biochem: cellular

Question 1

CDKs

Answer 1

constitutive and inactive

Question 2

cyclins

Answer 2

regulatory proteins that control cell cycle events; phase specific; activate CDKs

Question 3

cyclin-CDK complexes

Answer 3

phosphorylate other proteins to coordinate cell cycle progression; must be activvated and inactivated at appropriate times for cell cycle to progress

Question 4

tumor suppressors

Answer 4

p53 and hypophosphorylated Rb normally inhibit G1-to-S progression; mutations in these genes result in unrestrained cell division (e.g. li-fraumeni syndrome)

Question 5

phases of cell cycle

Answer 5

G0G1->S->G2->M->G1

Question 6

permanent cells

Answer 6

remain in G0, regenerate from stem cells. e.g. neuron,s skeletal and cardiac muscle, RBCs

Question 7

stable (quiescent) cells

Answer 7

enter G1 from G0 when stimulated. e.g. hepatocytes, lymphocytes

Question 8

labile cells

Answer 8

never go to G0, divide rapidly with a short G1. most affected by chemotherapy. e.g. bone marrow, gut epithelium, skin, hair follicles, germ cells

Question 9

rough ER

Answer 9

site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide additions to proteins.

Question 10

Nissl bodies

Answer 10

= RER in neurons. synthesize peptide neurotransmitters for secretion

Question 11

free ribosomes

Answer 11

= unattached to any membrane; site of synthesis of cytosolic and organellar proteins

Question 12

goblet cells and plasma cells are rich in:

Answer 12

RER. they’re secreting mucus/antibodies! so lots of export

Question 13

smooth ER

Answer 13

site of steroid synthesis and detoxification of drugs and poisons. lacks surface ribosomes

Question 14

hepatocytes, adrenal cortex, and gonads are rich in:

Answer 14

SER! they have to detoxify stuff/make steroids

Question 15

golgi

Answer 15

= distribution center for proteins and lipids from ER to vesicles and plasma membrane. also modifies N-oligosaccharides on arparagine and adds O-oligosaccharides on serine and threonine. Adds mannose-6-phosphate to proteins for trafficking to lysosomes

Question 16

endosomes

Answer 16

= sorting centers for material from outside the cell or from the golgi, sending it to lysosomes for destruction or back to the membrane/golgi for further use

Question 17

I-cell dz

Answer 17

= inherited lysosomal storage disorder. defect in N-acetylglucosaminyl-1-phosphotransferase -> failure of the golgi to phosphorylate mannose residues, so proteins are secreted extracellularly rather than delivered to lysosomes. -> coarse facial features, clouded corneas, restricted joint movement, and high plasma levels of lysosomal enzymes. often fatal in childhood.

Question 18

signal recognition particle (SRP)

Answer 18

abundant, cytosolic ribonucleoprotein that traffics proteins from the ribosome to the RER. absent or dysfunctional SRP -> protein accumulation in cytosol

Question 19

vesicular trafficking proteins

Answer 19

COPI: golgi->cis-golgi -> ER, retrograde. COPII: ER -> cis-golgi, anterograde. clathrin: trans-golgi -> lysosomes; plasma membraine -> endosomes (receptor-mediated endocytosis)

Question 20

peroxisome

Answer 20

membrane-enclosed organelle involved in catabolism of very-long-chain fatty acids, branched-chain fatty acids, and AAs

Question 21

proteasome

Answer 21

barrel-shaped protein complex that degrades damaged or ubiquitin-tagged proteins. defects in the ubiquitin-proteasome system have been implicated in some cases of PD

Question 22

microfilaments

Answer 22

usually fxn for muscle contraction, cytokinesis. e.g. actin

Question 23

intermediate filaments

Answer 23

maintain cell structure. e.g. vimentin, desmin, cytokeratin, lamins, GFAP, neurofilaments

Question 24

microtubules

Answer 24

usually fxn for movement, cell division. e.g. cilia, flagella, mitotic spindle, axonal trafficking, centrioles. made of alpha and beta tubulin dimers. grows slowly, collapses quickly.

Question 25

drugs that act on microtubules

Answer 25

Microtubules Get Constructed Very Poorly: mebendazole (antihelminthic), Griseofulvin (antifungal), colchicine (antigout), vincristine/vinblastine (anticancer), paclitaxel (anticancer)

Question 26

molecular motor proteins

Answer 26

transport cellular cargo toward opposite ends of microtubule tracks. dynein = retrograde (+ -> -), kinesin = anterograde (- -> +)

Question 27

kartagener syndrome

Answer 27

= primary ciliary dyskinesia. immotile cilia due to dynein arm defect. causes infertility, bronchiectasis, recurrent sinusitis, and situs inversus

Question 28

ouabain

Answer 28

inhibits Na-K-ATPase by binding to K site

Question 29

cardiac glycosides

Answer 29

= digoxin. directly inhibit Na-K-ATPase, indirectly inhibiting Na/Ca exchange -> increased [Ca] -> inc. cardiac contractility

Question 30

collagen type mnemonic

Answer 30

Be (So Totally) Cool, Read Books: I: bone, skin, tendon; II: cartwolage; III: reticulin (in skin, blood vessels, uterus, fetal tissue, granulation tissue); IV: basement membrane, basal lamina (type IV, under the floor)

Question 31

type I collagen defect

Answer 31

OI type I. problem forming triple helix during glycosylation step

Question 32

type IV collagen defect

Answer 32

alport syndrome, targeted by Abs in goodpasture syndrome

Question 33

steps of collagen synthesis

Answer 33

inside fibroblasts: 1. synthesis (RER). 2. hydroxylation (RER). 3. glycosylation (RER). 4. exosytosis. outside fibroblasts: 5. proteolytic processing. 6. cross-linking

Question 34

scurvy

Answer 34

caused by vit. C deficiency: hydroxylation of collagen requires it

Question 35

ehlers-danlos syndrome

Answer 35

faulty collagen, classically type V but can be type III in vascular type. causes hyperextensible skin, easy bruising, and hypermobile joints. variable genetics

Question 36

menke’s dz

Answer 36

x-linked recessive dz caused by impaired copper absorption and transport -> dec. activity of lysyl oxidase (part of collagen/elastin synthesis) (Cu = cofactor), -> brittle kinky hair, growth retardation, and hypotonia

Question 37

marfan syndrome

Answer 37

caused by defect in fibrillin = glycoprotein that forms a sheath around elastin

Question 38

alpha-1-antitrypsin

Answer 38

inhibits elastase. deficiency can cause emphysema because elastase breaks down elastin in the lungs.