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126 Cards in this Set

  • Front
  • Back
enzyme regulation methods (7)
1. enzyme [] alterations (synthesis or degradation)
2. covalent modification (ex: phosphorylation)
3. proteolytic modification (zymogens)
4. allosteric regulation (ex: allosteric inh.)
5. pH
6. temperature
7. transcriptional regulation (ex: steroid hormones)
regulates checkpoints that control transitions between phases of cell cycle
cyclins
cdk's
tumor suppressors
Gap or growth phase
G phase
Synthesis phase
S phase
stages of the cell cycle
G0->G1->S->G2->Mitosis
phases of mitosis
Interphase
Prophase
metaphasea
anaphase
telophase
shortest phase of cell cycle
mitosis
phase that forms proteins to make dna
g1
phase in which chromosomes replicate
S phase
only protein made at S phase
centriole
chemo drugs that target S phase
antimetabolites
etoposide
chemo drugs that target G2 phase
bleomycin
etoposide
chemo drugs that target M phase
vinka alkaloids and taxols
cells that remain in G0 phase
permanent cells
permanent cells
cells that remain in G0
how permanant cells regenerate
from stem cells
permanant cells
neurons
skeletal/cardiac muscle
rbc's
enter G1 from G0 when stimulated
stable cells
stable cells
hepatocytes
lymphocytes
divide rapidly; never go to g0
labile cells
labile cells
bone marrow
gut epithelium
skin
hair follicles
*rapidly dividing cells*
divide rapidly with a short g1
labile cells
cells rich in RER
mucus-secreting goblet cells of small intestine
ab-secreting plasma cells
site of synthesis of secreted proteins
RER
site of N-linked oligosaccharide addition to many proteins
RER
stain of RER in neurons
nissl bodies
synthesizes enzymes and peptide NT's in neurons
nissl bodies
the distribution center of proteins and lipids from ER to plasma membrane, lysosomes, and secretory vesicles
Golgi
modifies N-oligosaccharides on Asn
Golgi
adds O-oligosaccharide to Ser and Thr
Golgi
adds mannose-6-ph to specific lysosomal proteins
golgi
targets protein from golgi to lysosome
mannose-6-ph label
site of proteoglycan assembly
golgi
site of sulfation of sugars in PG's and of select Tyr on proteins
Golgi
failure of addition of mannose-6-ph to lysosomal proteins
I-cell disease
I-cell disease: where do the enzymes go?
enzymes are secreted out of the cell instead of being targeted by the lysosome
features of I-cell disease:
coarse facial features
clouded cornea
restricted joint movement
high plasma levels of lysosomal enzymes
*often fatal in children
trafficking protein that's retrograde (golgi -> er)
COPI
trafficking protein that's anterograde (RER -> cis-Golgi)
COPII
Clathrin
vesicular trafficking protein:
trans-golgi -> lysosomes
plasma membrane -> endosomes
receptor-mediated endocytosis
endosomes
vesicular trafficking protein that controls receptor-mediated endocytosis
cathrin
functions of golgi (6)
1. distribution center of protein and lipids from ER to plasma membrane, lysosome, and secretory vesicles
2. modifies n-oligosaccharides on asn
3. adds o-oligosaccharides to ser and thr
4. adds mannose-6-ph to lysosymal proteins; this targets it to lysosome
5. PG assembly
6. sulfation of sugars in PG's and tyr on proteins
structure of MT
cylindrical structure
24 nm in diameter
variable length
helical array of polymerized dimers of Alpha and Beta-tubulin
MT's are made up of.....
helical array of polymerized dimers of alpha and beta- tubulin
bound to a dimer of alpha or beta tubulin
2 gtp bound
cell structures with microtubules
flagella, cilia, mitotic spindles
slow axoplasmic transport in neurons
microtubules
grows slowly and collapses quickly
microtubules
drugs that act on microtubules (5)
1. griseofulvin - antifungal
2. taxol - anti-breast ca
3. mebendazole/thiabendazole
4. vincristine/vinblastine
5. colchicine - anti-gout
microtubule polymerization defect resulting in decreased phagocytosis
chediak-higashi syndrome
9+2 arrangement of microtubules
cilia
atpase that links peripheral 9 doublets of cilia
dynein
causes of bending of cilium by differential sliding of doublets
dynein
regrograde motion
dynein
anterograde motion
kinesin
immotile cilia due to a dynein arm defect
kartagener's syndrome
situs inversus
kartagener's
infertility due to immotile sperm
kartagener's
recurrent sinusitis due to inability of cilia to push bacteria and particles out
kartagener's
plasma membrane composition
assymetric fluid bylayer
substances that make of plasma membrane
50% cholesterol
50% phospholipids
sphingolipids, glycolipids, proteins
increased melting point of plasma membrane
with high cholesterol and long saturated fatty acids
major component of rbc membranes
lecithin/phosphatidyl choline
major component of bile
lecithin
major component of myelin
lecithin
major component of surfactant
lecithin
surfactanct aka
DPPC - dipalmitoyl phosphatidyl choline
used in esterification of cholesterol
lecithin
LCAT = lecithin-cholesterol acyl transferase
location of Na+-K+-ATPase
plasma membrane
location of ATP site
cytoplasmic side
for each atp consumed in sodium pump, ? Na go ? and ? K go ?
3 Na+ go out
2 K+ come in
drugs that inhibit sodium pump
Ouabain
Cardiac glycosides
drug that binds to K+ site
Ouabain
inhibits NaKatpase
cardiac glycosides
result of cardiac glycosides on the heart
high cardiac contractility
most abundant protein in the human body
collagen
organizes and strengthens extracellular matrix
collagen
Type I collagen
Bone
skin
tendon
dentin
fascia
cornea
late wound repair
type II collagen
cartilage (including hyaline)
vitreous body
nucleus pulposus
type III collagen
reticulin - skin, bs, uterus, fetal tissue, granulation tissue
type IV collagen
basement membrane or basal lamina
location of synthesis of collagen
RER
location of hydroxylation of collagen
ER
location of glycosylation of collagen
golgi
what cells synthesize collagen mostly
fibroblasts
what steps of collagen synthesis occur inside fibroblast
synthesis
hydroxylation
glycosylation
exocytosis
site of preprocollagen formation
RER
preprocollagen
through translation of collagen alpha chains
structure of preprocollagen peptide
Gly-X-Y peptide
x and y are Pro, hydroxypro, and hyroxylys
needed for hydroxylation of preprocollagen
vitamin C
gets hydroxylated
Pro
Lys
procollagen
triple helix of 3 collagen alpha chains
site of procollagen synthesis
Golgi
synthesis of procollagen by....
glycosylation of pro-alpha-chain Lys residues
exocytosis during collagen synthesis
exocytosis of procollagen into extracellular space
disease where hydroxylation of proline/lys is inhibited
scurvy
disease where glycosylation of pro alpha chain lysine are inhibited
osteogenesis imperfecta
disease where procollagen can not be formed
osteogenesis imperfecta
steps of collagen synthesis occurring outside of fibroblast
proteolytic processing
cross-linking
decifient proteolytic processing
ehlers-danlos
cleavage of terminal regions of procollagen
proteolytic processing
proteolytic processing yields
tropocollagen
reinforcement of many staggered tropocollagen by covalent lysine-hydroxylysine cross links
cross-linking
enzyme that makes covalent lysine-hydroxylysine cross-links
lysyl oxidase
collagen fibril
many staggered tropocollagens linked by covalent lys-hydroxylys cross-linkages
faulty peptide cleaveage of tropocollagen
ehler danlos
faulty collagen synthesis
ehler-danlos
collagen type most affected with ehlers-danlos
Type III
*blood vessel instability*
seen with ehlers-danlos pt
hyperextensible skin
tendency to bleed (bruising)
hypermobile joints
ehlers-danlos association
berry aneurysms
AD with abnormal Collagen type I
Osteogenesis imperfecta
osteogenesis imperfect patient
multiple fractures with minimal trauma
blue sclerae - translucency of conn. tissue over choroid
hearing loss - abnormal middle ear bone
dental imperfections - lack of dentin
type of osteogenesis imperfects that is fatal in utero/neonatal period
type II
maybe confused with child abuse
osteogenesis imperfecta
stains connective tissue
vimentin
stains muscle
desmin
stains epithelial cells
GFAP - glial fibrillary acid proteins
stain neurons
neurofilaments
locations of elastin in body
lungs
large arteries
elastic ligaments
protein rich in Pro and Lys - non hydroxylated form
elastin
tropoelastin has
fibrillin scaffolding
defective fibrillin
marfan's
conformations of elastin
relaxed or stretched
excess elastase activity
emphysema
inhibits elastase
alpha antitrypsin