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228 Cards in this Set

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What determines the strength of cell adhesion?
receptor density: often multiple weak binding interactions rather than 1 or 2 strong interactions
How do receptors interact with cytoskeleton?
usually through adapter proteins
What type of interactions lead to cell-signaling?
ligand-receptor interactions cause changes in gene expression, secretion, motility
What category of molecules connects ECM to cells?
adhesive glycoproteins such as laminin and fibronectin
What do laminin and fibronectin bind to?
different subtypes of integrins (transmembrane R's) via RGD sequences
What is the fxn of fibronectin?
helps to connect ECM to cells
Explain the structure of fibronectin.
large glycoprotein
forms dimers
"MODULAR" binding sites for ECM material and for cell surface receptors
What do the modular binding sites on fibronectin contain?
RGD sequences (Arg Gly Asp)
3 aa sequences
What binds the RGD sequences on fibronectin?
integrins
what secretes fibrillar fibronectin?
fibroblasts
When does fibronectin form dimers?
when binding to integrins at cell surface ..this stimulates fibril formation with other fibronectins via disulfide bond crosslinks
What adhesive glycoprotein is reqd for embryogenesis?
fibronectin
What happens with cells grown on matrix of fibronectin fibrils?
they flatten out and assemble intracellular actin bundles (stress fibers) aligned with fibronectin fibrils; intracellular actin filaments also promote assemby, orientation of fibronectin fibrils (they work together to secrete an oriented matrix)
What is the job of integrins?
they connect ECM to actin cytoskeleton
What is the structure of integrins?
alpha/beta heterodimer
many alpha and beta genes exist, alternatively spliced with subunits pairing in multiple ways
Wht is a ubiquitous membrane protien in our body?
integrins
What do integrins bind?
collagens, fibronectin, and laminin through many weak interactions that allow cell migration
What links the ECM with intracellular signaling?
integrins
the signalling is a adhesion-dependent activation of cytosolic signaling proteins that regulate anchorage-dependent growth
What effect do growth factor dependent cascades have on integin clustering?
they reverse integrin clustering, reduce adhesion=more cell mobility
What is Leukocyte Adhesion deficiency a mutation in?
integrin mutation..mutations in beta2 integrin preventing homodimerization..impaired leukocyte chemotaxis, extravasation, and capillary basement transmigration. patients suffer from repeated life threatening infections
absence of what leads to embryonic death/failure to implant?
integrin mutation..absense of beta1i integrin
What are the adaptors for integrin and actin?
vinculin and talin
What crosslinks actin stress fibers?
alpha actinin
What results in the clustering of integrins ?
vinculin and talin attach actin to integrin. alpha-actinin then cross links actin strss fibers bringing the integrins closer together and causing them to bind ECM proteins more tightly
How do integrins signal?
through focal adhesion kinase (FAK), regulating Rho and Arf
What are used as "feet" in migrating cells?
focal contacts
What results in a focal adhesion?
integrins binding to actin stress fibers and fibronectin
What results in a hemidesmosome?
integrins bind IFs (keratins) via adaptor proteins and to laminin
hemidesmosomes and focal adhesions are both what?
anchoring jxns..focal contacts used for mobility
What is the fxn of hemidesmosomes?
the link cells to EXM through integrins
What is the strongest anchor b/n cell and ECM?
hemidesmosomes
they form the basal surface in epithelial cells and basement mem. ..making them nonmotile
What are the IF's of hemidesmosomes embedded in?
keratins are embedded in plaques containing plectin
What links the plectin plaques in hemidesmosomes to laminin?
integrins
what anchors hemidesmosomes in ECM?
collagen VII fibrils in ECM
"anchoring collagen"
what causes the autoimmune blistering disease known as Bullous Pemphigoid?
autoantigens to hemidesmosomal antigens causing a disrupption in dermal-epidermal jxn leading to supepidermal blisters
What G proteins are important for cell mobility?
Rac and Cdc42
What G protein determines Filipodia movement?
Cdc42
What G protein determines Lamellipodia movement?
Rac
What is Lamellipodium?
leading edge of moving fibroblast..extended with broad, flattened ruffly veil projection
What is Filipodia?
thin spike like protrusions at leading edge of moving cell
Forces generated where move a cell foward?
in the actin rich cortex
What happens at leading edge of cell to protrude lamellipodium?
actin polymerization the move the edge foward by stretching actin cortex
What propels the cell body forward to relax tension?
contraction
Action of Rac in cell mobilty?
rearranges actin to stretch front out in a lamellopodium
How does Rho participate in cell mobility?
it mediates the formation of new focal contacts (induce assembly of new focal adhesions and cortical contraction)
Describe what leads up to fibrin forming the blood clot scaffold.
blood platelets aggregate, release granules containing platelet-derived growth factors (PDGF) and TGF-b
Vasoactive factors increase blood vessel permeabiliy and plasma fibrinogen cleaves to become fibrin
What is the job of PDGF?
attracts fibroblasts, immune cells which are then activated to secrete matrix metalloproteinases (MMPs) and fibroblast growth factors (FGFs)
What is the job of MMP's?
degrade ECM to remodel
What are the 4 fxns of MMP?
1. clear path through matrix
2.expose sites on cleaved proteins that promote cell binding and/or migration
3.promote cell detachment from matrix
4.release extracellular signal proteins that stimulate cell migration
What facilitates tissue remodeling?
MMP's
What are MMP's?
Zn dependent enzymes whose fxn is to degrade ECM at neutral pH
How are MMP's secreted?
as zymogens b/c we don't want them degrading anything and everything
** they only fxn following activation by other proteases
What is increased MMP activity involved with?
invasion and metastatis of cancer (ovary, lung, prostate, breast, pancreas)
What is the inactive plasminogen zymogen activated to? Fxn?
plasmin
breaks up clots
What cleaves plasminogen to plasmin?
tissue-type plasminogen activators (tPA) that breaks up blood clots after heart attack or stroke restoring blood flow
What is the fxn of tissue-type plasminogen activator?
converts inactive plasminogen to plasmin
**impt in dissolving clots b/c they activate the molecule that is largely responsible for chewing up the proteins that comprise the clot
What do serine proteases do?
activate zymogens (plasmin activates plasminogen)
What are the fxns of TIMPs and serpins?
negative regulators of proteases..keep enzymes in their inactive form
*they confine action of proteases to specific areas
What secretes TIMPs and serpins?
cells at margins of active protein degradation for PROTECTION
What do TIMPs inhibit?
MMPs
What do serpins inhibit?
serine proteases (plasmin, tPA)
What happens to plasminogen when converted to plasmin?
it bececomes active and fxns as a serine protease
what occurs in the E-M transition during wound healing?
epithelial cells around wound edges become fibroblast-like
-they lose their intercellular jxns
-unanchor from basal lamina
-form lamellipodia
-migrate to fill space (cover wound)
What occurs in the M-E transition during wound healing?
morph into epithelial cells to reheal..epithelium reconstucted, cell-cell, cell-ECM contacts reform
What transmembrane proteins use in recreating cell-cell jxns?
adherins jxns use E-cadherins
What is formed in response to wound healing?
new capillaries
During wound healing , what does the shortage of oxygen cuase? Fxn?
increase in hypoxia-induced factor 1 (HIF-1) that stimulates transcription of vascular endothelial growth factor (VEGF) gene
What is VEGF related to ?
PDGF
Why is VEGF mRNA stability and transcription tightly regulated?
dont want a lot of vasculature in cornea where it should be transparent
Besides activate VEGF, what else does HIF stimulate?
increase in glycolytic enzymes to enhance anearobic glucose metabolism
What does VEGF act on? HOw?
endothelial cells
-first MMPs degrade basal lamina of parent capillary
-endothelial cells migrate toward source of signal
-cells proliferate
-cells form tubes and differentiate into new capillary branch
What regulates VEGF? HOw?
HIF-1
as new vessels form, oxgyen levels rise, HIF-1 declines and VEGF production shuts off, angiogenesis halts
What is the normal level of HIF-1?
normally low due to continual degradation of HIF-1 by ubiquitylation
(see ubiquitin think degradation)
What do tumors resemble
wound healing sites
Why is there clumps of fibrin in tumor-associated stroma?
due to leak capillaries
from ECM for migrating cells
Why do many cancer cells continuously release?
PDGF that acts as a mitogen, stimulating growth particularly of stromal cells with PDGF R's:fibroblasts, smooth muscle cells, macrophages.
The stromal cells then incrase remodeling through MMP's
When cancer cells release PDGF what does it act as?
mitogen stimulating growth of stromal cells that then icrease remodeling through MMPs
Carcinogenesis cause a reverse in what?
reversibilty of EMT-MET in carcinogenesis
How does carcinogenesis work?
epithelial cancer cell invades stroma, stroma receives signal to become mesencymal. Now that they are fibroblast like they invade though basmement membrane, intravasate into circulation and extrvasate out as MET and metastasize
What can MMPs be secreted from?
stromal cells or cancer cells and create a space for cells to move and invade
What MMP is hugely associated with cancers?
MMP-9
What leads to activation of MMPs
activation of urokinase plasminogen activator (uPA)
What do stromal cells release?
inactive uPA that can bind to uPA receptor on cancer cells and becomes activated
After uPA is activated by cancer cells what does it do?
it coverts plasminogen to plasmin. plasmin then activates MMPs
What do human prostate cells make and secrete?
uPA leading to metastasis
Why do many cancer cells continuously release?
PDGF that acts as a mitogen, stimulating growth particularly of stromal cells with PDGF R's:fibroblasts, smooth muscle cells, macrophages.
The stromal cells then incrase remodeling through MMP's
Why do many cancer cells continuously release?
PDGF that acts as a mitogen, stimulating growth particularly of stromal cells with PDGF R's:fibroblasts, smooth muscle cells, macrophages.
The stromal cells then incrase remodeling through MMP's
When cancer cells release PDGF what does it act as?
mitogen stimulating growth of stromal cells that then icrease remodeling through MMPs
Carcinogenesis cause a reverse in what?
reversibilty of EMT-MET in carcinogenesis
How does carcinogenesis work?
epithelial cancer cell invades stroma, stroma receives signal to become mesencymal. Now that they are fibroblast like they invade though basmement membrane, intravasate into circulation and extrvasate out as MET and metastasize
When cancer cells release PDGF what does it act as?
mitogen stimulating growth of stromal cells that then icrease remodeling through MMPs
Carcinogenesis cause a reverse in what?
reversibilty of EMT-MET in carcinogenesis
What can MMPs be secreted from?
stromal cells or cancer cells and create a space for cells to move and invade
What MMP is hugely associated with cancers?
MMP-9
How does carcinogenesis work?
epithelial cancer cell invades stroma, stroma receives signal to become mesencymal. Now that they are fibroblast like they invade though basmement membrane, intravasate into circulation and extrvasate out as MET and metastasize
What can MMPs be secreted from?
stromal cells or cancer cells and create a space for cells to move and invade
What leads to activation of MMPs
activation of urokinase plasminogen activator (uPA)
What do stromal cells release?
inactive uPA that can bind to uPA receptor on cancer cells and becomes activated
What MMP is hugely associated with cancers?
MMP-9
After uPA is activated by cancer cells what does it do?
it coverts plasminogen to plasmin. plasmin then activates MMPs
What leads to activation of MMPs
activation of urokinase plasminogen activator (uPA)
What do stromal cells release?
inactive uPA that can bind to uPA receptor on cancer cells and becomes activated
What do human prostate cells make and secrete?
uPA leading to metastasis
After uPA is activated by cancer cells what does it do?
it coverts plasminogen to plasmin. plasmin then activates MMPs
What do human prostate cells make and secrete?
uPA leading to metastasis
Why do many cancer cells continuously release?
PDGF that acts as a mitogen, stimulating growth particularly of stromal cells with PDGF R's:fibroblasts, smooth muscle cells, macrophages.
The stromal cells then incrase remodeling through MMP's
When cancer cells release PDGF what does it act as?
mitogen stimulating growth of stromal cells that then icrease remodeling through MMPs
Carcinogenesis cause a reverse in what?
reversibilty of EMT-MET in carcinogenesis
How does carcinogenesis work?
epithelial cancer cell invades stroma, stroma receives signal to become mesencymal. Now that they are fibroblast like they invade though basmement membrane, intravasate into circulation and extrvasate out as MET and metastasize
What can MMPs be secreted from?
stromal cells or cancer cells and create a space for cells to move and invade
What MMP is hugely associated with cancers?
MMP-9
What leads to activation of MMPs
activation of urokinase plasminogen activator (uPA)
What do stromal cells release?
inactive uPA that can bind to uPA receptor on cancer cells and becomes activated
After uPA is activated by cancer cells what does it do?
it coverts plasminogen to plasmin. plasmin then activates MMPs
What do human prostate cells make and secrete?
uPA leading to metastasis
What induces the mobility of filopodia allowing them explore environment
epidermal growth factor induced mobility **this is important for breast cancer cell invasiveness..Rho, Rac and Cdc42 are involved
How do some small tumors "co-opt" exisiting vessels?
tumor cells grow along blood vessels. as they grow this leads to hypoxia and necrosis, angiogensis is then stimualated b/c of the hypoxia (HIF activated..activating VDGF)!
What is the diff b/n angiogenesis and vasculogenesis?
angio: formation of new blood vessels from pre-existing ones
vasculo:formation of new blood vessels where there are no pre-existing ones
Once angiogensis is stimulate, wat do tumor cells do?
invade into new blood vessels and travel creating metastatic sites
How is tumor vasuclature different from normal?
normal: very orderly, unbranched, nearly parallel vessels
tumor: coiling, irregularity, size heterogeneity, branched
What is the problem in von Hippel-Lindau (VHL) syndrome?
1 fxnl copy of VHL gene..defects in VHL that encodes for ubiquitin ligase
2nd mutation in good copy of VHL leads to uncontrolled HIF-1 causing overproduction of VEGF requardless of oxygen availability..leads to hemangioblastomas of CNS and retina (blood vessel tumors)
What happens in VHL syndrome to mutant cells that produce VEGF?
they proliferate by over-rich nourishment=viscous cycle promoting tumor growth
Why would an ubiquitin ligase produce pathology observed in VHL syndrome?
b/c ubiquitin normally keeps HIF-1 levels low by degradation. w/o it HIF is uncontrolled
What are the 3 major cytoskeletal fibers?
IF
MT
Microfilaments (actin)
What 2 cytoskeletal fibers are most closely alike?
IF and MT
Microfilaments are quite different
What is desmin?
IF of muscle
holds myotubules together in muscle cells
What are keratins?
epithelial IF
Where are IFs in cell?
surround nucleus then create a web throughout the cell, finally hooking up hemidesmosomes and desmisomes
What is the diff b/n desmisomes and hemides?
desmosomes: cell-cell adhesion
hemi: cell-ECM adhesion
What is the fxn of IF's?
tie cells to one another, and anchor cells to ECM
-limit max stretching of cells
what do IF's do as cells deform?
they limit max stretching of the cell before cell ruptures
What might happen if a patient has disfnxl keratins (epithelial IFs) as in Epidermolysis bullosa simplex?
skin can no longer withstand tensile forces, cells rupture leading to blistering
Does the assmebly of IF subunits into filaments require ATP or GTP?
no
and..IF subunits DO NOT bind nucleotides
Describe the structure of IFs.
great in tension
filaments made of 8 tetramers
as a tetramer, filament has NO polarity thus cannot be used as a track for a motor; only as a rope
-alpha-helical rods that assemble into ropelike filaments
What are IFs great for?
tension
acts as a rope
how is a IF tetramer created?
from the staggering of 2 coiled-coil dimers to form tetramer
then 2 tetramers pack together end to end and are twisted into a ropelike filament
8 tetramers form a filament!
What is the location of IF's ?
extend from the nucleus to the cell membrane
What do IFs crosslink with and how?
crosslink with other filaments like MT via plectin (linker adaptor protein)
What are lamins?
nuclear IF's that form a structural net on the inner surface of the nuclar envelope
What happens to lamins during mitosis?
1. they are associated with chromatin and the inner nuclear membrane during interphase.
2. during mitosis, they are phosphorylated by a cdk Kinase that triggers net breakdown
3. vesicles of the fragmented nuclear envelope remain bound by Lamin B to allow quick envelope reformation during telophase
What is the problem in Emery-dreifuss Muscular dystrophy?
mutated A or C lamin or a lamin connector--EMERIN
EMERIN is essential for normal fxn of skeletal and cardiac muscle
Progeria is also lamin related
what are neurofilaments?
axonal IF's
What is the disease marker of ALS?
NF tangles
What do NF's do?
they crosslink in an axon to create strong structure; this is needed b/c of extremely long length and narrow girth of axon
What crosslinks NF's to MT?
plectin
Where would you find NF's ?
in areas with lots of axons
Compare purpose of NFs vs MTs.
NF's: structure
MT's: transport
What is the IF of the muscle Z disc?
desmin
What does desmin do?
adds integrity to the sarcomere and myotube
Where will you find desmin in muscle?
areound each myofibril at the Z disk
What are GFAPs?
glial fibrillary acidic protein in astrocytes of CNS
* specific astroglial marker
Why are IFs used to identify the cellular origin of certain tumors?
typcially tumor cells lose their normal appearance so we can't tell where they came from. However, they retain many of the differentiated properties of the cells from which they were derived, including expression of certain IF proteins. So now we use fluor-labeled Ab to determine if tumor originated in epithelial, mesenchymal or neuronal tissue. if so.. it indicates metastisis
EX: a cell that was once an astrocyte then became a tumor cell will still contain GFAP so you will know that it originated in the CNS
What do ALS, Alzeimers, MS all exhibit?
abnormal tangles of protein: glial tangles, lewy bodies (NF tangles)
What is vimentin?
mesenchymal IF's
found in CT, muscle cells and neuroglial cells
What cell type will have lamins?
every cell type b/c tehy are associated with inner membrane of nucleus
Which cytoskeletal fiber is the only one w/o polarity?
IF's
Do IFs have enzymatic activty? what about MT and actin(microfilaments)?
IF's NO enzymatic activity
MT: GTPase
actin: ATPase
Describe the motor proteins of the cytoskeletal fibers.
MT: kinesins, dynein
IF: none b/c no polarity
actin:myosin
Compare the strcutre of the cytoskeletal fibers.
MT: stiff, hollow tube
IF:tough, rope-like fiber
actin:flexible, helical filament
what are IF's lousy at?
compression unlike MT
What characteristics are seen in Kartagener syndrome patients?
infundibular pulmonic stenosis
chronic renal failure
azospermia
situs inversus
**all MT axonemal related movement has been affected (flagellar movement in sperm)
Why is there no flagellar movement in kartagener syndrome?
b/c the motion of sperm tails depend on MT and in this sydrome there is no dynein motors
What are the 4 cytoskeletal fxns?
1. structure and support
2. intracellular transport
3. contractiltiy and motility
4. spatial organization
what are 2 ways in which movement is driven by?
1. motors on tracks
2. elongation and shrinkage of the tracks themselves
What are the minus ends of MT anchored to?
MTOC, near nucleus, MT then radiate outward towards cell periphery
What are MT made of?
tubulin dimers that add to protofiliaments to form tube that is hollow
describe the MT subunit/building block.
it is a alpha beta heterodimer of tubulin that stack to form tubulin dimers
These dimers are what are added or subtracted from tube in movement
what is the most rigid of filaments?
MT good in tension and compression
describe the MT motors:
kinesins: antegrade movement (plus directed)
dyneins: retrograde movement (minus directed)
Is tubulin tissue specific like IF's ?
no, same tubulin in every tissue
What is used as a scaffold for growth in the MTOC (centrioles)?
gamma tubulin
Which tubulin hydrolyzes GTP to GDP?
only beta; it is primed with GTP by replacement of GDP with GTP by GEF
What end of MT do dimers add to?
plus end: dimers add to plus end more easly espeically BEFORE GTP is hydrolyzed
beta tubulin end is + end
What does the + end of MT always have exposed?
beta tubulin to hydrolyze GTP
(GTP cap lost when hydrolyzed) You add to GTP cap before hydrolyzed
What happens if GTP is hydrolyzed to GDP before next dimer is added?
puase in growth, a GDP cap
What happens with the MT is shrinking?
GDP tubulin is released to the cytosol (tubulin molecules have bound GDP)
Shrinking means that hydrolysis catches up with dimer addition--addition needs to proceed faster than GTP hydrolysis
What is the tubule construction order?
tubulin monomer
tubulin dimer
protofilament
MT
axoneme
How many protofilaments make up singlet tube? and what are they for?
singlets:13 protofilaments
used to carry and move vesicles, organelles, etc
What are doublets for? triplets?
doublets:make up cilia and flagella
triplets: 9 triplets make up centrioles (MTOC)
describe the directionality of MT w/n cell?
minus end anchored at MTOC near nucleas with pos end extending out towards periphery
Where do MT start growing from?
gamma tubulin (nucleating sites) lining the pores in the sphere surrounding the centrioles (pericentriolar material)
What are basal bodies?
MTOC under cilia and flagella
describe the structure of MTOC/centrioles.
short cylinders
made up of 9 triplet MT connected by radial spokes to one another
contain gamma tubulin
Why do axons require an intracellular transport system?
b/c can't use diffusion to travel length-takes too long over long distances therefore need axonal transport
What do both kinesins and dyneins need to drive movement?
ATP needed for every step it takes to move cell body. It first binds to MT then ATP exchange takes place..hydrolysis leads to movement
What viruses can be carried by axonal transport?
rabies
herpes
west nile
tetanus
What types of diseases are linked to problems in axonal tranpsort?
neurodegenerative disease like CMT, parkinsons, alzheimers..find neuronal tangles
what is tau?
microtubule associated protein (MAP) that is involved in AD neurodengerative disease b/c it falls to a critical level and now MT depolymerize and disrupts axonal transport
What is the biomarker for AD in living patients?
abundance of MAP (tau in CSF)
What 2 types of MTs are involved in chromosome movment?
spindle MT and kinetochore MT
they line up chrom on metaphase plate, pull daughter chromatids apart
What drives flagellar and ciliary movement?
MTs
What is similar b/n cilia and flagella?
thy share an axonemal structure and dynein motor driven movement
describe the structure of axoneme.
9+2 arrangement; 9 doublets (outside) and 2 singlets (inside)
dynein motors
MTOC's are basal bodies
in intact flagellum, what is bending a consequence of?
dynein motion and the contraint of linkage proteins
What does Taxol block?
MT disassembly
What do Vinblastin, Vincristine, Colchicine block?
MT assmebly
What drugs block MT assembly used in chemotherapy?
Vinblastin, Vincristine, Colchicine
What drugs block MT disassemby ?
Taxol
What does Vinblastine bind?
tubulin, thereby inhibiting the assembly of MTs
What does Taxol bind?
MT and inhibits their depolymerization into tubulin: blocks cells ability to break down the mitotic spindle during mitosis
How are microfilaments (actin) similar to MT?
they form tracks with motors to create movement by either changing track length or using motors to propel tracks or carry items along a fixed track
What is the fxn of Arp 2/3?
Arp= actin related proteins
are small G proteins that nucleates actin monomers into dimers and trimers
How are microfilaments made/
G-actin monomers are nucleated by Arp to form dimers and trimers. Monomers need a bound ATP to then add to form F-actin filament. GEF exchanges ADP for ATP so the monomer can add
What is the rate of elongation or shortening of microfilaments dependpent on?
level of ATP-G-actin..if the monomers don't have bound ATP they won't add to filmaent
are microfilaments a double helix?
no they jsut look like one but it is single chain of F-actin
What happens in microfilament formation when the concentration of both monomers and ATP is high?
monomers are added to both ends but faster at the + end
when the concentration is low, it will add to the + end but come off the minus end
What is treadmilling?
when the monomer addtion to + end is matched by removal from the - end; filament length remains constant
In microfilaments what is capped?
F-actin to maintian stable length like in skeletal muscle
F-actin is also crosslinked and bundled
Why do certain Arps severe F-actin?
to modulate the ratio of gel:sol in the cell cortex
What does dystrophen do?
links actin to plasma membrane and ECM indirectly
when nonfxnl-DMD
What is the structural protein of microvilli?
actin--it is crosslinked by crosslinking proteins to strengthen the actin cytoskeleton
What are stereocilia packed with?
f-actin..they are more like microvilli b/c normally MT are packed with actin

*participate in hair cells for hearing
HOw does Listeria use the host cell's actin polymerization process?
it binds to the reptors on host cell stimuluing signals to PIP2-PIP3-Rac-PAK to drive their own motility
how does ARP participate in actin branching?
it promotes branchpoint formation by nucleating actin monomers
what motor proteins drive actin forward?
myosin
what are actin uses?
structural; in microvilli and stress fibers that connect to hemidesmosomes; lamellar movements
where is Myosin II found?
skeletal muscle
it is twisted together as a dimer
the head splits ATP
What does titin do? What does nebulin do?
titin: holds thck filament to Z disc
nebulin: stabilizes actin filament and extends from Z line to lenght of thin filaent
What does M line do?
holds thick filaments in register
in the power cycle, what happens when ATP binds myosin head?
it releases head from thin filament then splitting ATP, energizing head
What happens in power cycle when ADP-bound myosin head binds actin?
Pi comes off after binding actin then power stroke occurs and ADP comes off with the movement
What important stage of mitosis is actin important in?
cytokinesis
**also vescicular transport like MT
What small g proteins control actin assembly and organizatin?
Arf
Rab
Ran
*Rho -key player in actin that triggers movement during development
What g protein regulates actin cytoskeleton?
Rho--requires GAPs and GEF
What g protein is involved in growth factor signals?
Ras
What are some drugs that disrupt microfilaments?
cytochalasin D (mold)
Phalloidin (mushroom)
Latrunculin (sponge)
what does Phalloidin do?
binds to microfilament and freezes growth
What does cytochalasin D do?
binds to plus end of microfilaments, stops growth, minus end depolymerizes