| MTs | Actin | Motor Proteins | Cell Adhesion | ECM |
|---|---|---|---|---|
|
What is EB1
I am a + end TIP that does not visualize catastrophe
|
What is ADF/cofilin
I accelerate the rate of - end de-polymerization and pefer ADP-actin
|
What is dynein
I walk + to - towards the centrosome, in a drunken manner
|
What is tight/occulding junctions
I act as a selective barrier/fence with help from claudins
|
What is hyaluronan?
I occupy a HUGE volume and am made of up of non-sulfated repeating disaccharides
|
|
What is pericentriolar matter
I am a lattice of MT associated proteins, containing pericenrin and gamma-TURC
|
What is Arp 2/3
I am a complex of 7 proteins and need NPFs to be active
|
What is kinesin
I mediate anterograde transport
|
What is hemidesmosomes
I link cells to the matrix with help from intermediate filaments
|
What is aggrecan
I am the main component of cartilage, you can classify me as a proteoglycan
|
|
What is CAMSAPS (Patronin)
I am the only - end MT binding protein that stabilizes MTs
|
What is formins
I follow the + end and generate non-branched filaments. I also compete with capping proteins
|
What is myosin VI
I walk towards the pointed end on actin
|
What is integrins
I am an adhesion protein that has a alpha and beta subunit with an RGD sequence
|
What is laminin
I am a glycoprotein of three chains in a cross shape and contain binding sites for integrins
|
|
What is tyrosination
This type of PTM occurs in the distal axon on alpha tubulin
|
What is tropomodulin
I am the only known - end capping protein
|
actin's + end is oriented towards the z disc, myosin walks towards + end, causing the sacromere to shorten.
How does a sacromere shorten? tell me about actin, z disc and myosin directionality.
|
What are linkage/anchor proteins?
catenins, alpha-actinin, vinculin are part of this group of proteins
|
What is talin
I am a tension sensor at cell-matrix junctions, considered an adaptor protein as well involved in inside out signaling
|
|
KD= knocking out but OE=overexpressing and over-stabilizing MTs can be deterimental as well
TACC3 stabilizes MTs. TACC3 KD slows down growth velocity by 27% but TACC3 OE also slows down growth veloctity by 11% Explain how this is possible?
|
the actin tails would become short because profilin-actin (which binds to PRDs) can no longer be recruited by Sca2 for processive elongation
What would happen to actin tails on bacteria if the proline rich domains (PRDs) on Sca2 (bacterial formin) were mutated?
|
The regulatory domain of myosin acts as its lever arm. Myosin B with 10 light chains, has a lever 5x longer than myosin B so motility is faster.
Myosin A has 2 light chains while myosin B has 10. Myosin A and B have the same duty ratio. Yet after an in vitro motility assay, you notice the gliding rate of actin is higher for myosin B. How so?
|
The activation causes a conformational change in the integrin extracellular domains, allowing binding of fibronectin, and also resulting in a conformational change inside the cells, with separation of the alpha and beta cytoplasmic domains, and hence decrease of the FRET signal. This process is called outside-in signaling.
In an experiment, resting integrin has high FRET signal. It is activated by its agonist which binds to its ligand fibronectin. You add in agonist and fibronectin and FRET signal decreases. Why? Is this inside-out or outside-in signaling?
|
Active force (actomyosin, filopodia)
Passive force (shear stress, stretch, drag, substrate rigidity)
With respect to mechanosensing, give an example each of active force versus passive force generators. Many answers. (Hint: active force=applied by cell, passive=applied to cell)
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