Bis 104 Final

Front 1

MOA of Latrunculin?

Back 1

It's binds to and sequester free Actin monomers so that they are out of the available pool and cannot be added to filaments. In other words, it effectively lowers the concentration of free monomers leading to actin depolarization.

Hint 1

Uncle (latrUNCULin) thats ACTIN to get people (monomers) out of the POOL by grabbing (binding) to them.

Front 2

MOA of cytochalasin?

Back 2

Depolarizes actin filaments by binding to and capping the plus end of action filaments.

Note: Will depolarize the minus end of a steady state until it reaches 0.6 (the minus end Cc).

Hint 2

Stop CHALASIN (chasing) my end (+) with your CapZ on bro!

Front 3

MOA of phalloidin?

Back 3

Binds to sides of actin filaments and prevents depolymerization.

Hint 3

Like a the balls of a phallus, phalloidin binds to the sides...prevents shrinkage (aka. depolarization).

Front 4

MOA of thymosin?

Back 4

A protein that binds and sequester monomeric actin to prevent it from polymerizing (note: analogous to the drug latrunculin)

Hint 4

Uncle (latrUNCULin) Thompson (Thymosin) is ACTIN to get people (monomers) out of the POOL by grabbing (binding) to them.

Front 5

MOA of profilin?

Back 5

Binds monomeric actin and induces the exchange of ADP for ATP. In this manner, it activates monomeric actin which stimulates filament growth.

Hint 5

Front 6

MOA of cofilin?

Back 6

Recycles actin monomers by binding to actin in the ADP state near the pointed/minus end and inducing depolarization.

Hint 6

At the end (-) of his life, Akon (actin) is ripped into shreds and placed in a coffin (coffilin).

Front 7

MOA of CapZ?

Back 7

Binds to barbed/plus end of actin filament to block dynamics at that end (analogous to cytochalasin). Useful in inactive blood platelet cells.

Hint 7

Stop CHALASIN (chasing) my end (+) with your CapZ on bro!

Front 8

MOA of gelsolin?

Back 8

Activated from Ca2+ release after the wounding of a blood vessel, gelsolin binds to the sides of the short actin filaments and severs them. This creates new plus ends not blocked by CapZ.

Hint 8

A Cap wearing Zombie (CapZ), tried to make me bleed, but I kicked his hat off with my gel-soled shoes (gelsolin).

Front 9

MOA of filamin?

Back 9

Cross links actin filaments to form a 3D actin-gel that resists local mechanical pressures.

Hint 9

Fill-em-in. Fills A In. "Fills actin in" by binding them together.

Front 10

MOA of fimbrin and villin?

Back 10

Connect parallel arrays of actin filaments to begin to form spike-like structures seen in an activated platelet.

Hint 10

Fimbria and her Villains like ACTIN together to make the spikey things.

Front 11

MOA of ARP2/3?

Back 11

Serves as the major actin-nucleating factor (aka. the tiny seed required for the initiation of actin filament assembly)

Hint 11

Assembling Red Pipes (ARP)! Actin is always red in the diagram.

Front 12

MOA of WASP/WAVE?

Back 12

Recruit ARP2/3 to nucleate actin filaments.

Hint 12

WASPS Assemble Red Pipes (ARP).

Front 13

MOA of ActA?

Back 13

A transmembrane bacterial protein (eg. from Listeria) that is required for actin nucleation that results in propulsion of bacterial cell throughout the host cell.

Hint 13

In Act A of the play, hysteria (Listeria) erupted when the character was shot out of a cannon!

Front 14

MOA of Dystrophin?

Back 14

A spectrin-related protein that stretches from the interior actin filaments toward the plasma membrane, where it interacts with Dystrophin glycoprotein complex (DGC), which in turn spans the membrane and attaches to the ECM component laminin.

Hint 14

The orphan felt he was in distopia,so he left Akon's house to become a Sheppard to watch over lambs.

Front 15

MOA of Nesprin-1?

Back 15

Connects the actin network in the cytoplasm to lamin forming the cytoskeleton inside the nucleus.

Hint 15

Needing an Aspirin, Akon reached into Nicole's laminated cupboards.

Aspirin = Nespirin-1

Akon = Actin

Nicole = Nucleus

Laminated = Laminin

Front 16

MOA of Griscelli syndrome (albinism)?

Back 16

Defect in motor myosin-Va which normally distributed pigment-containing melanosomes throughout the cell. As a result the melanosomes remain stuck near the Golgi, leading to albinism.

Hint 16

The white witch Griselda confessed my 5 sins while eating a melon on a golf cart.

Griselda = Griscelli syndrome

White = Albinism

My 5 sins = Myosin-5

Melon = Melanosomes

Golf = Golgi

Front 17

MOA of Usher syndrome (deafness)?

Back 17

Mutations in myosin-VIIa disrupt the actin structures underlying the stereocilia in your ear, resulting in hearing loss.

Hint 17

Usher confessed his 7 sins so loudly through the stereo that Akon lost his hearing.

Usher = Usher's syndrome

His 7 sins = Myosin-7

Stereo = Stereocilia

Akon = Actin

Lost his hearing = Deafness

Front 18

MOA of colchine (drug)?

Back 18

Binds to and sequester free a-/B-tubulin dimers, And prevents them from polymerizing. This effectively lowers the concentration of free dimers and leads to depolymerization.

Hint 18

The coaching staff stole all the dimes sitting in the tub of water.

Front 19

MOA of taxol (drug)?

Back 19

Functions by binding to the side of a microtubule and stabilizes it to prevent depolymerization.

Hint 19

It's very taxing to hold onto a heavy tube from the sides.

Front 20

y-tubulin ring complex (y-TuRC)?

Back 20

Consists of a number of proteins (the Dgrips) that form a ring that serve as the template off of which the 13 protofilaments of a microtubule can grow (note: located at the minus end).

Front 21

Catastrophe?

Back 21

The point at which a microtubule switches from growing to shrinking due to the plus end of the microtubule being in a GDP-bounds state.

Front 22

Rescue?

Back 22

The point at which a microtubule switches from shrinking to growing due to the plus end of the microtubule reestablishing it's GTP cap.

Front 23

MAP2/Tau?

Back 23

Stabilizes microtubules by binding to the side and increasing frequency of rescue events.

Hint 23

According 2 the MAP they were lost. The only remaining chance of rescue was to attached a towel to the side of a long tube and wave it in the air!

Front 24

Kinesin-13?

Back 24

Induce catastrophes and shrinkage of microtubules.

Hint 24

13...as in Friday the 13th is always a catastrophic day!

Front 25

Axonemal dyenin?

Back 25

Functions in eukaryotic cilia/flagella. Tail is attached to A tubule and it's three, ATPase-functioning heads move B tubule toward minus end on basal body.

Front 26

Dynein?

Back 26

Delivers cargo to minus end.

Front 27

Kinesin?

Back 27

Plus-end directed proteins (mostly).

Front 28

Vanadate?

Back 28

Inhibits dynein.

Hint 28

You're so vain, that even when on a date all you could talk about was how you hated your dyed hair.

Front 29

Kinesin-5?

Back 29

Can push the two poles of a mitotic spindle apart when it cross-links antiparallel microtubules.

Hint 29

Kyle's 5 sins were confessed between the two spinning flagpoles

Front 30

Kinesin-14?

Back 30

The exception to the rule. The only of its class that moves toward the minus end of microtubules.

Hint 30

Put four teens together, and you'll get the exact opposite of what you want!

Front 31

UNC-83?

Back 31

A KASH protein responsible for nucleus migration in C. Elegans. It binds both kinesin-1 and dynein in order to switch between +/- end movements depending on the situation.

Hint 31

My cash-loaded uncle Nick just turned 83. All he can talk about are 1) his sins and about dying.

Front 32

Dam1?

Back 32

Forms a ring around a microtubule and is attached to the kinetochore by the Ndc80 complex. As the microtubules depolarizes, the ring is forced down the microtubule to the minus end.

Hint 32

DaM1 that 80-year nudist, delinquent cop (NDC80), forcing his ring down my tubular throat!

Front 33

Plectin?

Back 33

A protein that joins intermediate filaments with either actin filaments or microtubules.

Hint 33

Unlike electin intermediaries, plectin joins things together

Front 34

Chromokinesin?

Back 34

Generates the "polar ejection force" that move chromosomes toward the plus end of microtubules, away from the pole.

Hint 34

Chromosome kinetics = movement of chromosome in opposite directions

Front 35

Restriction/START point?

Back 35

The "no turning back" point at which a cell decides to proceed to S-phase or to remain in G1-phase.

Front 36

CyclinD/CDK?

Back 36

Active at the end of G1 and regulates entry into the cell cycle.

Front 37

CyclinE/CDK?

Back 37

Regulates the initiation of S phase.

Hint 37

Drunkard Elephants Appreciate Beer (CyclinD + E + A + B)

Front 38

CyclinA/CDK?

Back 38

Comes on in the early S phase and remains active until late G2 and prevents the reinitiation or S phase.

Front 39

CyclinB/CDK?

Back 39

Initiates mitosis. Also phosphorylates lamin, which leads to nuclear envelope breakdown. Also phosphorylates histone H1 and condensin, which initiates chromosome condensation. Also phosphorylates Separase to keep it inactive when Securin is absent.

Hint 39

Such a Beezee! He broke Nicole's laminated envelope. Then condensed his 1 stone on someone's chrome bumper. He also securely separated his absent-minded friend.

Front 40

E2F?

Back 40

A transcription factor that controls the initiation of S phase by binding to the promoters of cyclinE and cyclinA, turning on their transcription, in late G1 phase.

So, how is it regulated in early G1 phase?

Hint 40

At the end of the G-string was Enough Cyclic Activity for Everyone2F!

Front 41

Rb?

Back 41

A protein that binds to and inactivates E2F during early G1 phase so cyclinE and cyclinA are not expressed. This protein itself is inactivated by phosphorylation from cyclinD/CDK.

Hint 41

Ronaldo blocked (Rb) Everyone2Fu**

Front 42

Cdc6?

Back 42

A licensing factor for the firing of the origins of replication; the origin cannot fire without Cdc6 recruiting other components, but can also not fire until getting rid of Cdc6. As a result, at the beginning of S phase, it is quickly tagged by cyclinA/CDK and degraded.

Hint 42

******* during cuddly sex (Cdc6) leads to a firing of the replication of the orgin of the human species.

Front 43

Cdc20?

Back 43

Once activated by CDK1, it's a subunit of APC that attaches multiple ubiquitins to lysine residues on cyclinB so it can be degraded. It also targets Securin.

Hint 43

The center for disease control (Cdc20) is targeting 20 different circular Bacteria (cyclinB) by attaching ubiquitous (ubiquitin) antibiotics to induce lysis (lysine residues).

Front 44

Securin?

Back 44

A protein that binds to and inhibits Separase.

Front 45

Separase?

Back 45

A protease that cleaves Scc1. Is activated by kinetochore bipolar tension.

Hint 45

To separate some clumsy chickens you do it bi pulling on their wings to create tension.

Front 46

Scc1?

Back 46

A protein that closes the cohesion ring that connects sister chromatids.

Front 47

Mad1?

Back 47

A protein that binds to unoccupied kinetochores, and then recruits and activates Mad2.

Hint 47

For Kyle's to leave his number #1 chore unfinshed is pure MADness!

Front 48

Mad2?

Back 48

Once activated by Mad1, it functions to pause the cell cycle by inhibiting Cdc20. Once Cdc20 is stabilized, then Securin is stabilized and Separase remains inactive.

Hint 48

The CDCs plan is MADness! It must be stopped! The bacteria must be Secured another way!

Front 49

ATR?

Back 49

A protein kinase that recognizes DNA damage and proceeds to phosphorylate a second kinase Chk1.

Hint 49

Activate Total Repair! Check!

Front 50

Chk1?

Back 50

Delays the cell cycle by phosphorylating Cdc25...

Front 51

Cdc25?

Back 51

After being phosphorylated by Chk1, it then binds to protein called 14-3-3. 14-3-3 exports Cdc25 out of the nucleus and into the cytoplasm where it is inactive. Without Cdc25's activity, cyclinB/CDK remains inactive, giving time to the cell to repair it's DNA damage before entering mitosis.

Front 52

ATM?

Back 52

Recognizes DNA damage in G1 phase, then phosphorylates and activates Chk2, that phosphorylates and stabilizes p53.

Hint 52

Activate Total Maintenance! Check#2!

Front 53

P53?

Back 53

It's a transcription factor, that when stable will activate p21, which is a CDK inhibitor. This slows down the cell cycle, giving time to repair the DNA damage. In other words, p53 is a tumor suppressor gene.

Also, when a cell has too much damage, P53 will induce apoptosis.

Front 54

MDM2?

Back 54

MDM2 acts in opposition to P53 by inducing it's degradation. MDM2 acts as an oncogene.