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Cellular
First Aid - Biochem - Cellular
Question | Answer |
---|---|
Cell cycle phases | Mitosis (shortest phase): prophase-metaphase-anaphase-telophase, Interphase (G1, Go), (Rb, p53), S phase (diploid > haploid), G2 , mitosis (haploid back to diploid) |
Cell cycle checkpoints | CDK's, cyclines, cyclin-CDK complexes, and tumor suppressors |
Cell types: 3 | 1. permanent = remain in G0, regenerate from stem cells (neurons, skeletal/cardiac muscle, RBC's) 2. stable(quiescent) = enter from G1 from Go when stimulated (hepato/lymphocytes) 3. Labile = never go to G0 divide rapidly with short G1 (bone marrow, gut,. |
CDK's | cyclin-dependent kinases, constitutive and inactive. serine-threonine kinases (phosphorylators) |
cyclins | regulatory proteins that control cell cycle events, phase specific, and activate CDK's |
cyclin-CDK complexes | must be activated and inactivated for cell cycle to progress |
tumor suppressors | Rb and p53 normally inhibit G1-S progression; mutations in the genes = unrestrained growth |
Rough Endoplasmic Reticulum | syn of secretory (exported) proteins and N-linked oligosaccharide addition to many proteins - mucus secreting goblet cells of small intestine and antibody secreting plasma cells are rich in RER (studded with ribosomes) |
Free ribosomes | unattached to any membranes, site of syn of cytosolic and organellar proteins |
Smooth endoplasmic reticulum | syn of steroids and detoxification of drugs and poisons - liver hepatocytes and steroid hormone producing cells of adrenal cortex are rich in SER |
Golgi Apparatus | 1.distribution center of proteins and lipids from ER to plasma membrane, lysosomes, and secretory vesicles 2.modifies N-oligosaccharides on asparagine 3.adds O-oligosaccharides to serine and thereonine residues |
Golgi apparatus - continued functions | 4.addn of mannose-6-P to specific lysosmal proteins > targets proteins to the lysosome 5.proteoglycan assembly from core proteins 6.sulfation of sugars in proteoglycans and of selected tyrosine on proteins |
Golgi apparatus -- flow | Nuclear envelope > RER > Golgi (COP II) (golgi > ER (COPI)) >> trans-Golgi > lysosome, cytosol, or secretory storage (Clathrin using endosomes - receptor mediation endocytosis)) |
Vesicular trafficking proteins | COPI = retrograde, Golgi > ER COPII = anterograde, RER > cis golgi Clathrin = trans-golgi > lysosome, cytosol, plasma mem through endosomes (receptor mediated endocytosis) |
microtubulues | 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 slow,collapses quickly. and slow transport in neurons. |
molecular motor proteins | transport cellular cargo toward opposite ends of microtubule tracks powered by ATP hydrolysis. 1.Dynein = towards cell center (retrograde) along microtubules 2.Kinesin = away from center > periphery |
Cilia structure | 9+2 arrangement of microtubules - axonemal dynein = ATPase that links peripheral 9 doublets and causes bleeding of cilium by differential sliding of doublets |
Kartagener's syndrome | immotile cilia b/c dynein arm defect, male and female infertility (sperm immotile), bronchiectasis and recurrent sinusitis (bacteria and particles not pushed out) |
Cytoskeletal elements | provides cell with shape and structure, components = actin (microfilaments) and myosin, microtubules, intermediate filaments |
Actin and Myosin - location | microvilli, muscle contraction, cytokinesis, adherens junctions |
Microtubules - location | cilia, flagella, mitotic spindle, neurons, centrioles |
Intermediate filaments - location | vimentin, desmin, cytokeratin, glial fibrillary acid proteins, neurofilaments |
plasma membrane composition | 1.asymmetric lipid bilayer 2.cholesterol, phospholipids, sphingolipids, glycolipids,and proteins 3.high cholesterol or long saturated fatty acid content > increased melting temperature and decreased fluidity |
Collagen - basics | most abundant protein in the body, organizes and strengthens extracellular matrix. |
Type I collagen | 90%, bone, skin, tendon, dentin, fascia, cornea, late wound repair |
Type II collagen | cartilage |
Type III collagen | skin, blood vessels, uterus, fetal tissues, granulation tissue |
Type IV collagen | basement membrane or basal lamina |
Collagen Synthesis - in fibroblasts - main steps | 1.synthesis (RER) (preprocollagen) **(Scurvy)** 2.hydroxylation (ER) *vitamin C / **(OI)** 3.glycosylation (ER) (procollagen/triple helix) 4.exocytosis |
Collagen Synthesis - outside of fibroblasts - main steps | 5.proteolytic processing (tropocollagen) **(Ehlers-Danlos)** 6.cross-linking (collagen fibrils) |
collagen synthesis (RER) | translation of alpha collagen chains (preprocollagen) usually Gly-X-Y polypeptide (X,Y = proline, hydroxyproline, or hydroxylysine) |
collagen hydroxylation (ER) | hydroxylation of specific proline and lysine residues (requires Vit. C) |
collagen glycosylation (ER) | glycosylation of pro-alpha-chain lysine residues and formation of procollagen (triple helix of 3 collagen alpha chains) |
collagen exocytosis | exocytosis of procollagen into extracellular space |
collagen proteolytic processing (outside fibroblast) | cleavage of terminal regions of procollagen transforms it into insoluble tropocollagen |
collagen cross linking (outside fibroblast) | reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (by lysyl oxidase) to make collagen fibrils |
Ehler's Danlos Syndrome | Type III collagen (skin, blood vessels..) hyperextensible skin, tendency to bleed (bruising), hypermobile joints, 6 types, inheritance and severity vary, autosomal dominant or recessive, joint dislocation, berry aneurysms, organ rupture |
Marfan's syndrome/elastin | elastin = stretchy protein in lungs, large arteries, ligaments, vocal cords, ligaments to connect vertebrae, tropoelastin with fibrillin scaffolding > Marfan's = defect in fibrillin (fib is protein in connective tissue) (also effects TGF-B *problem) |