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62 Cards in this Set
- Front
- Back
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what is the shortest phase of the cell cycle
4 phases within that phase |
mitosis
prophase-meta-ana-telo |
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4 phases of the cell cycle
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G1, S, G2, Mitosis
G= gap S=synthsis |
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3 phases of the cell cycle associated with interphase
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G1, S, G2
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What are cyclins
When are they expressed |
regulatory proteins that bind to CDKs and activate them, promoting progression through cell cycle
Phase specific - different cyclins expressed at different points in the cell cycle |
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What are CDKs
When are they expressed When are they activated |
Cyclin-dependent kinases, regulate progression through the cell cycle
expressed constitutively activated when bound to cyclin |
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2 tumor suppressors that inhibit G1 to S progression
What happens when these are mutated |
p53, Rb
When mutated, unrestrained growth of cell can occur |
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What are permanent cell types
examples |
cells that remain in G0, regenerate from stem cells
Neurons, skeletal and cardiac muscle, RBCs |
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What are stable (quiescent) cell types
2 examples |
enter G1 from G0 when stimulated
Hepatocytes, lymphocytes |
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What are labile cell types
examples |
Never go to G0, divide rapidly with a short G1
bone marrow, gut epithelium, skin, hair follicles |
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2 events that occur in the RER
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1. synthesis of secretory proteins
2. addition of N-linked oligosaccharides to many proteins |
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What are Nissl bodies and what do they do?
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RER in neurons
Synthesize enzymes and peptide neurotransmitters |
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What are free ribosomes and what do they do?
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ribosomes that are unattached to any membrane, synthesize cytosolic and organellar proteins
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Difference between proteins synthesized in RER vs. free ribosomes
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RER = secretory proteins
Free = cytosolic and organellar proteins |
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Small intestine mucus-secreting goblet cells
Ab-secreting plasma cells What organelle are these rich in? |
RER
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Site of steroid synth and detox of drugs and poisons in the cell
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Smooth ER
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LIver hepatocytes
Steroid hormone-producing cells of adrenal cortex Which organelle are these rich in? |
SER
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Organelle responsible for distributing proteins and lipids from ER to PM, lysososomes, and secretory vesicles
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golgi
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Function of golgi on
a. asparagine b. serine, threonine c. lysosomal proteins d. proteoglycans, tyrosine |
a. modifies N-oligosaccharides
b. adds O-oligosaccharides c. adds mannose-6-phosphate to specific lysosomal proteins --> targets the protein to the lysosome d. assembles proteoglycans, sulfates sugars on proteoglycans and tyrosine |
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Vesicular trafficking proteins
Retrograde transport from golgi to ER |
COPI
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Vesicular trafficking proteins
Antegrade transport from RER to cis-Golgi |
COPII
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Vesicular trafficking proteins
Transport from trans-Golgi --> lysosomes, plasma membrane --> endosomes (receptor-mediated endocytosis) |
Clathirin
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Patient has
-coarse facial features -clouded corneas -restricted joint movement -high plasma levels of lysosomal enzymes dx? pathogenesis? course? |
I-cell disease (a lysosomal storage disease)
Failure of addition of mannose-6-phosphate to lysosome proteins --> enzymes that should go to the lysosome are instead secreted outside the cell Fatal in childhood often |
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Microtubule
structural makeup |
cylinder composed of a- and b-tubulin dimers in a helical array
each dimer has 2 GTP bound |
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Functions of Microtubules
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1. incorporated into flagella, cilia, mitotic spindles
2. axoplasmic transport in neurons |
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Microtubules
how fast does it grow and collapse |
grows slowly
collapses quickly |
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What are molecular motor proteins?
What are 2 examples and what do they do? |
transport cellular material along microtubule tracks
dynein = retrograde to microtubule (pos --> neg, towards center of cell) kinesin = antegrade to microtubule (neg --> pos, towards periphery of cells) |
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5 drugs that act on microtubules
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1. mebendazole/thiabenazole (antihelminth)
2. Griseofulvin (antifungal) 3. Vincristine/vinblastine (anticancer) 4. paclitacel (anti-breast cancer) 5. Colchicine (anti-gout) |
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Patient has
-recurrent pyogenic infections -partial albinism -peripheral neuropathy dx? pathogenesis |
chedaiak-higashi syndrome
microtubule-polymerazation defect leading to decreased phagocytosis |
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Cilia
structure what links the peripheral ones? |
9+2 arrangement of microtubules
9 peripheral microtubule doublets 2 central microtubule singlets peripheral 9 doublets linked by Axonemal Dynein (ATPase) |
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What is axonemal dynein
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ATPase that links peripheral 9 doublets of cilia, causes bending of cilum by differential sliding of doublets
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Patient has
-infertility -recurrent sinusitis -produces tons of sputum -imaging shows situs inversus -chest CT shows 'tree in bud' pattern What does the tree in bud pattern and sputum signify? dx? pathogenesis |
bronchiectasis
kartagener's syndrome immotile cilia due to a dynein arm defect Recurrent sinusitis because bacteria and particles not pushed out |
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Cytoskeletal elements involved in
-microvilli -muscle contraction -cytokinesis -adherens junctions |
actin and myosin
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cytoskeletal elements in
-cilia -flagella -mitotic spindle -neurons -centrioles |
microtubules
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cytoskeletal elements involved in
-vimentin -desmin -cytokeratin -GFAP -neurofilaments |
intermediate filaments
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What are 5 things found in the plasma membrane bilayer
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cholesterol (50%)
phospholipids (50%) sphingolipids, glycolipids, proteins |
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How does composition of a plasma membrane relate to melting point and fluidity
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higher cholesterol content or long saturated fatty acid content --> higher melting temp, lower fluidity
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Immunohistochemical stain - what kind of tissue can you find if you stain with
a. vimentin b. desmin c. cytokeratin d. GFAP e. neurofilaments |
a. connective tissue
b. muscle c. epithelial cells d. neuroglia e. neurons |
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Na/K ATPase
a. where is it located b. how does it work |
a. plasma membrane, ATP binding site on cytoplasmic side
b. ATP phosphorylates channel --> 3 Na out Dephosphorylation --> 2K in |
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Function of Oubain
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inhibits Na/K ATPase by binding to the K site
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How do cardiac glycosides work (digoxin, digitoxin)
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Directly inhibit Na/K ATPase --> inhibit Na/Ca exchange --> increased intracellular Ca --> increased cardiac contractility
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What is the most abundant protein in the body?
General function |
collagen
Organizes and strengthens ECM |
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Where does Type I collagen work?
How prevalent is it? |
Bone, Skin, Tendon, dentin, fascia, cornea, late wound repair
90% of collagen is type I |
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Where does Type II collagen work?
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Cartilage (including hyaline), vitreous body, nucleus pulposus
carTWOlage for type TWO |
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Where does type III collagen work?
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Reticulin fibers
skin, blood vessels, uterus, fetal tissue, granulation tissue |
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Where does type IV collagen work?
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Basement membrane or basal lamina
"Type four under the floor" |
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In general, where are 6 places with collagen
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Bone
Skin Tendon Cartilage (II) Reticulin (III) Basement membrane (IV) Be So Totally Cool, Read Books (in COLLAGEn) |
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Collagen synthesis
what happens inside the RER in fibroblasts Structure of the product |
Synthesis
Translate preprocollagen (alpha chains) Gly-X-Y (X, Y = proline, hydroxyproline, or hydroxylysin) |
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Collagen synthesis
What happens to preprocollagen in ER (2 steps) |
1. Hydroxylation of proline and lysine residues (requires vitamin C)
2. GLycosylation of pro-a-chain lysine residues, formation of procollagen (triple helix of collagen alpha chains) |
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Collagen synthesis
Where does procollagen go after exocytosis What happens there? |
Outside fibroblasts
Cleavage of terminal regions of procollagen --> insoluble tropocollagen Crosslinking tropocollagen (by covalent lysine-hydroxylsine cross-linkage by lysyl oxidase) --> collagen fibrils |
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In making collagen, I cannot hydroxylate the proline and lysine residues of preprocollagen in the ER
What is my disorder |
Scurvy
Hydroxylation of lysine and proline requires vitamin C |
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In making collagen, I cannot form a procollagen triple helix of glycosylated pro-a collagen chains
what is my disorder |
osteogenesis imperfecta
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In making collagen, I cannot crosslink my tropocollagen to form collagen fibrils
What is my disorder |
Ehlers Danlos
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Patient has
-hyperextensible skin -easy bruising (tendency to bleed) -hypermobile joints + -joint dislocation -berry aneurysms -organ rupture condition? genetics? |
Ehlers Danlos
Faulty collagen synthesis, most often type III can be autosomal dominant or recessive |
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Patient has
-multiple fractures with minimal trauma, can occur during birth -blue sclera (translucency of CT of choroid) -hearing loss (abnormal middle ear bones) -dental imperfections (lack of dentin) dx? pathogenesis? Most common type? |
Osteogenesis imperfecta
Brittle bones due to inability to crosslink preprocollagen to form procollagen Most commonly is autosomal dominant, affecting type I collagen |
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What is the difference between osteogenesis imperfecta affecting type I vs. Type II collagen
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type I = fractures, blue sclera, hearing loss, dental imperfections
type II = fatal in utero or neonatal period |
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Incidence of osteogenesis imperfecta
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1:10,000
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Patient has
-progressive, hereditary nephritis -deafness -may have ocular disturbances dx? pathogenesis genetics |
Alport's syndrome
abnormal type IV collagen Most commonly x-linked recessive |
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where is type IV collagen found that is affected by Alport's?
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kidneys, ears, eyes
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what is elastin
where is it found |
stretchy protein
lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava |
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elastin composition
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tropoelastin protein crosslinked with fibrillin scaffolding
rich in proline and glycine, nonglycosylated forms |
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how is elastin broken down?
one enzyme that prevents this? |
elastase
a1 antitrypsin |
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a. disease caused by a defect in fibrillin (component of elastin)
b. disease caused by defect in a1 antitrypsin - what happens? |
a. Marfan's - defective elastin
b. Emphysema - excess elastase --> breakdown of elastin |
