Cellular Flashcards
regulatory proteins that control cell cycle events
phase specific
activate CDKs
cyclins
phosphorylates other proteins to coordinate cell cycle progression
must be activated/inactivated at approp times
cyclin-CDK complexes
p53 & hypophosphorylated retinoblastoma which normally inhibit G1 to S transition
tumor suppressor genes
permanent cells in G0 that regenerate only from stem cells
neurons, skel m, cardiac m, RBCs
stable quiescent cells that enter G1 when stimulated
hepatocytes
lymphocytes
labile cells that never enter G0 with short G1
bone marrow, gut epithel, skin, hair follicles, germ cells
site of secretory protein synth & N linked oligosaccharide addition to proteins
RER
synthesize peptide NT’s for secretion
nissl bodies (RER in neurons)
site of synth of cytosolic & organellar proteins
free ribosomes
site of steroid synth & detox of drugs/poisons
smooth ER
cell types rich in smooth ER
liver hepatocytes
steroid hormone producing cells of adrenal cortex & gonads
modifies N oligosaccharides on asparagine, adds O oligosaccharides on serine & threonine, adds mannose 6 phosphate to proteins to traffic to lysosome
golgi distribution center for proteins & lipids from ER to vesicles & p.m.
inherited defect in N-acetylglucosaminyl-1-phosphotransferase causing failure of golgi to phosphorylate mannose residues - causes proteins to be secreted extracellularly instead of to lysosomes - course facial features, clouded corneas, restricted joint movement, high level lysosomal enzymes
I-cell disease (inclusion cell disease)
cytosolic ribonucleoprotein that traffics proteins from ribosome to RER
if absent, causes proteins to build up in cytosol
signal recognition particle
leads things from golgi to golgi (retrograde) or from cis-golgi (side opp. p.m.) to ER
vesicular trafficking protein COPI
leads things from ER to cis golgi (anterograde)
vesicular trafficking protein COPII
leads things from trans golgi to lysosomes
or leads things from p.m. to endosomes (receptor mediated endocytosis ie. LDL receptors)
vesicular trafficking protein clathrin
organelle that catabolizes VLCFA, branched chain FA, a.a.
peroxisomes
protein complex that degrades damaged/ubiquinated proteins
proteasome
vimentin immunohistochem stain for intm filaments
in connective tissue
desmin immunohistochem stain for intm filaments
muscle
GFAP immunohistochem stain for intm filaments
neuroglia
molecular motor protein that moves retrograde to microtubule (pos to neg)
dynein
molecular motor protein that moves anterograde to microtubule (neg to pos)
kinesin
drugs that act on microtubules
‘Microtubules Get Constructed Very Poorly’
Mebendazole, Griseofulvin, Colchicine, Vincristine/vinblastine, Paclitaxel
ATPase that links peripheral 9 doublets and causes bending of cilium by differential sliding of doublets
axonemal dynein
immotile cilia d/t dynein arm defect - M/F infertility, high risk ectopic pregnancy, bronchiectasis, recurrent sinusitis, situs inversus
Kartagener syndrome (primary ciliary dyskinesia)
ergosterol
in fungal plasma membranes
Na/K pump ion movements
1 ATP - 3 Na+ exit cell and 2K+ enter cell
inhibits Na/K pump by binding K+ site
Ouabain
drugs that directly inhib Na/K pump which inhib Na/Ca exchange - increases intracell Ca - increases cardiac contractility
Cardiac glycosides: digoxin, digitoxin
type I collagen
bone, skin, tendon, dentin, fascia, cornea, late wound repair
‘type one = bONE’
type II collagen
cartilage, vitreous body, nucleus pulposus
‘carTWOlage’
type III collagen
reticulin: skin, blood vessels, uterus, fetal tissue, granulation tissue
deficient in vascular subtype Ehlers Danlos
type IV collagen
basement membrane, basal lamina, lens
‘type 4 under the floor’
defective collagen type in Alport syndrome
type IV collagen
where does synthesis, hydroxylation, glycosylation of collagen occur in the cell?
inside fibroblast RER
preprocollagen content
Gly-X-Y where X & Y are proline or lysine
vitC
hydroxylates proline & lysine residues
deficiency of vitC = scurvy
glycosylation of pro alpha chain hydroxylysine residues forms _____ via hydrogen & disulfide bonds
triple helix of 3 collagen alpha chains = procollagen
problems forming triple collagen helix via glycosylation
osteogenesis imperfecta
cleavage of disulfide terminal regions of procollagen forms…
tropocollagen (outside of fibroblast)
covalent lysine-hydroxylysine cross linkage by lysyl oxidase makes
collagen fibrils
problems with cross linking of tropocollagens causes
Ehlers Danlos & Menkes disease
auto dominant decreased production of type I collagen, blue sclera, hearing loss, dental abnormalities
osteogenesis imperfecta
auto dom or recessive
assoc with joint dislocation, berry aneurysm, organ rupture
hyperextensible skin, bleeding tendency, hypermobile joints
Ehlers Danlos syndrome
classical type is mutated type V collagen
vascular type is mutated type 3 collagen
X linked recessive CT disease from impaired copper absorption/transport d/t defective menkes protein ____
ATP7A
low activity of lysyl oxidase of which copper is a necessary cofactor causing brittle, kinky hair + growth retardation + hypotonia
Menkes disease
rich in non hydroxylated proline, glycine, lysine residues (before collagen synthesis)
tropoelastin with fibrillin scaffolding
extracellul cross linking
elastin
defect in fibrillin (glycoprotein that forms sheath around elastin)
Marfan’s
alpha 1 anti trypsin function
inhibits elastase activity from breaking down too much elastin
(deficiency of this enzyme causes emphysema)
