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Flashcards in Biochemistry Deck (293)
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Chloramphenicol mechanism

inhibits 50S peptidyltransferase


Macrolides mechanism

act on 50S subunit and block translocation (step 3 of elongation factor)


Clindamycin and Chloramphenicol mechanism

act at 50S; block peptide bond formation


Regulation of cell cycle by:
-Cyclic-dependent kinases
-Cylcin-CDK complexes
-Rb and p53 (tumor suppressors)

*CDKs = cyclin-dependent kinases: constitutive and inactive; expressed constantly, but inactive unless activated
*Cyclins = activate CDKs
*Cyclin-CDK complexes: must be both activated and inactivated for cell cycle to progress
*Rb and p53: inhibit G1-->S progression; p53 also inhibits G2-->Mitosis


Which cell types are "permanent", remaining in G0, regenerating from stem cells?

neurons, skeletal and cardiac muscles, RBCs


Which cell types are stable/quiescent --> enter G1 from G0 when stimulated?

hepatocytes, lymphocytes


Which cell types are labile --> never go to G0, divide rapidly with a short G1?

bone marrow, gut epithelium, skin, hair follicles (this type are most susceptible to cancer drugs)


Nissl bodies

RER in neurons (in dendrites; not in axons) --> synthesize enzymes and peptide neurotransmitters


What types of cells are rich in RER?

mucus-secreting goblet cells of the small intestine and antibody-secreting plasma cells


What types of cells are rich in SER?

liver hepatocytes (for drug and poison detox) and steroid-hormone producing cells of the adrenal cortex


Which amino acids are modified by the golgi?



Failure to add mannose-6-phosphate to lysosome proteins results in what disease?

I-cell disease = Inclusion cell disease;
inherited lysosomal storage disease. Since not tagged by mannose-6-phosphate, enzymes are secreted outside the cell instead of to the lysosome.
-Features: coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes; often fatal in childhood


Peroxisome function

catabolism (breakdown) of very long fatty acids and amino acids


Proteasome function

barrel-shaped; degrades damaged or unnecessary proteins tagged for destruction with ubiquitin


Dynein and Kinesin

microtubule proteins:
-dynein: retrogradeto microtubule (+ to -)
-kinesin: anterograde to microtubule (- to +)


Immune disease due to a defect in microtubule polymerization?

Chediak-Higashi syndrome: microtubule polymerization defect resulting in decreased fusion of phagolysosomes and lysosomes; get recurrent pyogenic infections, partial albinism, peripheral nueropathy


Drugs that act on microtubules

1)-Bendazoles (anti-helminthic)
2) Griseofulvin (anti-fungal)
3) Vincristine/Vinblastine (anti-cancer) - block polymerization of microtubules
4) Paclitaxel (anti-breast cancer) - stabilizes microtubules
5) Colchicine (anti-gout)


Kartagener's syndrome: cause, presentation

*immotile cilia due to a dynein arm defect
-infertility (male and female)
-recurrent sinusitis (because can't push bacteria/particles out)
-situs inversus


Cytoskeletal elements

-actin and myosin
-microtubule (for movement)
-intermediate filaments (for structure: vimentin, desmin, cytokeratin, lamins, GFAP, neurofilaments)


Contents of the plasma membrane

-50% cholesterol
-50% phospholipids (phosphatidylcholine, lecithin, phosphatidyl inositol)
-also: sphingolipids, glycolipids, proteins


Stains for intermediate filaments: What types of cells do these stains stain?
-GFAP (glial fibrilary acid proteins)

-Vimentin-->Connective tissue (so use for sarcomas, some carcinomas)
-Desmin --> muscle (rhabdomyosarcoma, leiomyosarcoma)
-cytokeratin--> epithelial cells (carcinomas, some sarcomas)
-GFAP --> neuroglia
-Neurofilaments --> neurons (adrenal neuroblastoma,primitive neuroectoderm tumors)


Oubain mechanism

inhibits the Na/K-ATPase by binding to the K site


Cardiac glycosides (digoxin, digotoxin) mechanism:

inhibit Na/K-ATPase, leading to indirect inhibition of Na/Ca-exchange; resulting in increased intracellular Ca and thus increased cardiac contractility


What are the 4 types of collagen?

"Strong, Slippery, Bloody BM!"
Type I: (90%) = Strong --> bone, skin, tendon, dentin, fascia, cornea, late wound repair
Type II: Slippery --> Cartilage (including hyaline)
Type III: Bloody --> skin, blood vessels, uterus, fetal tissue, granulation tissue (early wound healing)
Type IV: BM --> basement membrane and basal lamina


Collagen synthesis steps:

--Within Fibroblasts--

1) Synthesis in RER: Preprocollagen: Gly-X-Y polypeptide (X and Y are proline or lysine)
2) Hydorxylation of proline and lysine in ER: requires Vitamin C
3) Glycosylation in ER: formation of procollagen
4) Exocytosis of procollagen into extracellular space

--outside fibroblasts--

5) Proteolytic processing: procollagen is cleaved to become tropocollagen
6) Cross-linking: Collagen fibrils are formed by cross-linking tropocollagen molecules


Osteogenesis imperfecta:
-what type of collagen is defective?

="brittle bone disease"
-Autosomal dominant, abnormal type 1 collagen (type 2 is fatal in-utero)
-defect is in the glycosylation phase (step 3) of collagen synthesis; can't form triple helix (procollagen) from the pro-alpha-chain

-multiple fractures (may be during birth; may look like child abuse)
-blue sclerae
-hearing loss
-dental problems due to lack of dentin


Blue Sclerae?

Osteogenesis imperfecta


Defect in Type III collagen?

Ehlers-Danlos syndrome (defect is ouside fibroblasts, can't crosslink tropocollagen to make collagen fibrils)
*"bloody" collagen defect (can be other types, but type III is most common)
-hyperextensible skin
-tendency to bleed (easy brusing, berry aneurysms, organ rupture)
-hypermobile joints (joint dislocation)


Type IV collagen defect

Alport syndrome --> "can't see, can't pee, can't hear"
-usually X-linked recessive
-progressive hereditary nephritis and deafness; may have ocular disturbances too.


Which two amino acids is elastin rich in?

glycine and proline