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23 Cards in this Set

  • Front
  • Back
what energy factor is required for:
1. tRNA aminoacylation?
2. loading tRNA onto ribosome?
3. translocation
4. how much total energy is expended
1. ATP-->AMP (NOTE: 2 phosphoanhydride bonds!!!)
2. GTP-->GDP
3. GTP-->GDP
4. 4 high energy phopspoanhydride bonds
define these post-translational modifications:
1. trimming
2. covalent alterations
3. proteasomal degradation
1. trimming = removal of N- or C-terminal propeptides from ZYMOGENS to generate mature proteins
2. covalent alterations: phosphorylation, glycosylation, hydroxylation
3. proteasomal degradation: attachment of UBIQUITIN to defective proteins to TAG THEM FOR BREAKDOWN
list the enzyme regulation methods
- enzyme concentration alteration (synthesis and/or destruction)
- covalent modification (eg - phosphorylation)
- proteolytic modification (zymogen)
- allosteric regulation (eg - feedback inhibition)
- pH
- temperature
- transcriptional regulation (eg - steroid hormones)
cell cycle phases
- mitosis (SHORTEST PHASE!): prophase, metaphase, anaphase, telophase
- G1 - variable duration (at which time you can go in and out of G0 - variable duration
- S
- G2
factors which control transitions between phases (3 things)
1. cyclins - phase, specific and activate CDKs
2. CDKs - constitutive and inactive
Cyclin-CDK complexes must be both activated and inactivated for cell cycle to progress
3. tumor supressors -
Rb
p53
- both INHIBIT G1-->S PROGRESSION; mutations in these genes result in unrestrained growth!
Permanent cells
- what phase of cell cycle are they in?
- how to they regenerate
- 4 examples of this cell type?
remain in G0
- regenerate from stem cells
- neurons
skeletal muscle
cardiac muscle
RBCs
Stabile (quiescent) cells
- how are they involved with cell cycle?
- examples? (2 of them)
- enter G1 from G0 when stimulated!
- hepatocytes
lymphocytes
Labile cells
- how are they involved with cell cycle?
- examples? (4 of them)
- NEVER GO to G0!!!
- divide rapidly with SHORT G1
- bone marrow
gut epithelium
skin
hair follicles
RER
- site of synthesis of SECRETORY PROTEINS
- site of synthesis of N-LINKED OLIGOSACCHARIDE
- site of synthesis of many other protiens too :)
- NOTE: Mucus-secreting GOBLET CELLS of small intestine and Ab-secreting PLASMA CELLS are rich in RER!!!
Nissl bodies
found in neurons
- synthesize enzymes (ChAT) and peptide neurotransmitters
free ribosomes
unattached to any membrane
- site of synthesis of CYTOSOLIC and ORGANELLAR PROTEINS
Smooth ER
- function
- what cells are rich in it?
- site of STEROID SYNTHESIS (smooth steroid!)
- site of DETOXIFICATION OF DRUGS (smooth out the bad effects of drugs by detoxifying!)
- LIVER HEPATOCYTES and steroid-hormone producing cells of ADRENAL CORTEX - rich in SER!!!
Functions of the golgi apparatus
(6 of them)
1. distribution center of proteins and lipids from ER to plasma membrane, lysosomes, secretory vesicles
2. modification of N-oligosaccharides on asparagine
3. addition of O-oligosaccharides to SERINE and THREONINE residues
4. addition of MANNOSE-6-PHOSPHATE to specific lysosomal enzymes, which targets the protein to the lysosome (NOTE: Failure of this ftn --> I-Cell Disease!)
5. proteoglycan assembly from proteoglycan core progeins
6. sulfation of sugars in proteoglycans and of selected tyrosine proteins
vesicular trafficking proteins
- COPI
- COPII
- Clathrin
COPI:
- retrograde!!!
- GOLGI-->ER
COPII
- anterograde
- RER-->cis-Golgi
CLATHRIN:
- trans-Golgi-->lysosomes
- plasma membrane-->endosomes (receptor mediated endocytosis)
- key for internalization of lysosomal enzymes
- key for internalization of LDL receptor
microtubule
- cylindrical structure composed of HELICAL array of polymerized DIMERS of alpha- and beta-tubulin
- each dimer has 2 GTP bound
- incorporated into flagella, cilia, mitotic spindles
- grows SLOWLY
- collapses QUICKLY
- also involved in SLOW AXOPLASMIC TRANSPORT IN NEURONS!
drugs that act on microtubules (5 of them)
1. mebendazole/thiabendazole (anti-helminthic)
2. paclitaxel (taxol) - anti-breast cancer
3. Griseofluvin (antifungal)
4. Vincristine/Vinblastine (anti-cancer)
5. Colchicine (anti-GOUT!)
chediak higashi syndrome
microtubule polymerization defect!
--> decreased phagocytosis!!!
celia structure
9+2 arr of microtubules
- DYNEIN is an ATPase (not use of ATP!!!) that links peripheral 9 doublets and causes bending of cilium by differential sliding of doublets
- DYNEIN = RETROGRADE to microtubule (+ --> -)
- KINESIN = ANTEROGRADE to microtubule (- --> +)
kartagener's sydnrome
immotile cilia due to dynein arm defect
--> male and female infertility (sperm immotile)
- bronchiectasis
- recurrent sinusitis (bacteria and particles not pushed out)
- associated with SITUS INVERSUS
cytoskeletal elements - give examles of where each of these are found:
1. actin and myosin
2. microtubule
3. intermediate filaments
1. ACTIN & MYOSIN:
- microvilli
- muscle contraction
- cytokinesis
- adherens junctions (along with E-cadherin)
MICROTUBULE:
- cilia
- flagella
- mitotic spindle
- neurons
- centrioles
INTERMEDIATE FILAMENTS:
- vimentin
- desmin
- cytokeratin
- glial fibrillary acid proteins (GFAP)
- neurofilaments
plasma membrane composition
asymmetric fluid bilayer
- cholesterol (50%)
- phospholipids (50%)
- spingolipids
- glycolipids
- proteins

HIGH CHOLESTEROL or LONG SATURATED FATTY ACID CONTENT --> increased melting temperature & decreased fluidity
phosphatidycholine function
- aka?
aka LECITHIN!
- major component of:
rbc membranes
myelin
bile
surfactant (DPPC - dipalmitoyl phosphatidycholine)

phosphatidylcholine/lecithin is used in ESTERIFICATION OF CHOLESTEROL (LCAT = lecithin-cholesterol acyltransferase)
immuno histochemical stains - name what staining these proteins allows you to see:
1. vimentin
2. desmin
3. cytokeratin
4. GFAP
5. neurofilaments
1. vimentin for connective tissue
2. desmin for muscle
3. cytokeratin for epithelial cells
4. GFAP for neuroglia
5. neurofilaments for neurons