Which statment best describes what a cancer cell is?

a. cells that divides uncontrolably

b. cells that divides uncontrollably that invade nearby tissues and spread to other parts of the body

c. cells that grow in places they aren't supposed to

d. cells that have mutated genes

-Proliferation is not anchor dependent (cancer cells don't need an anchor to grow unlike normal cells)

-Loss of contact inhibition (cancer cells never stop growing, even will grow ontop of eachother)

-They are immortal (cancer cells can replenish the lost telomere sequences by producing telomerase, unlike normal cells)

They are normal genes that regulate cell division.

-If they become mutated, they become an oncogene

-Point mutation

-Gene amplification (ex. ERBB2 gene is rep. several times which causes breast cancer)

-Chromosomal translocation (ex.philadelphia chromosome causes chronic myelognous leukemia (take a peice of 19 & 22 and switch them around)

-DNA rearrangments (deletions, insertions,inversions)

-Insertional mutagenesis (insert a base, or parts of DNA that disrupts how gene is expressed)

-Viruses (cause cancer by inserting in a region containing a proto-oncogene)

What is different about a cancer cell?

a. It's growth is anchorage dependent

b. It stops dividing when it is in contact with other cells.

c. It has one or more mutated proto-oncogenes

d. All of the above

The correct response is: C

-Chemicals (Carcinogens; directly & indirectly)

-UV and ionizing irradiation

-Viruses (ex. Epstein-Barr virus= Burkitt's lymphoma, Hepatits B & C= liver cancer, Human papillomavirus= uterine cervical cancer).

-Presence of oncogenes (need more than 1 to transfer into cancer)

G1= first cap phase, is where teh cell lives

S Phase= synthesize dna in thise phase

G2= Getting ready for mitosis, is where centrioles divide)

M Phase= Where mitosis occurs

They are normal genes that regulate cell proliferation in which it regulates the passage of cell from G1 to S Phase.

If you lose or inactivate these, it causes cancer.

In the unphosorylated state, RB binds to E2F preventing E2F from activating transcription of genes coding for proteins required for replication (S Phase).If DNA is damaged, p21 blocks bad DNA from being replicated.

Growth factors stimulate Ras which activates a kinase that adds PO4 groups to RB which phosporylates it.

Phosphorylated RB can't bind to E2F which releases E2F to bind to promoters and activing transcription of genes involved in the transition to S phase in order to replicate DNA.

-It helps repair damanged DNA

-Triggers cell cyle arrest and apoptosis

When DNA is damged, it activates ATM protein kinase which adds phospate groups to p53, and links p53 to ubiquitin. This activates cell death by transcribing genes involved in apoptosis.

If we wanted to develop a cancer drug, what would it need to specifically do at the cellular level? How would it work?

a. Turn on tumor suppressor genes like P53?

If we wanted to develop a cancer drug, what would it need to specifically do at the cellular level? How would it work?

b. Turn on oncongenes

If we wanted to develop a cancer drug, what would it need to specifically do at the cellular level? How would it work?

c. Affect the process of mitosis

If we wanted to develop a cancer drug, what would it need to specifically do at the cellular level? How would it work?

d. Affect the process of cell migration.

It occurs in order for development and protenction.

-virus infected cells

-turn off immune reponse (gets rid of immune cell that reongnize self antigens)

-DNA damaged cells

-Cancer cells

-eliminates excess cells

1. Death signal is sent (can be either extrinsic or intrinsic)

-reversible

2. Execution (irreversible)

-DNA segregates, apoptoic bodies form, eat me signal builds up,  brekaing of chromosomes into fragments.

3. Englufment by either macrophages or neighboring cells.

-destroys apoptic bodies

Is a series of enzymes called caspases.

-begins with the activates of Caspase-8 which is an initiator of the cascasde

-key action is to activate caspase-3= executioner caspase

In general, which of the following best describes cytoskelteons?

a. nucleoprotein filaments

b. protein filaments

c. nucleoprotiens

d. ribonucleoprotein flaments

Microtubules are made up of..

a. flagellin

b. actin

c. desmin

d. tubulin

Microfilaments are made up of..

a. flagellin

b. actin

c. desmin

d. tubulin

Which of teh following is the most heterogeneous type of cytoskeletal filament?

a. intermediate filaments

b. microfilaments

c. microtubules

d. all of these

The intermediate filament present in nail & hair is the..

a. keratins

b. lamins

c. vimetins

d. tubulines

e. GFAP

Crhomsome movement during cell division is regulated by..

a. microfilaments

b. microtubules

c. intermediate filaments

d. all of these

Cillia & flagella are made up of..

1. Intermediate filaments

2. Microfilaments

3. Microtubules

a. 1 only

b. 1 & 2

c. 2 only

d. 2 & 3

e. 3 only

Microfilaments are inovled in..

a. cyclosis

b. amoeboid movment

c. cytokinesis

d. all of these

Which of the following statements correctly describes intermediate filaments?

a. they are the only cytoskeletal filaments that are not composed of protein

b. these filaments help the cell to withstand mechanical stress

c. intermediate filaments are the principal component of the cell cortex.

d. these filaments are always found outside of the cell

Lamellipodia and filopodia frequently occur near the edges of cells. These membrane features...

a. result from the polymerization of actin filaments

b.are supported by intermediate filaments such as keratin

c. probably do not serve any useful puerpose to the cell

d. are directly linked to the microtubule organizing center

-cell motility

-cell shape

-strength & rigidity

Axonemal MT (found in cilia, flagella, basal bodies; 9 +2 arangment)

Cytoplasmic MT (microtub highways in cytoplasm; form spindle fibers)

1. Tubluin dimers

2. Oligomers

3. Protofilament

4. Sheets of protofilamenets form

5. Elongating of microtubule

6. Plateau phase

Microtubules growing in legth have tubluin... at plus end

-GTP

(tubulin GTP has greater affinity for each other than tubulin GDP)

-GTP cap stabilizes the end of a MT

Shrinking= GDP at end

It is when there is no net gain/loss of dimers.

(if it falls below=shrink; if it falls above= growth)

-It is where MT assembly is initiated

- Acts as an anchor for one end of the MT

-direct teh local polymerization of tubulin dimers

It causes free tubulin to assmeble and makes them stable. (prevents MTs from growing or shrinking)

-Stops mitosis

It causes tubulin to aggregate, or group together, inside the cell.

-Forms spindle fibers

-they provide mechanical strength to teh cell by forming a band under the plasma membrane

-they link transmemrbane protins to cytoplasmic proteins

-they form contractilel ring during cytokinesis in animal cells

-cytoplasmic streaming

-generate locomotion in cells such as white blood cells

-interact with myosin to provide force of muscular contraction

1. 3 to 4 subunits nucleation center

2. G actin is added to both ends (+ & -)

3. As filament assembles, ATP slowly turns into ADP

4. Hydrolysis of ATP to ADP for depolymerization

5. Reaches steady state with no net addtion

It nucleates actin filament growth from the - end allowing rapid elogngation at the + end.

-It also can attatch to the side of another actin filament while rmaining bound to the - end of the filament that has nucleated.

-Free G actin can be bound by it

-it keeps g actin in an unpolymerizable form

-it is essential for maintainging small cytoplasmic pool of free G-actin

-it is found bound to PIP2 in membrane and is inactive in this state

-in reponse to an extracellular signal it is released from the membrane by the hydrolysis of PIP2

-Profilin competes with TB4 for the G-actin and takes it

-Profilin catalyzes the exchange of actin-bound ADP to ATP

It disrupts actin filament formation by binding to the + end which prevents any more G actin bidings.

What is the basic structure of intermediate filaments?

-Cenral helical core

-Flanking N terminal domain

-Flanking C terminal domain

1. Monomer

2. Parallel dimer twists together

3. Antiparallel tetramer

4. Protofilament formation

5. Protofilbril

6. Intermediate filament is formed

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

Involved in muscle contraction

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

Involved in movement of cilia and flagella

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

More important for chromsome movements than for cytokinesis

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

Can be detected by immunoflorescence microscopy

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

Assemble from protofilaments

For each statement is it is true of
a.  MT    b.  MF    c. IF  
d.  All    e.  None of these.

Differ in composition between muscle and nerve cells

The energy required for tubulin and actin plymerization is provided by the hydrolysis of a nucleoside triphosphate.

True or false

As long as actin monomers continue to be added to the plus end of a MF, the MF will continue to elongate.

True or False

The minus end of MTs and MFs is so amed because subunits are lost and not added there

True or False

State the conclusion that be be drawn from the following statments:

State the conclusion that be be drawn from the following statments: