Flashcards in Biochemistry Deck (293)
inhibits 50S peptidyltransferase
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:
-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?
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)
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
catabolism (breakdown) of very long fatty acids and amino acids
barrel-shaped; degrades damaged or unnecessary proteins tagged for destruction with ubiquitin
Dynein and Kinesin
-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
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)
-actin and myosin
-microtubule (for movement)
-intermediate filaments (for structure: vimentin, desmin, cytokeratin, lamins, GFAP, neurofilaments)
Contents of the plasma membrane
-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)
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:
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
5) Proteolytic processing: procollagen is cleaved to become tropocollagen
6) Cross-linking: Collagen fibrils are formed by cross-linking tropocollagen molecules
-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)
-dental problems due to lack of dentin
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)
-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.