Cell Biology Flashcards
(103 cards)
1
Q
Nuclear localization signals are rich in which AA
A
Proline, Arginine, Lysine
To get in you need a PAL
2
Q
What proteins inactivate cyclin-CDK complexes
A
p21, p27, p57
3
Q
G1 to S phase cyclins and CDK
A
Cylcin D –CDK4 –> phosphorylation of Rb –> Rb released from E2F –> with E2F unbound cell can now transcribe
Cyclin E binds to CDK 2 allows progression to S phase
4
Q
G2 to M phase cyclins and CDK
A
Cyclin A – CDK2 –>mitotic prophase
Cyclin B – CDK1 activated by cdc25 –> breakdown of nuclear lamins
5
Q
Deficiency in Mannose phosphorylation leads to
A
I-ceel disease
- No mannose-6-phosophate to target lysosome
- corneal clouding, coarse facies, hepatosplenomegaly, skeletal abnormalities, joint movement prob
- Death by 8
6
Q
Peroxisomes purpose
A
Beta-oxidation of long chain FA and branched chain FA
- Synthesis of plasmalogens
- oxidases and catalase for metabolizing ethanol
7
Q
Plasmalogens
A
Important phospholipids in myelin
8
Q
COP II
A
RER –> cis golgi
9
Q
COP I
A
cis Golgi –> RER
10
Q
Clathrin
A
Trans Golgi –> lysosomes
-Plasma memb into cell
11
Q
Golgi post-translational modifications
A
- modifies N-oligosaccharide on ASPARAGINE
- adds O-oligosaccahrides to SERINE and THREONINE
12
Q
Rx for MT
A
Vincristine, Vinblastine (prevents growth)
Paclitaxol, Docetaxel (prevents breakdown)
Benzimidazoles (worm inf, worms are BENDY)
Griseofulvin (fungal inf)
Colchicine (anti-infl, phagocytes use MT to move)
13
Q
Dynein
A
+ to - retrograde back towards center of cell
14
Q
Kinesin
A
- to + away from nucleus anterograde
15
Q
Kinase
A
adds phosphate with ATP
16
Q
Phosphatase
A
Removes Phosphate
17
Q
Phosphorylase
A
Adds Pi without ATP
18
Q
Carboxylase
A
Adds COOH requires BIOTIN
19
Q
Decarboxylase
A
Removes carboxyl group
20
Q
Hydroxylase
A
Adds OH
21
Q
Dehydroxylase
A
Removes OH
22
Q
Dehydrogenase
A
Oxidize a substrate using electron acceptor (NAD+ or NADP+)
23
Q
PDGF and GF receptor type
A
Tyrosine Kinase rec
-SIngle-pass transmembrane protein
24
Q
Insulin and IFG-1 receptor
A
Tyrosine Kinase rec
- 2 alpha subunits (disulfide bonds) bind extrecellular ligand [harsh conditions need the disulfide bonds]
- 2 beta subunits: tyrosine kinase activity
25
Receptor-mediated endocytosis
-Molecules bind to receptors --> receptors interact with clathrin by adaptin protein --> clathrin polymerizes with other clathrin molecules to form a vesicle --> Dynamin pinches vesicle off --> vesicle is uncoated --> vesicle fuses with lysosome --> receptor recycled and lysosome breaks down contents
26
Histologic signs of apoptosis
-Pyknosis (condensation of nuclear chromatin), membrane blebbing, karyorrhexis (nuclear fragmentation), apoptotic bodies, phagocytosis, NO inflammation
27
Intrinsic pathway of apoptosis
Bcl-2 is anti-apoptotic --> DNA damage of apoptotic signals activates Bax (pro-apoptotic) --> Bax creates channels in mitochondrial membrane --> Cytochrome C moves from mitochondria to cytsol --> activates caspases --> caspases intitate apoptosis
28
Extrinsic pathway of apoptosis using the Death receptor
TNF receptors and Fas receptors are located on cell membrane --> TNF-alpha and Fas ligand activate receptors --> activated receptors lead to acctivation of caspases
29
Extrinsic pathway of apopptosis using Cytotoxic T cells
CD8+ T cells release perforin and granzyme B --> perforin punches holes in membrane and granzyme enters and activates caspases
30
Necrosis def
Cell death not orderly
| -Spilling out of cytoplasmic contents --> inflammation
31
Coagulative Necrosis
- gelatinous substance in dead tissue
- common in heart, liver, kidneys
- caused by ischemia (MI, wedge ischemia in liver)
- histo: "death cells" cells with no nuclei
32
Liquifactive Necrosis
- viscous liquid mass
- common in brain, bacterial abscess, pleural effeusion
- histo: homogenous eosinophilic (lots of MP)
33
Caseous Necrosis
- combination of coagulative and liquifactive
- MP walling off the infecting organism
- "clumpy cheese"
- seen in TB and systemic fungal infections
- histo: acellular cells in the middle of a granuloma with multinucleated giant cells
34
Fat necrosis
- Damaged cells release lipase, breaks down triglycerides in fat cells
- seen in pancreatitis (enzymatic) and breast trauma (nonenzymatic)
- histo: white fat spots and inflammatory giant cells, dark blue on H&E stain
35
Fibrinoid necrosis
- seen in blood vessels
- typically immune-mediated vascular damage
- histo: area of fibrosis with eosinophils
36
Gangrenous necrosis
- Distal extremity after chronic ischemia
- Wet: bacterial infection, extremities (liquefaction and coag)
- Dry: ischemia, toes and feet (coag)
37
Why do we get reperfusion injury?
- Drastic free radical production and massive influx of calcium
- free radicals --> cell damage through membrane lipid peroxidation, protein modification and DNA breakage
38
MOI in cyanide poisoning
ATP depletion
39
Enzymes responsible for free radical degradation
- Catalase
- Superoxide dismutase
- Glutathione Peroxidase
- Antioxidants
40
Granuloma
cluster of MP, lymphocytes and fibroblasts, typically contains multinucleated giant cells
41
Neutrophil Extravasation rolling molecules
selectins
42
Neutrophil Extravasation Tight binding
ICAM-1 (endo) and LFA-1 (integrin on NP)
43
Neutrophil Extravasation Diapedesis
PECAM-1
44
NP chemotactic signals
C5a, IL-8, LTB4
45
Acute inflammation mediators
IL-1
IL-6
TNF-alpha
46
Vasodilation and increased vascular permeability --> fluid exudation caused by
Histamine
Serotonin
Bradykinin
47
Tissue remodeling occurs by
Metalloproteinases (Req ZINC)
48
ESR
Erythrocyte Sedimentation Rate
- rate at which RBCs sediment to bottom of test tube
- inflammatory debris coat RBCs to cause them to clump faster, increased in inflammatory states
49
C-reactive protein
- synthesized
- why
synthesized by the liver with acute inflammation
| -Part of innate immune response: opsonized bacteria and activates complement (C-reactive protein, Complement)
50
Cells that generate fibrinogen and C-reactive protein
Heaptocytes LIVER
51
Type I Collagen
Bones, skin, dentin, scar tissue
Strong, slippery, stretchy, BM
SCAB
52
Type II Collagen
Cartilage, virtreous body, nucleus pulposos
Strong, slippery, stretchy, BM
SCAB
53
Type III Collagen
blood vessels, skin,uterus, embryonic, fetal, granulation tissue
Strong, slippery, stretchy, BM
SCAB
54
Type IV Collagen
Basement Membrane
Strong, slippery, stretchy, BM
SCAB
55
Collagen Synthesis
1. Basic peptide synthesis in RER of Fibroblasts (Preprocollagen, becomes alpha chain)
2. Hydroxylation of lysine and proline (req VITAMIN C)
3. Glycosylation of Hydroxylated Lyzine (Procollagen)
4. Exocytosis
5. Cleave terminal regions of procollegen (Tropocollagen)
6. Cross link tropocollagen mol to make collagen fibrils (covalent bonds to form a triple helix)
56
Angiogensis
- Grow new branch off existing vessel
- uses metalloproteinases (w ZINC) --> remodeled ECM
- VEGF causes vascular endothelium to proliferate
- FBGF
57
Which metal facilitate generation of free radials
Iron and Copper
58
Wound healing
0-3 hrs: hemorrhage and clotting
12-24 hrs: acute inflmmation NP
1-3 days: MP, granulation tissue (fibroblasts and vascular endothelial cells), Epitherlializations
wks-months: Collagen production (type III then Type 1 to form scar
59
AA high in collagen
Proline, Glycine, Hydroxyproline
60
AA high in elastin
Proline, Glycine
| -elastin held together by fibrillin
61
Lipofuscin granules
Residual body with yellow-brown pigment --> incomplete free radical-infuced lipid oxidation
62
Remain in G0 regenerate from stem cells
Permanent cell types
63
Ex of permanent cell types
Neurons, skeletal and cardiac muscles, RBCs
64
Enter G1 from G0 when stimulated
Stable (quiescent cells)
65
Examples of stable cells
Hepatocytes, lymphocytes
66
Never go to G0, divide rapidly with a short G1, most affected by chemo
Labile cells
67
Examples of labile cells
Bone marrow, gut epithelium, skin, hair follicles, germ cells
68
The RER in neurons
Nissl bodies
| -synthesis peptide NT for secretion
69
Site of N-linked oligosaccharide addition
RER
70
Cells rich in RER
- Mucus-secreting goblet cells of the SI
| - Ab-secreting plasma cells
71
Where is glucose-6-phosphatase located and what does it do?
- Smooth ER
| - last step in gluconeogenesis
72
Deficiency in Glucose-6-phosphatase
Von Gierke's disease
73
Purpose of an endoscope
Sorting center for material from outside cell or from Golgi --> sending to lysosomes for destruction of back to membrane/Golgi
74
Cytosolic ribonucleoprotein that traffics protein from ribosome to the RER
Signal Recognition Particle
| -now protein synthesis can continue in the RER
75
Eukaryote ribosomal subunits
40S + 60S = 80S
76
Prokaryotic Ribosomal subunits
30S + 50S = 70S
77
Initiation factor role in protein sythesis
- Help assemble 40S subunit with initiator tRNA and release when mRNA and 60S subunit assemble
- initiated by GTP hydrolysis
78
Purpose of ribozymes in protein synthesis
Catalyes peptide bond formation
79
ATP in protein synthesis
tRNA Activation (charging of tRNA, the attachment of the AA)
80
GTP in protein synthesis
TRNA Gripping and Going places: Translocation
81
Removal of N or C terminal peptides from zygote not to generate mature protein
Trimming
82
Chaperone proteins that prevent shock-stressed proteins from misfolding
-hsp70 and hsp90 (heat shock proteins)
83
Fxn of muscle contraction and cytokinesis
Microfilaments
| Ex: actin, microvilli
84
Fxn of maintaining cell structure and ex
Intermediate filaments
| Ex: Vimentin, Desmin, GFAP, neurofilaments, cytokeratin
85
Fxn of movement and cell division and ex
Microtubules
| -ex: cilia, flagella, mitosis spindle, centrioles
86
Drugs that act on MT
```
Microtubes Get Constructed Very Poorly
Mebendazole (anti helminthic)
Griseofulvin (antifungal)
Colchicine (antigout)
Vincristine/Vinblastine (chemo)
Paclitaxel (anticancer)
```
87
Large component of Fungal membranes
Ergosterol
What you say to fungus: ERRRR GO STARE AT A WALL
88
Toxin that inhibits binding to the K+ site in Na/K ATPase
Ouabain
89
Relocates a functional group within a molecule
Mutate
90
How does Bcl-2 prevent apoptosis?
Prevents cytochrome c release by binding to and inhibiting APAF-1
-APAF-1 normally binds cytochrome c and induces activation of caspase 9 initiating the cascade
91
Which extrinsic death receptor pathway is used in thymic medullary negative selection?
Fas-FasL interaction
92
Regions most vulnerable to hypoxia/ischemia in brain
ACA/MCA/PCA bound areas (watershed most likely)
93
Regions most vulnerable to hypoxia/ischemia in heart
Subendocardium (LV)
94
Regions most vulnerable to hypoxia/ischemia in kidney
Straight segment of PT (medulla), thick ascending limb (medulla)
95
Regions most vulnerable to hypoxia/ischemia in liver
Area around central vein (zone III)
96
Regions most vulnerable to hypoxia/ischemia in colon
Splenic flexure and rectum (both watershed areas)
97
Red infarct
- Hemorrhagic infarcts in venous occlusion and tissues with multiple blood supplies
- common in liver, lung, intestine, testes, reperfusion injuries
98
Pale infarct
- anemic infarcts in solid organs with 1 blood supply
| - heart, kidney, spleen
99
Causes of exudate
- Lymphatic obstruction (chylous)
- Inflammation, infection
- Malignancy
100
Causes of Transudate
Increased hydrostatic pressure (HF, Na+ retention)
| Decreased oncotic pressure (cirrhosis, nephrotic syndrome)
101
Increased ESR assoc
- Anemia
- Infection
- Inflmmation
- Cancer
- Renal disease
- Pregnancy
102
Decreased ESR levels
- Sickle Cell anemia
- Polycythemia (inc RBC dilute aggregation factors)
- HF
- Microcytosis
- Hypofibrinogenemia
103
Elastin is high in what areas of the body?
Skin, lungs, large arteries, Elastic ligaments, vocal cords, ligamenta flava
