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58 Cards in this Set

  • Front
  • Back
What regulates cell cycle phases? (3)
a) cyclins
b) CDKs
c) tumor suppressors
which is the shortest phase of the cell cycle?
Mitosis
List the phases of the cell cycle
Prophase, Metaphase, Anaphase, Telophase
Which phases of the cell cycle are of variable duration?
G0 and G1
What are CDKs?

2 descriptive words
cyclin-dependent kinases

constitutive and inactive
what are cyclins?
specific to?
activate?
regulatory proteins that control cell cycle events;

phase specific
activate CDKs
what must both be activated and inactivated for cell cycle to progress?
Cyclin-CDK complexes
What are tumor suppressors and what do they inhibit? a mutation results in?
Rb and P53
Rb suppress G1-S
P53 suppress G1-S, S-M

mutation --> unrestrained growth
-retinoblastoma
-osteoscarcoma
where do permanent cells regenerate from? list 4 examples
from stem cells
1. neurons
2. skeletal muscle
3. cardiac muscle.
4. RBCs
give examples of 2 stable/quiescent cells (and define)
cells that can enter G1 from G0 when stimulated.
1. Hepatocytes
2. Lymphocytes
define labile cells and give 4 examples
labile cells never go to G0.
1) bone marrow
2) gut epithelium
3) skin
4) hair follicles
RER
a) site of synthesis of?
b) what is RER in neurons called?
c) what do nissl bodies do?
d) give an example of an enzyme that is made by nissl bodies. what is the function of this enzyme?
secretory (exported) proteins and of N-linked oligosaccharide addition to many proteins

b) Nissl Bodies
c) synthesize enzymes and peptide neurotransmitters
d) ChAT (choline acetyltransferase) --> makes Ach
where are cytosolic and organellar proteins made?
free ribosomes
give two examples of cells that would be rich in RER
mucous secreting goblet cells (of small intestine)

anti-body secreting plasma cells
smooth endoplasmic reticulum (SER) is the site of?

which types of cells are rich in SER? (2 examples)
steroid synthesis and detoxification of drugs and poisons

b) liver hepatocytes and steroid hormone producing cells of the adrenal cortex
Golgi apparatus
a) function
b) golgi modifies? on?
c) golgi adds? on?
d) 2 additional functions?
distribution center for proteins and lipids from ER to plasma membrane and vesicles

b) N-oligosaccharides on asparagine

c) O-oligosaccharides on Serine and Threonine
and
Adds mannose-6-phosphate to proteins for trafficking to lysosomes

d) glycosylations proteins and sulfation (of sugar and tyrosine)
which amino acids can be modified by the golgi?
serine, threonine, asparagine, tryosine
I-Cell Disease
a) stands for?
b) acquired or inherited?
c) what type of disorder?
d) caused by?
e) clinical features?
f) actual enzyme missing that causes the failure of addition of the mannose-6-phosphate?
a) inclusion cell disease

b) inherited

c) lysosomal storage disorder

d) failure of addition of mannose-6-phosphate to lysosome proteins (enzymes are secreted outside of cell instead of being targeted to lysosome)

e)
1) coarse facial features
2) clouded corneas
3) restricted joint movement
4) high plasma levels of lysosomal enzymes
5) often fatal in childhood

f) N-acetylglucosaminyl-1-phosphotransferase
COPI
-what is it, what does it stand for, what is its function
vesicular trafficking protein
-coat protein I
-retrograde (golgi--> ER)
COP II
-what is it, what does it stand for, what is its function
vesicular trafficking protein
-coat protein II
-anterograde (ER-->cis-golgi)
Clathrin
a) helps with what?
b) explain function of adaptin, clathrin, dynamin,
a) vesicular trafficking from trans-golgi --> lysosomes

plasma membrane -> endosome
(receptor mediated endocytosis)

b) cargo attaches to receptor, receptor attaches to "adaptin", clathrin attaches to adaptin and to other clathrin's attached to other adaptins . a bunch lined up attached to each other now
-dynamin pinches this bunch (vesicle)
-adaptin and clathrin recyles.
-naked vesicle (endosome) fuses with lysosome and cargo gets hydrolyzed so cell can actually use it.
what is the function of a peroxisome?
membrane enclosed organelle involved in catabolism of very long fatty acids and amino acids . also, generation of plasmalogens (imp for neural tissue)
what are three mechanisms for proteolysis?
a) degradation within lysosome
b) Calcium dependent enzyme
c) ubiquitin mediated proteosomal degradation
what is the shape and function of a proteosome?
a barrel-shaped protein complex that degrades damaged or unnecessary proteins tagged for destruction with ubiquitin
Microtuble
a) what is the shape of a microtubule?
b) what is a microtubule composed of?
c) what is bound to each dimer?
d) what are three structures that microtubules are incorporated into?
e) compare the speed of microtuble growth vs collapse
f) microtubules are involved in what kind of transport?
g)what do molecular motor proteins do?
h) dynein does what? what dir, +/- signs
i) kinesin does what?
a) cylindrical
b) helical array of polymerized dimers of alpha and beta tubulin
c) 2 GTP
d) flagella, cilia, mitotic spindle
e) grow slowly, collapse quickly
f) slow axoplasmic transport in neurons
g) transport cellular cargo toward opposite ends of microtubule track
h) retrograde to microtuble (+-->-)
i) anterograde to microtuble (- -->+)
list 5 types of drugs that act on microtubules and what they are used to treat.
1)mebendazole/thiabendazole(antihelminthic)
2) Griseofulvin (antifungal)
3) Vincristine/Vinblastine (anti-cancer)
4) Paclitaxel (anti-breast cancer)
5) Colchicine (anti-gout)
Chediak-Higashi Syndrome
a) what is it?
b) results in?
a) Microtuble polymerization defect resulting in decreased fusion of phagosomes and lysosomes (phagosomes need MT to get to places in the cell)

b) recurrent pyogenic infections,
partial albinism,
peripheral neuropathy
a) describe Cilia Structure
b) on what subunit is the dynein ATPase attached to?
c) what allows cilia to move in a coordinate fashion?
9+2 arrangement of microtubles.
9 dimers outside ring, 2 in center.
b) to the A subunit
c) gap junctions (communication)
Kartagener's Syndrome
a) what is it?
b) results in?
c) associated with?
d) also called?
a) immotile cilia due to dynein arm defect
b) male/female infertility (sperm immotile)
bronchiectasis, recurrent sinusitis (bacteria and particles not pushed out)
c) situs inversus
d) primary ciliary dyskinesia
cytoskeletal elements

actin and myosin make/involved in (4)?
microvilli, muscle contraction, cytokinesis, adherens junctions
cytoskeletal elements

microtuble
a) function
b) form/examples/function (5)
a) movement
b) cilia, flagella, mitotic spindle, axonal trafficking, centrioles
cytoskeletal elements

intermediate filaments
a) function
b) examples
a) vimentin, desmin, cytokeratin, lamins (ABC), glial fibrillary acid proteins (GFAP), neurofilaments (axons), peripherin (neurons)
plasma membrane composition
a) describe
b) contains? how much?
c) what happens if high cholesterol or high long saturated FA content?
a) asymmetric bilayer
b) cholesterol (50%), phospholipids (50%),
sphingolipids, glycolipids, proteins
c) increased melting temperature, decreased fluidity (no double bonds)
Vimentin
a) cytoskeletal component?
b) cell type?
c) id?
a) Intermediate filaments
b) connective tissue
c) sarcoma, some carcinoma
desmin
a) cytoskeletal component?
b) cell type?
c) id?
a) intermediate filament
b) muscle
c) rhabdomyosarcoma, leomyosarcoma
cytokeratin
a) cytoskeletal component?
b) cell type?
c) id?
a) intermediate filaments
b) epithelial cells
c) carcinoma, some sarcoma
GFAP
a) cytoskeletal component?
b) cell type?
c) id?
a) intermediate filament
b) neuroglia
c) astrocytoma
Neurofilaments
a) cytoskeletal component
b) cell type?
c) id?
a) intermediate filaments
b) neurons
c) adrenal neural blastoma (primitive neuroectodermal tumor)
Sodium Pump
a) located where?
b) ATP site is on what side?
c) ratio?
d) explain whats going with ATP and the pump
e) name 2 drugs that inhibit sodium pump
a) Na+-K+ ATPase in the plasma membrane
b) ATP site on the cytoplasmic side
c) 3 Na+ leave the cell, 2 K+ enter the cell
d) ATP attaches, gives phosphate (pump is phosphorylated), 3 Na leave. then, phosphate given off, 2 K+ enter.
e) Ouabain, Cardiac Glycosides
what does Ouabain do?
Ouabain inhibits the sodium potassium pump by binding to the K+ site
how do cardiac glycosides work? give two examples.
Digoxin, Digitoxin.

directly inhibit Na/K ATPase (sodium out, K in), which leads to indirect inhibition of Na/Ca (sodium in, calcium out) , therefore increase in intracellular calcium.

increased calcium = increased cardiac contractility.
what is the most abundant protein in the body?
collagen
a) what is the function of collagen generally?
b) type 1
c) type 2
d) type 3
e) type 4
a) organize and strengthen extracellular matrix
b)1: strong: bone, skin, tendon, dentin
c) 2: slippery: carTWOlage (hyaline), vitreous body, nucleus pulposis
d) 3: bloody: reticulin, skin, blood vessels, uterus, fetal tissue, granulation tissue
e) 4: basement membrane or basal lamina (of kidneys, ears, eyes)
collagen synthesis: step 1
1) synthesis (RER): translation of collagen alpha chains (pre-pro-collagen) . usually glycine-x-y (proline, lysine)
collagen synthesis: step 2
in ER. hydroxylation of specific proline and lysine residues (requires vitamin C)
collagen synthesis: step 3
in ER. glycosylation of pro-alpha-chain hydroxylysine residues and formation of procollagen via hydrogen and disulfide bonds (triple helix of 3 collagen alpha chains)
collagen synthesis: step 4
exocytosis of procollagen into extracellular space
collagen synthesis step 5
proteolytic processing. cleavage of terminal regions of procollagen transforms it into insoluble tropocollagen
collagen synthesis step 6
cross-linking. reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (by lysyl oxidase) to make collagen fibrils.
collagen synthesis: step 1-6 titles
1: synthesis (RER) : pre-procollagen alpha
(glysine-proline-lysine)
2: hydroxylation: proline lysine residues
3: glycosylation: of pro-alpha-chain hydroxylisine + procollagen by hydrogen bonds/sulfides (triple helix of 3 alpha chains)
4: exocytosis
5: proteolytic processing. cleavage (proteolysis) of terminal regions of procollagen -->tropocollagen (insoluble)
6: cross-linking: reinforcement of staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (by lysyl oxidase) to make collagen fibrils
osteogenesis imperfecta
a) also called?
b) how do you get it?
c) mc form inheritance? type? collagen?
d) 4 clinical features
e) why the blue sclera?
f) what can this disease be confused with?
g) type II incidence? clinical features?
a) brittle bone disease
b) inherited
c) AD, type 1, type 1 collagen
d) multiple #s, blue sclerae, hearing, dental
e) translucency of CT over choroid
f) child abuse
g) 1:10,000, fatal in utero or neonatal period
Ehlers-Danlos Syndrome
a) what is it?
b) 3 clinical features?
c) how many types?
d) 3 associations?
e) which type of collagen most frequently affected?
a) faulty collagen synthesis
b) 1) hyperextensible skin, 2) hypermobile joints, 3) tendency to bleed (easy bruising)
c) 6 types
d) berry aneurysms, organ rupture, joint dislocation
e) type III
Alport Syndrome
a) cause?
b) whats abnormal?
c) inheritance of mc form?
d) characterized by?
a) variety of gene defects
b) type IV collagen
c) X-linked recessive
d) progressive hereditary nephritis & deafness. maybe ocular disturbance. (lenticonus: thinning around capsule of lens)
elastin
a) where is elastin found?(5)
b) what is the function of ligamenta flava
c) elastin is rich in what amino acids? what forms of these?
d) how is elastin held together?
e) what breaks down elastin?
f) what inhibits elastase?
1) lungs 2) large arteries 3) elastic ligaments 4) vocal cords 5) ligamenta flava

b) ligamenta flava connect vertebrae --> relaxed and stretched conformations

c) proline, glycine (non-hydroxylated forms)

d) tropoelastin with fibrillin scaffolding
e) elastase
f) alpha 1 antitrypsin
Marfan's Syndrome
a) what is it
b) clinical features
caused by a defect in fibrillin

b) hyperelastic joints, problem with heart valves, aorta (dissection), tall long limbs, arachnodactyly
Emphysema
a) cause
a) alpha 1 antitrypsin deficiency (excess elastase activity)
why do we get wrinkles?
reduced collagen and elastin production
c
c