycle or promoting apoptosis

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27
Q

G0

A

State of withdrawal from the cell cycle, it may be transient or permanent (as with termially differentiated cells such as neurons)

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28
Q

Myc

A

Gene regulatory protein, its production increased in response to the MAP kinase cascade, which promotes cell-cycle entry by several mechanisms, including increased expression of genes encoding G1 cyclin

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29
Q

Retinoblastoma protein (Rb) family

A

Protein family which, in their unphosphorylated form, bind to and inhibit E2F gene regulatory factors, thus blocking entry into S-phase. This protein family was originally identified in children with an inherited form of eye cancer.

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30
Q

_ inhibits Rb, causing Rb to

A

G1-Cdk inhibits Rb, causing Rb to release and activate a group of gene regulator factors called E2F proteins

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31
Q

DNA damage response with p53

A

p53 = cell cycle arrest
* p53 usuallt bound and ub by Mdm2 and destroyed in proteasomes
* phosphorylation of p52 blocks Mdm2 binding, buildup of p53
* p53 binds p21 regulator region, stimulate expression of p21
* p21 inactivate G1/S-Cdk, arresting cells in G1

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32
Q

DNA damage response with Chk1/Chk2

A
  • M-Cdk initional inactive due to presence of inhibitory phosphates
  • Cdc25 remove inhibitory phosphates
  • when DNA damage, Chk1 and Chk2 phospho and inhibt Cdc25, blocking progression into mitosis
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33
Q

replicative cell sencence

A

Phenomenon in which cell proliferation halts after a finite number of cell divisions, apparently due to loss of telomeres

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34
Q

Arf

A

In response to abnormal mitogenic stimulation, this protein associates with Mdm2, preventing its binding and ubiquitylation p53, resulting in p53 accumulation and the triggering of p53-driven cell cycle arrest or apoptosis

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35
Q

TOR

A

A protein kinase activated by the PI 3-kinase cell growth pathway, it is an important component of growth regulatory pathways in all eukaryotes. It activates many targets that stimulate metabolic processes, including increased protein synthesis

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36
Q

for a cell to maintain its size,

A

it must double in size before dividing

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37
Q

nerve growth factor

A

secreted by neuron to make neuron larger

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38
Q

A large multiprotein complex called ___________________ binds to replication origins throughout the cell cycle.

A

origin replication complex

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39
Q

The formation of prereplicative complexes is referred to as _____________________ since initiation of DNA synthesis may only occur at origins containing a pre-RC.

A

licencing of replication

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40
Q

When cells undergo nuclear division without cytoplasmic division a ___________________ is formed.

A

syncytium

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41
Q

Extracellular signal molecule that stimulates cell proliferation.

A

mitogen

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42
Q

Stage of mitosis when the mitotic spindle disassembles.

A

telophase

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43
Q

The assembly and contraction of the contractile ring is controlled by

A

the small GTPase RhoA.

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44
Q

APC/C is a member of the

A

ubiquitin ligase family of enzymes.

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45
Q

The major components of the contractile ring are

A

actin filaments and myosin II filaments.

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46
Q

The continued activation of APC/C into G1 is due to the binding of ___________________, a process which only occurs in the absence of M-Cdk activity.

A

chd1

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47
Q

The_ triggers both anaphase and cytokinesis.

A

inactivation of Cdks by the action of APC/C

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48
Q

DNA replication begins at sites scattered at numerous locations on each chromosome called

A

origins of replication.

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49
Q

For full activation of a cyclin-Cdk complex, an enzyme called _______________ must phosphorylate an amino acid near the Cdk active site.

A

Cdk-activating kinase

50
Q

For full activation of a cyclin-Cdk complex, an enzyme called _______________ must phosphorylate an amino acid near the Cdk active site.

A

Cdk-activating kinase

51
Q

Complex of proteins that holds sister chromatids together until they segregate at anaphase.

A

cohesion

52
Q

the duplication of centrosomes occurs in

A

S phase

53
Q

At least half of all human cancers have mutations in .

A

p53

54
Q

The _ ends of kinetochore microtubules are attached to the _ by the _

A

plus, kinetochores of chromatids, Ndc80 complex

55
Q

Many human cells divide a finite number of times before going into permanent arrest, a phenomenon called _ which appears to be caused by the loss of telomeres.

A

Replicative cell senescence

56
Q

Many human cells divide a finite number of times before going into permanent arrest, a phenomenon called _ which appears to be caused by the loss of telomeres.

A

Replicative cell senescence

57
Q

Cell cycle checkpoint at which APC/C is activated.

A

Metaphase-to-anaphase transition

58
Q

The assembly of pre-RCs is inhibited by _ and stimulated _

A

Cdk activity (S phase to early mitosis), by APC/C activity (late mitosis to early G1)

59
Q

Nuclear envelope breakdown occurs during

A

prometaphase

60
Q

cell death is important

A

in both developing and adult tissues

61
Q

apoptosis

A
  • cell remains intact
  • rapidly removed by phagocytes
  • no inflammation
  • more common
  • cell shrinkage
  • cytoskeleton collapse
  • mediated by proteolytic enzymes called caspases
62
Q

necrosis

A
  • cell burst and spill content
  • inflamation
63
Q

necrosis

A
  • cell swell and burst and spill content
  • inflamation
  • triggered by acute insult (e.g. trauma or ischemia)
64
Q

_ make apoptotic cells recognizable to

A

macrophages

65
Q

caspases

A
  • mediate apoptosis
  • proteases specialized
  • cys in active site, target Asp
66
Q

procaspases

A

inactive soluable form of initiator caspases, need to be cleaved to become active caspases

67
Q

apoptotic signals trigger

A

binding of caspases to proteins causing dimerization and acivation
* each caspase cleaves the protease domain of its dimer partner
* cleaved protease domains rearrange into a large and small subunit, active complex

68
Q

executioner caspases usually exist as

A

inactive dimers

69
Q

executioner caspases are activated when

A

cleaved by intiator caspases

70
Q

amplifying proteolytic cascade

A

Self-amplifying and irreversible series of events which lead to cleavage of target proteins and programmed cell death

  • happens because one initiator caspase can activate many executioner caspases
71
Q

executioner capases cleave

A

many specific target proteins leading to controlled cell death

72
Q

extinsic pathway of apoptosis activation

A
  • triggered by binding of ligands from TNF family of signal proteins to death receptors of the TNF receptor family
  • intercellular death domain recruits FADD
  • FADD death effector domain binds to intiator caspase to form a death inducing signaling complex (DISC)
  • initiator caspases (procaspases) cleave one another to activate and trigger pathway
73
Q

FLIP inhibits

A

DISC by binding in so inhibits extrinsic pathway of apoptosis

74
Q

intrinsic pathway of apoptosis is a response to

A

injury, DNA damage, ROS, mitochondrial problems, etc

75
Q

intrinsic pathway of apoptosis

A
  • internal stimuli and Bcl2 Bek and Bax release cytochrome C from IM space of mitochondria
  • cyt c binds Apaf1 and form apoptosome
  • each Apaf1 contains CARD which each CARD domain binds initiator caspase 9, activation of CARD domain
76
Q

anti apoptotic Bcl2 protein

A
  • contain all four BH domains
  • Bcl2 and BclX
  • Proteins which inhibit apoptosis by binding to effector Bcl2 proteins and preventing their oligomerization within the outer mitochondrial membrane
77
Q

pro apoptotic Bcl2 proteins

A
  • contain BH1, 2, 3 domains (Bax, Bak) or
  • only contain BH3 domain (Bad, Bid)
78
Q

Bek is located in _ and Bax in _ and both

A

outer MM, cytosol and both trigger release of cyt C

79
Q

BH3 only proteins

A

Pro-apoptotic Bcl2 proteins which bind to and inactivating anti-apoptotic Bcl2, thus allowing the oligomerization of effector Bcl2 proteins within the outer mitochondrial membrane
* promote apoptosis

80
Q

Bid

A
  • links extrinsic and intrinsic pathways
  • extrincsic pathway active then capse 8 cleaves and activates Bid
  • Bid then inhibits anti apoptotic Bcl2 proteins and triggers intrinsic pathway
81
Q

Inhibitors of apoptosis (IAPs)

A

Proteins which bind to and inhibit (or ubiquitylate) active caspases; they set an inhibitory threshold to prevent the accidental triggering of apoptosis due to spontaneous activation of initiator caspases

82
Q

_ must be inactivated for apoptosis to occur

A

IAPs

83
Q

A large ring complex composed of cytochrome c-bound Apaf1, it recruits and activates initiator caspase-9.

A

apoptosome

84
Q

An amplifying proteolytic cascade triggered in response to cell injury, DNA damage, lack of O2, lack of extracellular survival factors or presence of intracellular developmental signals.

A

intrinsic pathway

85
Q

Proteases which cleave thousands of specific targets resulting in controlled cell death.

A

executioner caspases

86
Q

An amplifying proteolytic cascade triggered in response to the binding of extracellular signal molecules to death receptors.

A

extrinsic pathway

87
Q

This domain is missing from decoy receptors, making them incapable of initiating a proteolytic caspase cascade.

A

death domain

88
Q

decoy receptors

A

Cell surface receptors which bind death ligands but lack the cytosolic death domains required to trigger the extrinsic pathway of apoptosis

89
Q

Abnormal regulation of apoptotic programs often occurs in

A

cancer cells.

90
Q

Abnormal regulation of apoptotic programs often occurs in

A

cancer cells.

91
Q

Proteins which bind to and inhibit (or ubiquitylate) active caspases; they set an inhibitory threshold to prevent the accidental triggering of apoptosis due to spontaneous activation of initiator caspases.

A

IAPs

92
Q

Domain found on both adaptor proteins and initiator caspases; it promotes their association within death-inducing signaling complexes (DISCs)

A

death effector domain

93
Q

Homotrimeric transmembrane proteins which are members of the tumor necrosis factor receptor family.

A

death receptors

94
Q

Proteolytic enzymes which are the intracellular mediators of apoptosis.

A

caspases

95
Q

A type of programmed cell death which causes cells to swell and burst, spilling their contents into the extracellular matrix and potentially triggering immune and inflammatory responses.

A

necrosis

96
Q

Decoy receptors…

A

inhibit extrinsic apoptosis by competing with death receptors for ligand.

97
Q

Death-inducing signaling complexes (DISC) are formed during the _ pathway of apoptosis.

A

extrinsic

98
Q

Domain found on Apaf1 adaptor proteins and initiator caspase-9, it mediates the recruitment of the initiator caspase into an apoptosome.

A

CARD

99
Q

An intracellular blocker of apoptosis, it resembles an initiator caspase but lacks a proteolytic domain.

A

FLIP

100
Q

Complex in which initiator caspases are brought into close proximity and activated in the extrinsic pathway of apoptosis.

A

DISC

101
Q

The amplifying proteolytic caspase cascade begins with the self-activation of _ caspases.

A

initiator

102
Q

cancer arises from mutations that cause a cell

A

to become asocial and behave selfishly

103
Q

cancer cells two properties

A
  • abnomal proliferation
  • invasiveness
104
Q

neoplasm

A

A term meaning ‘new growth’, it describes a tumor arising from the growth and proliferation of a cell in defiance of normal controls

105
Q

benign tumor

A

A tumor which is self-limiting in growth and non-invasive; it can be cured by removing or destroying the mass

106
Q

malignant tumor

A

A tumor whose cells have acquired the ability to invade other tissues, an essential characteristic of cancer

  • form metastases
107
Q

metastases

A

A secondary tumor that arose from a malignant primary tumor

108
Q

carcinoma

A

Derived from epithelial cells, it is the most common type of human cancer

109
Q

adenocarcinoma

A

Cancer derived from glandular tissue

110
Q

sarcoma

A

Cancer derived from connective tissue or muscle cells

111
Q

leukemias

A

Blood cancer derived from white blood cells and their precursors

112
Q

lymphoma

A

Cancer derived from lymphocytes and found mainly within lymphoid organs

113
Q

tumors develop

A

years before detection

114
Q

primary tumors

A
  • located at original site where a mutated cell was formed
  • arise form proliferation ofo a single abnormal cell
115
Q

as cells of a primary tumor proliferate,

A

more mutations accumulate

116
Q

for a single cell to give rise to a tumor, its aberration must be

A

inheritable
* mutagenic changes to DNA sequence (caused by carcinogens)
* epigenetic changes
* inheritaed genetic effects (ex. impaired gene repair)

117
Q

if a single mutation could cause cancer

A

we would all be yeeted

118
Q

tumor progression

A

Process in which a mild disorder of cell behavior evolves gradually into a full-blown cancer

119
Q

chronic myelogenus leukemia (CML)

A

Chronic overproduction of white blood cells due to the Philadelphia chromosome translocation

120
Q

clonal evolution

A

repeated rounds of mutation, proliferation and natural selection
* as the number of tumor cells increase, so does the chance that at least one cell will undergo a change that favors it

121
Q

genetic instability results from

A

mutations that interfere with replication and genome maintainance, therby increasing the mutation rate

122
Q

cancer cells transformed phenotype

A
  • abnormal cell shape
  • abnormal cell motility
  • abnomral response to growth factors

Cell Bio (BIOL 4004) (8 decks)

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