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Flashcards in Exam 4 Deck (109)
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1
Q

ER

A

continuous network of membranous tubules and sacs that run throughout the cell
gives rise to golgi, lysosomes, and new cell membrane
rough ER
transitional ER
smooth ER

2
Q

rough ER

A

has ribosomes on cytosolic surface

important in protein processing

3
Q

transitional ER

A

involved with budding that sends vesicles to the golgi

important in protein processing

4
Q

smooth ER

A

no ribosomes attached

involved in lipid metabolism

5
Q

translocation

A

process of sending a protein into the ER

some proteins targeted for lumen of ER or to be embedded in its membrane

6
Q

where does all protein synthesis begin

A

free ribosomes in the cytosol (unattached to ER)

proteins destined to remain in cytosol complete synthesis on free ribosomes

7
Q

destination of proteins that complete synthesis on free ribosomes

A
remain in cytosol
nucleus
mitochondria
chloroplasts
peroxisomes
8
Q

destination of proteins that complete synthesis on membrane bound ribosomes

A

plasma membrane
secretory vesicles
endosomes –> lysosomes

9
Q

cotranslational translocation

A

some proteins headed for lumen of ER enter as they are being made (during translation)

10
Q

cotranslational translocation process

A

synthesis begins on a free ribosome in the cytosol
proteins have a unique signal sequence near the N-terminus that is about 20 AA long and contains a stretch of hydrophobic AA
signal recognition particle (SRP) that is a protein-RNA complex recognizes signal sequence and binds to the SS and ribosome which halts translation
mRNA-ribosome-polypeptide-SRP complex binds to protein on ER called SRP receptor (SRP receptor binds SRP and SS on polypeptide binds to protein complex next to SRP receptor called translocon
translocon forms channel into ER lumen
binding of SRP receptor to SRP causes SRP to be released from SS and ribosome allowing translation to resume
growing polypeptide inserted into channel in translocon but the SS is retained within the translocon bound to the wall of the channel
signal peptidase associated with translocon on lumen side and cleaves SS releasing polypeptide into lumen when translation is complete

11
Q

posttranslational translocation

A

some ER lumen proteins made on free ribosome then translocated into ER

12
Q

ER membrane proteins with an N-terminus SS and an internal stop transfer sequence

A

single pass membrane proteins
translocation proceeds as described in cotranslational translocation but midway through synthesis there is a stop transfer sequence that stops translocation (by altering translocon) so the remainder of polypeptide remains on cytosolic side
stop transfer sequence passes through wall of translocon into phospholipid bilayer
when finished - N-terminus on lumen side and C-terminus on cytosolic side with stop transfer sequence embedded in membrane

13
Q

ER membrane proteins with internal signal sequence(s) and/or internal stop transfer sequence(s)

A

single or multiple pass membrane proteins
orientation of single pass membrane proteins may be in either orientation (N-terminus or C-terminus on outside)
some proteins have multiple internal signal sequences and stop transfer sequences which results in multiple pass membrane proteins

14
Q

protein folding and processing in the ER

A

chaperones/folding
cleavage
disulfide bridge formation
glycosylation/other modifications

15
Q

chaperones and folding

A

polypeptides must be in correct folding patter to function properly
correct folding mediated by chaperones (which are also proteins)
complete polypeptide will assume correct folding spontaneously but before translation is complete it can assume an incorrect pattern or aggregate with other partially complete polypeptides
chaperones in ER and cytosol bind to nascent polypeptide to keep it from interacting with anything else until synthesis is complete

16
Q

prion

A
improperly folded protein
can be disease causing unit
can't be destroyed by heat
can interact with other properly folded proteins and turn them into prions
ex: mad cow disease
17
Q

cleavage

A

many polypeptides have AAs removed after translation
removal of inital methionine
extensive cleavage as with preproinsulin

18
Q

cleavage process to form insulin

A

preproinsulin has N-terminal SS which is removed inside Er to make proinsulin
proinsulin becomes insulin when internal AA sequence is removed in ER lumen and 2 polypeptide fragments are joined by disulfide bridges

19
Q

disulfide bridge formation

A

protein disulfide isomerase responsible for making and breaking disulfide bridges until most stable configuration is formed
ONLY IN LUMEN
disulfide bridge is a covalent bond between 2 cysteine residues
disulfide bridges only found in proteins that are to be secreted or are exterior membrane proteins because the cytosol contains reducing agents that would break the bonds

20
Q

glycosylation and other modifications

A

other chemical modifications occur in the ER lumen
glycosylation: addition of oligosaccharides (carbs)
external membrane proteins glycosylated this way

21
Q

lipids synthesized in the smooth ER

A

most membrane lipids including phospholipids, glycolipids, and cholesterol

22
Q

phsopholipid synthesis

A

occurs in outer layer of ER membrane bilayer

enzyme flippase moves phospholipids to inner membrane layer after synthesized on outer membrane layer

23
Q

export from ER

A

vesicles bud off the ER from transitional ER and carry ER lumen content and ER membrane components to the golgi
vesicles first fuse to ER-golgi intermediate compartment which gradually becomes cis-face cisternae of golgi which gradually becomes trans-face cisternae
from trans-face cisternae vesicles bud off to fuse with cell membrane (secretion and cell membrane formation) or fuse with endosomes/lysosomes

24
Q

where is golgi most abundant

A

secreting cells (exocytosis)

25
Q

clathrin coated vesicles

A

as vesicles bud off the ER, the region to form a vesicle first becomes coated in protein (ex: clathrin) through complex series of reactions
protein forms in network pattern
binding stimulates budding because it distorts membrane
after vesicle buds off, clathrin is removed

26
Q

membrane fusion

A

a vesicle fuses with either cell membrane or another membrane (ex: endosome)
process involves binding of v-SNARES (on vesicle) to t-SNARES (on target membrane)

27
Q

lysosomes

A

small membranous sacs containing lysosomal acid hydrolases (powerful hydrolytic enzyme)

28
Q

lysosomal hydrolases

A

about 50 kinds
can break down all cellular organic compounds
only work in acidic environment (pH ~5) of lysosome (cell would be okay if one burst because wouldn’t be functional in non-acidic cytosol)

29
Q

endocytosis

A

extracellular material brought into a vesicle by this

30
Q

pinocytosis

A

small scale endocytosis

involves clathrin-coated endocytic vesicles

31
Q

endosome formation

A

small endocytic vesicles fuse with early endosomes (larger vesicle than endocytic vesicles)
membrane recycled to cell membrane and early endosome becomes late endosome
hydrolases in golgi carried by vesicles to late endosome and material brought in from outside by pinocytosis is digested

32
Q

lysosome formation

A

late endosomes mature into lysosomes with a high concentration of acid hydrolases

33
Q

phagocytosis

A

endocytosis on a large scale
phagocytized material enters cell and a phagosome is formed
lysosome fuses with phagosome and digests phagocytized material

34
Q

autophagy

A

old organelles surrounded by ER membrane and sac becomes autophagosome
lysosomes fuse with autophagosome and old organelles are digested

35
Q

mitochondria

A

organelles specialized for aerobic respiration

believed to have arisen by endosymbiosis of a prokaryote in an ancestral eukaryotic cell

36
Q

structure of mitochondria

A

double membrane with inner membrane folded creating cristae
between 2 membranes is inner membrane space and inside inner membrane is the matrix
outer membrane highly permeable to small molecules due to channels formed by porin proteins
inner membrane impermeable to most ions and small molecules

37
Q

genetic material of mitochondria

A
circular DNA (like bacteria)
16 kb long in most animals (plant mitochondrial DNA considerably longer)
many copies of circular DNA in each mitochondrion
38
Q

mitochondrial genes include what

A

genes for a few of the proteins needed for oxidative phosphorylation (the rest are encoded by nuclear genes)
all mitochondrial rRNA genes (bc they have their own ribosomes)
all mitochondrial tRNA genes

39
Q

human mitochondrial genome

A

about 16 kb long
encodes 13 proteins that are embedded in inner mitochondrial membrane and are involved in oxidative phosphorylation
encodes the 16S and 12S rRNA and the 22 tRNAs
mitochondrial genetic code deviates from universal genetic code
may contain other genes that are found in open reading frames hidden in other genes

40
Q

mitochondrial ribosomes

A

16S and 12S rRNA
16S - large subunit (39S)
12S - small subunit (28S)

41
Q

ribosomal proteins

A

all coded for by nuclear genes and the proteins are transported into the mitochondrion
lower RNA/protein ratio in mitochondria versus E. coli

42
Q

mitochondrial large subunit

A

16S rRNA
29S
48 proteins (28 similar to E. coli)

43
Q

mitochondrial small subunit

A

12S rRNA
28S
30 proteins

44
Q

mitochondrial gene inheritance

A

usually passed to the zygote only via the egg and not the sperm (maternal inheritance)
mitochondrial genes seem to have a higher mutation rate so they’re useful in revealing genetic differences between closely related organisms
multiple copies of each mitochondrial gene in every cell so recovery of mitochondrial genetic material from minute samples is easier than recovery of genetic material

45
Q

evidence for endosymbiosis of mitochondria

A

circular chromosome with one origin of replication
formylmethionine used in initiation of protein synthesis
similarity of rRNAs to bacteria

46
Q

other mitochondrial components

A

majority of mitochondrial proteins imported from cytosol (at least ~1000 proteins encoded by nuclear genes and imported in)

47
Q

TOM

A

protein used in outer membrane transport

48
Q

TIM

A

protein used in inner membrane transport

49
Q

signal cell/signaling cell

A

cell releasing signal

50
Q

target cell

A

cell picking up signal

51
Q

direct cell-cell signaling

A

communication via direct connection between cells

seen in some embryonic development

52
Q

types of signaling by secretion

A

endocrine signaling
paracrine signaling
autocrine signaling

53
Q

endocrine signaling

A

hormones (signal molecules) released from endocrine organ and travels through circulatory system to target organ

54
Q

endocrine organs

A
pituitary
thyroid
parathyroids
pancreas
adrenal glands
gonads
many others
55
Q

paracrine signaling

A

signal molecules travel to local target organs (not via circulatory system)
ex: neurotransmitters that cross synapse in nervous tissue

56
Q

autocrine signaling

A

signaling cell and target cell are the same
signal molecules travel very locally (same cell)
ex: proliferation of T cells of immune system which is induced by antigens released by T cells

57
Q

steroid hormones

A

can cross cell membrane of target cells because they’re small and hydrophobic
bind to receptor in cell cytosol then travels through nuclear pore into nucleus and acts on DNA to activate transcription of gene
made from cholesterol
testosterone
estrogen
progesterone (sex steroids made chiefly by the gonads)
corticosteroids (made by adrenal gland)

58
Q

molecules that act like steroids but aren’t steroids

A

thyroid hormone
vitamin D
retinoic acid

59
Q

nitric oxide (NO)

A

important in certain paracrine signaling pathways
involved in signaling that results in blood vessel dilation
half life of only a few seconds making it paracrine signaler

60
Q

how is NO synthesized

A

nitric oxide synthetase (enzyme) uses arginine as substrate to form NO

61
Q

NO effect process

A

endothelial cells of vessels synthesize NO in response to neurotransmitters
NO travels and enters nearby smooth muscle cells where it activates guanylyl cyclase which synthesizes cGMP (second messenger molecule)
cGMP relaxes smooth muscle which dilates the vessel

62
Q

nitroglycerin

A

used in treating heart disease
converted to NO
releases such large amount of NO that it can have affect even with short half life

63
Q

neurotransmitters

A
paracrine signalers
move from a neuron to another neuron (or muscle), diffuse across the synaptic cleft, and bind to receptor on the surface of the target
hydrophilic so can't cross membrane
bind to receptor on membrane which opens ion channels on the target cell initiating nerve impulse
acetylcholine
dopamine
epinephrine
serotonin
histamine
glutamate
glycine
GABA
64
Q

epinephrine

A

neurotransmitter but can also function as a hormone secreted by the adrenal gland (called adrenaline in this case)

65
Q

peptides

A

a few to more than 100 AA
can’t cross cell membrane so bind to receptors on membrane
insulin and glucagon (pancreas)
hormones of pituitary (growth hormone and FSH)

66
Q

eicosanoids

A

lipids that bind to cell surface receptors (paracrine)

prostaglandins

67
Q

prostaglandins

A

some promote inflammation

68
Q

prostaglandin synthesis

A

enzyme cyclooxygenase (COX) responsible for synthesis

69
Q

COX

A

inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin
COX-1
COX-2

70
Q

effect of blocking COX-1

A

gastrointestinal problems

71
Q

aspirin

A

blocks both COX-1 and COX-2

72
Q

g protein coupled receptors

A

largest family of surface receptors
7-pass membrane proteins
may be as many as 1000 types encoded by human genome
epi and prostaglandins
olfactory and taste (bitter and sweet)
behavioral and mood regulation (nt including serotonin, dopamine, GABA, and glutamate)

73
Q

GCPR process

A

when signal molecule binds to GPCR the protein undergoes a conformational change on cytosolic side that causes G protein on cytosolic side to release its GDP and exchange it for GTP
alpha chain of G protein tis released and can interact with adenylyl cyclase to form cAMP from ATP
cAMP (second messenger) then travels within the cell and elicits further responses

74
Q

intracellular signal transduction

A

cAMP and others
signal molecules may cause increase in intracellular cAMP (second messenger) concentration by activating adenylyl cyclase
cAMP may then activate protein kinase A
protein kinase phosphorylates proteins and in some cases activates them while in other cases inactivates them
protein kinase can also enter nucleus and activate transcription

75
Q

exosomes

A

vesicles released from cells with proteins or RNAs

76
Q

stages of dividing cells

A
cell growth
DNA replication
mitosis
cytokinesis
G1, S, G2, M
77
Q

S

A

synthesis

DNA replication occurs during this phase

78
Q

G1

A

cell growth

first phase

79
Q

M

A

mitosis

80
Q

G0

A

non-dividing cells enter this phase after G1 if certain growth factors aren’t present
restriction point

81
Q

4 major checkpoints in cell cycle

A

G1/S
S
G2/M
M

82
Q

G1/S checkpoint

A

DNA damage checkpoint
checkpoint near end of G1
cell cycle will halt if DNA has been damaged and need repair

83
Q

S checkpoint

A

DNA damage checkpoint
mid-S
cell cycle will also halt here if DNA has damage that needs repair

84
Q

G2/M checkpoint

A

DNA damage checkpoint
near end of G2
cell cycle will halt if DNA replication is not complete or if DNA damage is detected
regulated by MPF

85
Q

M checkpoint

A

spindle assembly checkpoint
around anaphase
mitosis halted unless chromosomes have properly aligned
colchicine is agent that inhibits spindle fiber assembly so cells will not not divide and stay at this point until inhibitor gone

86
Q

MPF

A

maturation promoting factor
cyclin B/Cdk1 complex phosphorylated at one amino acid, dephosphorylated at 2 other amino acids
active form regulates entry into mitosis at G2/M checkpoint

87
Q

CDK

A

cyclin dependent kinase

88
Q

how does MPF regulate entry into mitosis

A

related to continual synthesis of cyclin, its degradation, a kinase that phosphorylates Cdk1, and a phosphatase that dephosphorylates Cdk1
DNA damage activates separate kinase that results in deactivation of MPF (so cell can’t enter into mitosis)

89
Q

examples of Cdk1/cyclin B’s action

A

condensins are activated by phosphorylation by Cdk1/cyclin B
initiates breakdown of nuclear envelope that occurs at outset of prophase
fragmentation of golgi apparatus
spindle formation

90
Q

condensins

A

protein complexes that are responsible for chromosome condensation during mitosis and meiosis

91
Q

nuclear envelope breakdown process

A

involves phosphorylation of lamins by Cdk1/cyclin B causing their depolymerization
phosphorylation of lamins, nuclear pore complexes, and inner nuclear membrane proteins

92
Q

p53 protein

A

tumor suppressor gene on short arm of chromosome 17
when DNA is damaged p53 protein causes other proteins to bind to Cdk thereby inactivating it so cell cycle halts
involved in stimulating DNA repair (and if damaged beyond repair stimulates apoptosis)
if p53 damaged - cells with damaged DNA will continue to divide (possibly leading to cancer)

93
Q

Li-Fraumeni syndrome

A

person with only 1 copy of p53 gene

have high chance of developing tumors

94
Q

fragmentation of golgi apparatus process

A

phosphorylation of golgi matrix proteins via Cdk1/cyclin B activity

95
Q

spindle formation process

A

phosphorylation of centrosome and microtubule-associated proteins via Cdk1/cyclin B activity

96
Q

genetics of cancer

A

involves 2 classes of gene alterations that produce cancer
oncogenes
tumor suppressor genes

97
Q

oncogenes

A

changes in genes that regulate the proliferation of cells is a prerequisite to becoming a cancer cell
oncogene stimulates cell to divide in an unregulated fashion
ras gene family

98
Q

how do oncogenes enter cells

A

tumor virus

mutation(s) that occur to existing cell-cycle genes (proto-oncogenes) - more common!!

99
Q

types of mutations that turn proto-oncogenes into oncogenes

A
point mutations
translocations
deletions
duplications
gene amplification
100
Q

tumor suppressor genes

A

in normal cells these genes are present to inhibit growth of cells containing oncogenes
these genes must be altered or deleted in order for a tumor to become malignant
p53

101
Q

role of miRNAs in tumor production

A

increased tumor activity is often associated with loss of some normal miRNA activity

102
Q

percentage of tumors that arise from mutation to proto-oncogene producing oncogene

A

80%

103
Q

ras gene family

A

most common oncogene family in human cancers
25% of all cancers
50% of colon carcinomas
25% of lung carcinomas
point mutations convert a ras proto-oncogene into an oncogene (changes 1 important AA)

104
Q

normal ras gene activity

A

normal ras protein made by proto-oncogene bound to cytosolic face of cell membrane and may be inactive (bound to GDP) or active (bound to GTP)
when growth factor (such as platelet derived growth factor - PDGF or epidermal growth factor - EGF) is recognized by a cell it binds to a target cell membrane receptor and cytosolic face of the receptor is phosphorylated
this results in recruitment of GDP-GTP exchange factor to membrane which converts ras protein into active form
this sets off series of reactions that activate cell division
after activation has occurred, the ras protein hydrolyzes its GtP to GDP and cell division is turned off

105
Q

mutant ras gene activity

A

altered ras protein made by oncogene is incapable of hydrolyzing GTP to GDP so cell division is constitutively turned on

106
Q

percentage of cancers with altered p53 gene

A

50%

107
Q

normal p53 gene activity

A

controls cell cycle, DNA repair, and apoptosis
p53 always made but usually is bound to MDM2 protein which degrades and inactivates it
when DNA is damaged, MDM2 dissociates from p53 making it more stable and turning its activity on
p53 is a transcription factor so if DNA damage is not repaired it results in cell-cycle arrest and apoptosis

108
Q

how does MDM2 dissociate from p53 when DNA damage present

A

ATM (protein kinase) stimulated by damage

ATM phosphorylates MDM2 and p53 causing MDM2 to lose its ability to bind to and degrade p53

109
Q

mutant p53 gene

A

altered p53 can’t arrest the cell cycle, stimulate DNA repair, and cause apoptosis so cells will survive and will have higher mutation rates
BRCA1 and BRCA2 (common in breast and ovarian cancers) have similar ignoring of cell cycle checkpoints