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28 Cards in this Set
- Front
- Back
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CDKs
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cyclin-dependent kinases; expressed constantly, inactive
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Cyclins
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Regulatory proteins that control cell cycle events; phase specific
**activate CDKs |
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Cyclin-CDK complexes
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must be both activated and inactivated for cell cycle to progress
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Tumor suppressors
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Rb & p53 inhibits G1 to S progression
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Cell types
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Permanent: remain in G0; regenerate from stem cells
-neurons, skeletal and cardiac muscle, RBCs Stable (quiescent): enter G1 from G0 when stimulated -hepatocytes, lymphocytes Labile: never go to G0; divide rapidly with a short G1 -bone marrow, gut, skin, hair follicles |
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RER
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synthesis of secretory (exported) proteins and N-linked oligosaccharide addition to many proteins
rich in RER: goblet cells, plasma cells |
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Nissl bodies
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RER in neurons; in dendrites, not axons
-synthesize enzymes (ChAT) and peptide neurotransmitters |
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Free ribosomes
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unattached
synthesize cytosolic and organellar proteins |
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SER
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Steroid synthesis
Detoxification of drugs and poisons SER-rich: hepatocytes; adrenal cortex; gonads Sarcoplasmic reticulum (specialized SER) in straited muscle |
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Nucleus localization signals
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4-8aa sequence made of Lys, Arg, Pro (+ charged)
-mutation in single AA leads to impaired transport -required for transport in and out of nucleus Transported out: ribosomal subunits and mRNA ATPase allows NLS to go into nucleus |
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Golgi
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"Nasty Asparagus"
"OST: O for Ser and Thr" 1. distribution center of proteins and lipids from ER to plasma membrane, lysosomes, and secretory vesicles 2. modifies N-oligosaccharides on asparagine 3. addis O-oligosaccharides to Ser and Thr 4. Adds mannose-6-P to specific lysosomal proteins --> targets the protein to the lysosome 5. Proteoglycan assembly from core proteins 6. Sulfation of sugars in proteoglycans and of selected tyrosine on proteins |
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COPI and COPII
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COPI: retrograde
golgi to ER COPII: anterograde RER to cis-Golgi |
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Clathrin
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trans-Golgi to lysosomes
plasma membrane to endosomes (receptor-mediated endocytosis) |
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I-Cell disease
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Inclusion Cell Disease
inherited lysosomal storage disorder; defective phosphotransferase, which normally adds P to mannose residues -lysosomal proteins are then secreted outside the cell instead of being targeted to the lysosome findings: coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes |
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Molecular motor proteins
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transport cellular cargo toward opposite ends of microtubule tracks:
Dynein: retrograde (+ to -) Kinesin: anterograde (- to +) |
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Chediak-Higashi
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Microtubule polymerization defect --> decreased phagocytosis
CH-AIN of Ps Albinism (partial) Infxns (pyogenic) Neuropathy (peripheral) |
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Drugs that act on microtubules
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1. Bendazole
2. Griseofulvin 3. Vincristine/vinblastine 4. Paclitaxel 5. Colchicine |
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Axonemal dynein
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ATPase that links peripheral 9 doublets and causes bending of cilium by differential sliding of doublets
*gap junctions for coordinated contraction of ciliated cells |
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Kartagener's syndrome
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primary ciliary dyskinesia
immotile cilia due to dynein arm defect --> infertility, bronchiectasis, recurrent sinusitis **assoc with situs inversus |
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Intermediate filaments
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Vimentin: connective tissue
Desmin: muscle Cytokeratin: epithelial cells GFAP: neuroglia (ependymal, astrocytes, oligodendrocytes) Neurofilaments: neurons Nuclear lamins: nuclear envelope and DNA within Peripherin: neurons |
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Plasma membrane composition
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asymmetric lipid bilayer
contains cholesterol, phospholipids (phophotidylinositol --> PLA2; lecithin- phosphatidylcholine), sphingolipids, glycolipids, proteins high chol aor long saturated FA content --> increased melting temperature, decreased fluidity |
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Ouabain
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inhibits Na/K-ATPase by binding to K+ site
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Collagen
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Strong, Slippery, Bloody, B.M.
I: bONE, skin, tendon, dentin, fascia, cornea, late wound repair II: carTWOlage: vitreous body, nucleus pulposus III: Reticulin: skin, vessels, uterus, fetal tissue, granulation tissue (early wound healing) IV: Basement membrane |
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Collagen synthesis
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She Has Given Everything to CC
Inside fibroblasts: 1. Synthesis (RER) translation of collagen alpha chains (preprocollagen) -Gly-X-Y (X & Y are Pro, hydroxypro, hydroxylys) 2. Hydroxylation (ER): of specific pro and lys residues (need vit C) **Scurvy 3. Glycosylation (ER): of pro-alpha-chain lys residues and formation of procollagen (triple helix of 3 collagen alpha chains) ***Osteogenesis Imperfecta 4. Exocytosis: of procollagen into extracellular space Outside fibroblast 5. Proteolytic processing cleave terminal regions of procollagen --> insoluble tropocollagen 6. Cross-linking: reinforcement of staggered tropocollagen by covalent lys-hydroxylys cross-linkage (by lysyl oxidase) to make collagen fibrils **Ehlers-Danlos |
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Ehlers-Danlos
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ED3
Ehlers-DanLYS Faulty collagen synthesis (impaired Lysine cross-linking) **type III collagen most often affected hyperextensible skin, easy bleeding, hypermobile joints can be assoc with joint dislocation, berry aneurysm, organ rupture |
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Osteogenesis Imperfecta
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MC form is auto dom with abnormal type I collagen
**impaired glycosylation of preprocollagen fractures, blue sclerae (translucent connective tissue over choroid), hearing loss, dental imperfections (lack of dentin) type II fatal in utero or neonatal |
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Alport's syndrome
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FOUR alPORt
can't pee, can't see, can't hear Abnormal type 4 collagen progressive nephritis deafness ocular disturbances |
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Elastin
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stretchy protein within lungs, large arteries, elastic ligaments, vocal cords, ligamenta flava (connect vertebrae)
-rich in proline and glycine, nonglycosylated forms -tropoelastin with fibrillin scaffolding -broken down by elastase, which is normally inhibited by A1A Elastin gene affected by Williams microdeletion Marfan's: defect in fibrillin |
