Exam 1 Flashcards | Quizlet

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Exam 1

Key Concepts:

Terms in this set (411)

Tumors arise from ____ tissue

Tumors do not arise through ______ agents

4 reasons for COD from cancer

- obstruction of vital organs
- infection
- wasting (cachexia)
- hemorrhage

4 features of cancer cells

- increased division and survival
- loss of normal characteristics
- spread into unrelated tissue
- unresponsive to regulatory signals

Invasiveness is

There is a homeostatic ______ of cancer cells

Cancer is a ____-_______ phenomena

multi-mutational

There is no evidence that ______ mutation causes cancer

Cancer does not occur in ______ or ______ because they are unicellular organisms

yeast, bacteria

Cancer only happens in ______ organisms

Cancer cells have lost _______ decision making

Individuals mutations happen at ______ due to genetic _____

random, environment

Cancers are examples of ______ selection

Regulated cell division, differentiation and controlled death are all ________ in the evolution of cancer

What cells continue to divide in adult organisms?

stratified squamous epithelium

Histological criteria in staging cancers measures the ______ of the cancer

progressiveness

Changes in disorganization correlate to gradual loss of multiple ______ controls

Neither invasive nor metastatic, can be cured surgically

Invasive and metastatic, beyond scope of surgery

Metastasis limits treatment to ______ and _____

chemo and radiation

-asia that is growth of excessive numbers of cells

-asia that cells appear normal, retain ability to form normal looking tissues despite deregulated proliferation

-asia that one type of normal cell layer replaced by another cell type not normally found at a particular site in the body

example of metaplasia

Barrett's Esophagus

Disease where normal secreting epithelial cells found in the stomach

Barrett's Esophagus

-asia that is cytologically abnormal

-asia that changes size/shape of cell nucleus, increased mitotic activity, lack of normal cytoplasmic features present in differentiated cells

Dysplastic cells result in major changes in

tissue architecture

Transitional state between benign and premalignant (invasive) growth

- asia that is abnormal, disorganized growth that leads to formation of a distinct mass

-asia that refers to both malignant and nonmalignant growth

Tumor cells that have de-differentiated

When tumor cells are anapestic, it is no longer possible to use ___________ criteria to identify tissue of origin

histopathological

Cancer cells growth past normal stromal boundaries are

An enclosure in connective tissues capsule, derived from host tissue, suggests a _____ tumor

Invasiveness is sometimes seen in slow growing

malignancies, but rare

Spread to, and growth in foreign sites

Metastasis is a central feature of

All but a few cancers can develop the ability to metastasize, these are

gliomas and basal cell carcinomas of the skin

Gliomas and basal cell carcinomas of the skin are highly

invasive, cannot metastasize

-omas are usually

4 general groups of tumors

carcinomas
sarcomas
leukemia/lymphomas
neuroectodermal tumors

The most common type of cancer

Carcinomas are of ______ origin

Epithelial cancer with glandular or mucin-secreting cells

Lung, breast, colon, prostate cancers are the most common _______ cancers

Cancer of mesenchymal/connective tissue origins

Fibroblast, bone, muscle cancers are examples of _____ cancers

2 cancers of the blood, of hematopoietic cells

leukemias and lymphomas

Gliomas, glioblastomas, neuroblastoma, schawannomas, are all ______ tumors

neuroectodermal

2 types of tumors that do not fit into the 4 categories of tumors

melanoma and small cell lung carcinomas

Melanomas arise from primitive cells originating in the _____ ______

SCLCs resemble ________ cells found in the adrenal glands

Frequency of cancer is much _______ for an 80 year old than a 10 year old because we are living _____

_______ mutations are required

Somatic mutations arise from a _____ source, not from _______ cells

______ mutations may play an important role in the development of cancer, but it really requires additional hits, called the _______ hypothesis

inherited, 2-hit

These cause additional mutations and exacerbate risk of cancer

The idea of carcinogens was first proposed in 1775 by

Percival Post noted a high incidence of ______ cancer among chimney sweeps, soot causes cancer = carcinogen

These cause mutations in DNA, not necessarily cancer causing or not

Carcinogens are ______, but mutagens aren't ______

mutagens, carcinogens

Lots of mutations occur all the time in critical genes, but do not necessarily result in ______

Cancers overcome ______ controls

Tumor growth is ______clonal

2 cancers that prove cancer grows monoclonally

Leiomyomas and myelomas

Leiomyomas are benign tumors of the _____

Leiomyoma tumors express only one of the two variant forms of ______, not both

Because leiomyoma tumors express ONE of the two variant forms of G6PD, not both, this represents that growth of cancer is

Each leiomyoma arose from a single progenitor cell that expressed only that particular ______ of G6PD

The gene for G6PD is on what?

the X chromosome

The two allelic forms of G6PD have different sensitivities to

heat inactivation

All of the cancer cells in a heterozygous G6PD patient express the same version of ______, suggesting

the G6PD enzyme, monoclonality

Cancer that involves B cell precursors of AB producing plasma cells and represents monoclonality

Cells of myeloma tumors all produce the same _______, suggesting monoclonality

Normal B cells secrete many different ______, but myeloma cells secrete the ______ types of antibodies

antibodies, same

Leiomyomas and myelomas prove that tumor cells descend from a ______ progenitor cell

The site of cancer in the body is determinant of different _______ stresses

Are cancers caused because of genetic or environmental factors?

Environmental factors

Japanese people who live in Japan have different rates of cancer compared to Japanese people who live in

3 environmental factors that contribute to cancer

viruses, carcinogens, lifestyle

Cancers caused by viruses are ______

Viruses make up ____% of all human cancer

How do these 3 environmental factors contribute to cancer? what must we focus on?

the mutations in key genes that control cell division, survival, migration, proliferation, development, etc.

The first example of a specific genetic alteration linked to cancer

the philadelphia chromosome

The philadelphia chromosome causes what type of cancer?

chronic myelogenous leukemia

Abnormality in chromosome 22 is called the

philadelphia chromosome

The ABL gene on chromosome 9 takes the place of the BCR gene on chromosome

The philadelphia chromosome has a fusion gene on it called the

BCR-ABL fusion gene

The Ames Test determines the relative ________ of a suspected cancer-causing compound

The Ames Test tells if a compound is a _______, not a ________

mutagen, carcinogen

If you want to tell if a compound is a carcinogen, you have to use an ______ model

Salmonella is an _______ strain

Salmonella has a natural mutation that does not allow it to produce its own _______

Without histidine, Salmonella cannot

The test compound induces a mutation in the Salmonella, making it a reversion mutant. The test compound is now known to be a

Homogenized rat liver releases enzymes that ______ compounds

How many mutations does it take to produce cancer?

Mutation/hits must occur in a _______ order

Mutations in _____ genes repeatedly shown to play important role in most cancers

Seven hallmarks of cancer

- loss of growth factor dependence
- loss of responses to anti-growth signals and differentiated state
- resistance to apoptosis
- limitless replication
- recruitment of blood/lymph
- invasion/metastasis
- genetic instability

There is some evidence that specific mutations accumulate in a _______ order

Reductionist view of tumors is a collection of _______ cells

identical in a pheno/genotypically way

Heterotypic view of tumors is includes _______ cells in tumors

Normal cells in tumors provides _____ for tumor growth

Autocrine tumor growth means that the _______ itself is working on its own to keep it alive

Autocrine growth is cell-________

Paracrine growth is ______ - cell-________

non-cell autonomous

Two ideas that support the tumor interacts with normal cells and the stromal environment

heterotypic view and paracrine growth

Molecules that have a gain of function mutation

proto-oncogenes

Molecules that have a loss of function mutation

tumor suppressors

2 examples of proto-oncogenes

3 mechanisms of oncogene formation

- gene amplification
- point mutations
- chromosomal translocations resulting in gene deregulation and fusion proteins

Example of gene amplification as a mechanism for oncogene formation

Her2/ERBB2 in breast cancers. The more copies of these genes, the worst the prognosis is

Weinberg's group in 1981 showed what?

Took tumor cells from coal-tar painted mice and injected it into normal mice. The transformed cells generated tumors. The normal cells in the normal mice did not grow tumors. First represented that a proto-oncogene had been activated in some way

Wigler and Cooper in 1982 showed what?

Weinberg's same experiment, but on humans with bladder and colon carcinomas. Same results.

Mutated form of Ras that induces tumor, shown in Wigler and Cooper's experiments

Altered form of Ras leads to what cancers?

pancreatic, colon, lung

Altered form of Myc leads to what cancer?

Burkitt's lymphoma

Altered from of ERBB leads to what cancers?

stomach, breast, ovarian, brain

Altered form of Her2/neu leads to what cancer?

Oncogenes encode proteins that control ________ in signal transduction pathways that tell cells to ______ and _______

regulation; grow and divide

Gain of function mutations activate pathways telling the cell to _______

Loss of function mutations involve critical genes that normally _______ cell division

Ras is found in everything from ______ to _______

yeast to humans

Inappropriate activation of Ras affects ________ control

_____% of human cancers show Ras mutations, specially L61S and G12V

3 major forms of Ras

K-Ras
H-Ras
N-Ras

most mutated form of Ras

Mutated K-Ras forms what cancers?

pancreatic, lung, colon

Mutated H-Ras forms what cancers?

bladder, urinary tract cancers

Mutated N-Ras forms what cancers?

What kind of protein is Ras?

Where does Ras reside?

plasma membrane

______ and _______ anchors Ras to the plasma membrane and these are potential targets for therapy

farnesyl and palmitoyl

Inactive Ras is bound to

Active Ras is bound to

Ras is a GTPase and hydrolyzes _______ to ______, inactivating itself

Ras acts as a ______ _______

molecular switch

Ras is ______-regulated

Does GEF inactivate or activate Ras?

GEF promotes the release of

When GDP comes off, _____ comes on to Ras

When Ras is bound to GTP, it is activate and further activates _______ signaling

Does GAP inactivate or activate Ras?

Hydrolysis reaction/GTPase reaction induced by

When Ras is mutated to the RasG12V mutation, it cannot _______ GTP

When GTP is not hydrolyzed, Ras is always

RasG12V mutation results in ______ being inactivated, which cannot hydrolyze ______ to ______

GTPase, cannot hydrolyze GTP to GDP

EGFR is an RTK that binds and transmits signals from soluble _____

GFs (EGF, NGF, FGF, PDGF, insulin)

Dimerized RTKs activate

Dimerized RTKs lead to the activation of catalytic _______ domains

Dimerized RTKs have the ability to

autophosphorylate

When dimerized RTKs phosphorylate, they create phosphorylated ________, which binds to SH2 on Grb2

Grb2 has one _______ domain and two ______ domains

Phosphorylated tyrosine binds to the ____ domain on _____

SH2 domain on Grb2

_____ domain on Grb2 binds to SOS

SOS is a ______ for Ras, which activates it

Kinase cascade induced when ______ is activated

Activated Ras phosphorylates _______ which phosphorylates ________ which phosphorylates ________ which goes into the nucleus to induce gene expression

4 Ras-Activated pathways

Raf-MAPK
PI3K-Rac
RalGDS
PLCepsilon

What happens to Ras when there's cancer?

Ras is mutated in a way that renders it always active, inactivating GTPase, which doesn't allow it to hydrolyze GTP to go into inactive state

What happens to RTK when there's cancer?

Overexpression of Her2/neu subunit of EGFR = increased signaling of RTKs

Cancers designated Her2 positive have a _____ prognosis

_______ is the oncogene in erythroblastosis

What happens to Raf when there's cancer?

It's overactive

Raf is over expressed in what tumors?

Activating mutations in B-Raf in what cancers?

melanoma and colon carcinomas

GAP acts as a ______ _______

tumor suppressor

NF-1 is an example of a _____ ______

tumor suppressor

If there's no GAP, Ras cannot be

GAP is deficient in what cancers?

neurofibrosarcomas, pheochromocytomas, leukemias

Loss of NF-1 leads to excessive ______ signaling

4 reasons for Ras complexity

- 4 different EGF receptor subunits that can all dimerize each other
- 3 major forms of Ras
- 3 major forms of MAPK
- 3 other Ras effector pathways

Her2 plays biggest role in promoting ____ signals

3 major forms of MAPK

FTI inhibits _____ activity in cancers

FTI keeps Ras away from the ______ to keep it _______

membrane, inactive

Myc is a ____ _____

transcription factor

Myc is a ______-dimer

Myc regulates genes linked to cell _____ and _____

growth and proliferation

Overexpression of Myc leads to what kind of cancer?

Burkitt's lymphoma

Burkitt's lymphoma does not have a _____ protein

fusion (BCR-ABL)

Oncogenic Myc arises due to _____ and _____

amplification and translocation of the gene

What kind of transcription factor is Myc?

bHlH-Zip DNA binding protein

Myc binds DNA only as a _______ with ______

heterodimer, Max

Specificity of Myc/Max binding is mediated through _____ and ______ domains

HLH and leucine zipper

In order for Myc to be functional, it must form a ______ with Max

There are a lot of gene promoters that bind to ______, but a few that are ________ by Myc

When Myc is over expressed in cells, it reduces dependence on

When Myc is over expressed in cells, it blocks exit from the

When Myc is over expressed in cells, it increases

When Myc is over expressed in cells, it accelerates the progression through the

Partial loss of function mutations in Drosophila Myc (Dmyc) leads to

Gain of function mutations in Drosophila Myc (Dmyc) leads to

B cells in Burkitt lymphoma patients are ______ than healthy patients

Activating Myc is not the only thing that needs to happen to form a tumor, you also need to

inhibit apoptotic factors

Forced expression of Myc induces

Myc:Max/Mga promotes

activation and HAT, leads to proliferation

Myc:Mad/Mnt promotes

repression and HDAC, leads to differentiation

Myc activates the expression what what 2 CDK promoters to promote cell division?

cyclinD2 and CDK4

Myc represses what CDK inhibitor to promote cell division?

What Myc is over expressed in Burkitt's?

3 main differences between Myc and other oncogenes

- no fusion protein
- no known mutation to Myc
- transforming activity

EBV causes proliferation of what cells?

When you have EBV, you have an increased chance of getting _____ activation through _______

Myc, translocation

The higher amount of Myc copies, the higher change of

N-Myc is found over active in what cancer?

childhood neuroblastoma, loss of negative regulatory loci

Molecules that have a loss of function mutation

tumor suppressors

2 examples of tumor suppressors

Mutations in Rb cause inherited childhood _______

Disease associated with retinal tumors that usually develop in both eyes

If retinoblastoma tumors are removed prior to becoming malignant, patients generally ________

Retinoblastoma is inherited as an _______ ________ trait

autosomal dominant

Mutations in Rb lead to ______ of function

2 types of retinoblastoma

hereditary and sporadic

When Rb heterozygotes _______ function of remaining WT allele in retina, tumors arise

_____% of Rb heterozygotes develop tumors

In hereditary retinoblastoma, there are _____ mutant RB gene copies after the first somatic mutation

In hereditary retinoblastoma, mice homozygous for loss of RB ______ during embryogenesis

Sporadic retinoblastoma is less ______ and _______ likely to occur than hereditary retinoblastoma

Caused by spontaneous loss of both Rb alleles in one cell

sporadic retinoblastoma

In sporadic retinoblastoma, there is _____ mutant Rb allele after the first somatic mutation, and _____ mutant Rb alleles after the second somatic mutation

Inactivation of the sole WT copy of Rb in a heterozygote is called ______ of _______

loss of heterozygosity

LOH is a common feature in what kinds of molecules?

tumor suppressors

5 mechanisms that can cause LOH

- missegregation
- alteration of chromatin structure
- deletion and methylation of Rb
- mitotic recombination

Who first came up with evidence for TS genes in the 1970s?

Harris put together _____ and _____ cells and discovered tumor suppressors

normal and cancer cells

Harris observed the fused cells stop ______, so there must be something in the normal cells controlling the tumor division

Who developed the 2-hit hypothesis in 1971?

Knudson correctly predicted a general role for _____ in TS genes

Inactivation of both WT alleles of a TS genes promotes

Proteins evolved for homeostatic growth control, not for

tumor suppressing

In G0, hyperphosphorylated Rb binds tightly to transcription factor _______

E2Fs activate genes necessary for cell cycle _______

Are E2Fs functional or nonfunctional when bound to Rb?

Cyclin-CDK complexes phosphorylate Rb, which releases

When E2Fs are released, what are activated?

target genes that promote DNA synthesis, cell cycle progression/differentiation

E2F target genes do what?

progress the cell cycle, make DNA

Examples of viral oncoprotein that can bind to the same place on Rb that E2F can and has same function of Rb bound to E2F: stop cells from dividing

Large T antigen
E7
E1A

Large T antigen, a viral oncoprotein, is from

E7 protein, a viral oncoprotein, is from

E1A, a viral oncoprotein, is from

The 3 viral oncoprotein have what kind of binding motifs?

E2Fs do not have _______ binding motifs like viral oncoproteins do

E2Fs can be bound to DNA with or without

When Rb and E2F are bound, what is recruited?

In HDAC, histones are _______ and chromatin are _______, so gene expression is not permitted

de-acetylated, closed

When Rb and E2F are not bound, what is recruited?

In HAT, histones are _______ and chromatin are _______, so gene expression is permitted

acetylated, open

Rb related proteins ______ and ______ are required for cell cycle exit

Which E2Fs repress gene expression?

Which E2Fs activate gene expression?

E2Fs 1, 2, and 3

Rb only binds to what E2Fs?

E2Fs 1, 2, and 3

Loss of Rb promotes genomic _______

Loss of Rb promotes increase of what molecule?

Increase of Mad2 affects mitotic

E2F has a transcriptional target, ______, which affects mitotic inability, promoting gene expression

Rb controls what point of the cell cycle?

restriction point

Rb is a target for what complexes?

Rb loss of function accelerates the

The TS that was mistaken for an oncogene originally

______% of all human tumors have inactivating mutations in p53

Why was p53 considered an oncogene? It was found in _____levels in tumor cells, but _____ levels in normal cells

Half life of p53 in tumor cells

Half life of p53 in normal cells

p53 was found to be a TS, not an oncogene, when it was transfected into cells and did not

immortalize (keep alive)

Inactivation of one allele through missense mutation can _____ all p53 complexes in the cell

p53 mutations act as

dominant negatives

Rb has no _____ _____ function, like p53 does

dominant negative

Missense mutations are ______ mutations

Missense mutations, mutant proteins can still assemble, but p53 function is

Null mutations produce no ______ at all

Inheritance of one null mutant of p53 causes what syndrome?

Li-Fraumeni syndrome

p53 is not required for ____ and ______

growth and development

Why don't mutations in Rb act as dominant negatives? Rb works as a ______, while p53 acts as a ________

monomer, tetramer

What genes does p53 regulate?

- Bax
- MDM2
- GADD45
- p21
- IGF-BP3

p21 is a ______ inhibitor

When p53 activates p21, the cell cycle

When p53 activates GADD45, the cell cycle

When p53 activates IGF-BP3, it blocks signaling of

mitogenic growth factors

When p53 activates Bax, it activates

When p53 activates MDM2, it stabilizes

Regulating the amount of p53 in the cell is done by what gene?

3 regulatory mechanisms of p53

- protein stability
- nuclear localization
- activate p53

E3 ligase attaches ______ to p53 to stabilize it

Protein stability of p53 is achieved by

ubiquitilzation

E1 is the Ub _______ enzyme

E2 is the Ub _____ enzyme

E1 and E2 are ______; they can work with a lot of different proteins

E3 is _______ for particular proteins

E1 binds to ______ and transfers it to E2

E2 passes Ub to

E3 ligase binds to p53 and forms _____ chain which targets the protein for degradation

Specificity of ub reaction lies within

p53 levels in normal cells are

Under conditions of stress, degradation is inhibited and p53 levels

Under conditions of stress, degradation is inhibited and p53 levels increase, which is regulated by what gene?

MDM2 facilitates the degradation of p53 using Ub in what conditions?

normal (you don't need to have over expression p53)

When MDM2 is inhibited, p53 levels

MDM2 is part of the _______ specific for p53

MDM2 binds to p53 and brings it into association with ______ in normal conditions

When in contact with Ub, both ______ and _______ are degraded in the proteosome 26

MDM2 has a ______ pocket to which p53 binds to

p53 accumulates when interaction with MDM2 is

Phosphorylation of p53 on N-terminial residues by _______ impairs ability to bind MDM2

Kinases that phosphorylate p53 to have it not bind to MDM2 include

ATM ATR CHK1 and 2

ATM ATR CHK1 and 2 are activated by

ATM ATR CHK1 and 2 are activated when p53 must

When MDM2 is over expressed, p53 levels go up or down?

p19ARF is what kind of molecule?

tumor suppressor

p19ARF increases levels of

p19ARF inhibits ______ and increases p53

Proliferative signals of Myc and Ras are checked by up regulating what molecules?

oncogenic forms of Myc and Ras lose _____ function

4 characteristics of stem cells

- self-renewal
- limitless replication
- pluripotent
- arise from embryonic stem cells, but potential more limited

Embryonic stem cells are derived from

Embryonic stem cells are

Totipotent, opposed to pluripotent, means that they can make _____ tissues in vivo

Embryonic stem cells can be primed to differentiate into an increasing number of cell types ___ ______

Adult stem cells are

Multipotent stem cells can develop into more than one cell _____, but have limited potential

Pluripotent stem cells can develop into _______ types of cells

Totipotent stem cells can give rise to any and all

cell types, even a whole organism

Two types of stem cell factors

c-kit and steel ligand

Mutations of c-kit and steel lead to what disease?

Piebald disease

3 phenotypic features of Piebald disease

- defects of melanocytes
- hematopoietic lineages
- neural structures

Null mutations in mice are embryonic _____

Fluorescence activated all sorter (FACS) is used in order to ____ and _____ mixed cell populations

identify and isolate

Two general models of how SCs divide to produce one cell and one progenitor

environmental and divisional asymmetry

Loss of molecular signals from critical stromal cells should disrupt stem identity - what model is this?

environmental model

Environmental asymmetry is consistent with what disease?

Evidence for function of Numb in Drosophila nerve cell differentiation is in what model?

Notch is inhibited by ______ in Drosophila to promote neuronal differentiation

HSCs are found where in adults?

HSCs are found where in blood islands?

HSCs are found where in developing embryos?

How can we study HSCs in the laboratory?

adoptive transfer

Bone marrow transplant is technically _____ ______

adoptive transfer

2 techniques to isolate and study stem cells

Adoptive transfer and FACS

Separate bone marrow cells by virtue of the cell-surface proteins they express

Injected stem cells would colonize hematopoietic tissues and generate steady supply of new blood cells

Adoptive transfer

HSCs can differentiate into both _____ and _____ cells

myeloid and progenitor

GM-CSFs and EPOs promote

differentiation

Only a small number of cancer cells could proliferate extensively to producing new tumors either _______ or _______

in vitro/in vivo

First real evidence of a true stem cancer cell was in what cancer?

acute myeloid leukemia

Progeny of CSCs are not

CSCs, like normal SCs, have limited proliferative ______

Multiple additional mutations are needed to _____ CSCs

2 different ways CSCs could have originated

- Normal SC mutation
- De-differentation of progenitor, gaining self-renewal properties

Cells that have high levels of CD44 and low levels of CD24 formed

CSCs differ from normal SCs in 2 ways

- higher growth potential
- most resistant to treatments

C. elegans have 1090 cells and exactly _______ die during apoptosis

During embryogenesis, only _____ of total neurons generated survive at birth

Apoptosis is important for _____ ______ during embryogeneisis

sculpting tissues

Greater than ____% of developing T cells die in the thymus

Apoptosis ot T cells prevent development of ______ and _______ T cells

nonfunctional, auto-reactive

Apoptosis is ______ dependent

Intense membrane "blebbing" produces apoptotic bodies containing cellular debris which are then engulfed by what kind of cells?

Cell lysis is triggered by _______

ischemia releases

cellular contents

Apoptosis is _______ , while necrosis is triggered by stress

Extrinsic is _____ mediated

Intrinsic is _______ mediated

Death receptor pathway aka

Mitochondrial pathway aka

Intrinsic releases

4 assays to measure apoptotic cells

- dye exclusion
- TUNEL assay
- Annexin V
- Proteolytic cleavage of caspase-3 or PARP

Dye exclusion tells ____ cells from ______ cells

Dye exclusion does not distinguish ______ death from apoptosis

Dyes in dye exclusion

trepan blue and propidium iodide

TUNEL assay attaches dUTP residues to ends of oligonucleaosomes generated from ______ during apoptosis

Annexin V binds to phosphatidyl-serine which is flipped from the PM to the _______ face during apoptosis

Extrinsic pathway involves death receptors which include

Fas, TNF, DR3, TRAIL-R1, TRAIL-R2

Fas, when bound to FasL, recruits

How does Fas recruit FADD- by what areas?

_______ in FADD recruits pro-caspase 8

When activated by DEDs on FADD, pro-caspase 8 auto activates and triggers ________ _________

effector caspases

FADD acts as a ______ protein

3 advantages of Death receptors

- Fas is on a lot of cells
- FasL is tightly regulated
- Lymphocytes up regulate Fas and FasL to stimulate death

FasL is induced in lymphocytes, MPs and NKs to always be expressed in non-immune cites like the

eyes and testes

Cytotoxic T cells and NKs express _____ inducing apoptosis

2 mechanisms of of negative regulation of death receptor signaling

FLIP has similar structure to

FLIP lacks _____ site, can dock with FADD, but cannot be _______ = apoptosis does not happen

proteolytic, cleaved

Death receptor signaling can induce expression of

NF-kB is a TF associated with ______ and _______apoptosis

differentiation and protection from apoptosis

Death receptor signaling can induce Nf-Kb transcription factor properties - differentiation and protection from apoptosis - could be a mechanism whereby ______ _____ ______ are retained after ________

memory immune cells are retained after infection

Decoy receptors look like ______ receptors, but cannot interact with FADD

Decoy receptors bind to ______ _______ ligands

Decoy receptors do not induce _______

Decoy receptor 3 amplified in what cancers?

Prosurvival apoptotic molecules

Bcl proteins maintain

Proapoptotic molecules

BH3 only bind to _______ and Bax is recruited to the OMM in response to ________ stimuli

Bax and Bak produce pores in OMM releasing

Cytochrome c activates

Overexpression of BCl family can block

Over expression of BH3 can promote

Initiator caspases

Effector caspases

Cytochrome c binds to

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