Cell Bio Exam 1

Front 1

Where is the nuclear lamina located? What does it do?

Back 1

- lies on inside of nucleus and is closely associated with inner nuclear membrane & nuclear pore complexes

- connect nuclear membrane to chromatin

Front 2

outer nuclear envelope is continuous with the _____

Back 2

ER

Front 3

Nuclear envelope is connected to the cytoplasm by ______. What size do you have to be to fit through a nuclear pore?

Back 3

- nuclear pores

- less than 10,000 Da

Front 4

What is the gene defect in progeria? What class of diseases is it?

Back 4

- Lamin A

- laminopathy

Front 5

What happens in rest of restrictive dermopathy? What class of diseases is it?

Back 5

- loss of gene that cleaves pre-lamin into lamin

- laminopathy

Front 6

Nuclear membrane assembly/disassembly?

Back 6

- during interphase lamins are unphosphorylated

- early in mitosis they are phsophorylated causing chromatin-nuclear membrane connection to break & begins disassembling

- late in mitosis phosphatase brings them back to unphosphorylated state permitting reassembly to occur

Front 7

What happens in huntington's disease?

Back 7

- protein huntingtin accumulates in nucleus of cells

Front 8

What happens in Systemic Lupus Erythromatosus (SLE)? How do you test for it?

Back 8

- ANA

- presence of ANA in the blood

Front 9

What is the structure of the nuclear pore?

Back 9

- annular ring with cage & plug --> need to move out of way & expand for protein bigger than 10,000

Front 10

What does the NLS look like?

Back 10

- very short, basic (positivey charged), 4-5 amino acids

Front 11

In huntingtons the proteins abnormally acquire a ______

Back 11

NLS

Front 12

Cargo smaller than_____ kDa can enter nucleus via diffusion—nuclear pores may be used but not required

Back 12

- 5-10 kDa

Front 13

Chaperone proteins (e.g., ________) bind to NLS on cargo and escort cargo to nuclear pore

Back 13

- importin & exportin

Front 14

membranes are about ____% of the total cell volume

Back 14

- 50%

Front 15

Most membranes are a little less than half _____, a little less than half ______, and have a small amount of _____. However, this can vary greatly depending on the function of the membrane. Ie: myelin has more ______ b/c wan't to propagate charge, mitochondria has more _____ because has ox phos

Back 15

- protein

- lipid

- carbohydrate

- lipid

- proteins

Front 16

integral membrane protein vs peripheral proteins

Back 16

- means embedded in the membrane at all, not just transmembrane

- peripheral closely associated, but not embedded

Front 17

what are the classes of membrane lipids in order of abundance in the membranes?

Back 17

1) phospholipids
2) sphingolipids
3) cholesterol
4) eicosanoids

Front 18

lipids are _________ distributed in the membrane

Back 18

- asymetrically

Front 19

PGE2 is derived from an __________. what is it important for?

Back 19

- eicosanoid

- induces uterine contractions

Front 20

TXA2 is derived from an _______. what is it important for?

Back 20

- eicosanoid

- induces platelet aggregation

Front 21

LTCA4, LTD4 & LTE4 are derived from __________. what are they important for?

Back 21

- eicosanoids

- branchoconstriction & vasodilation in asthma

Front 22

which two viruses take advantage of the fusogenic properties of phospholipids?

Back 22

- HIV

- measles

Front 23

__________ have fusogenic properties while _______ do not.

Back 23

- phospholipids

- sphingolipids

Front 24

Tay-sach's disease is a disease of ________ metabolism, aka an _______

Back 24

- sphingolipid

- LSD

Front 25

Gaucher's disease is a disease of ________ metabolism, aka an _______

Back 25

- sphingolipid

- LSD

Front 26

Fabry's disease is a disease of ________ metabolism, aka an _______

Back 26

- sphingolipid

- LSD

Front 27

Niemann-Pick disease is a disease of ________ metabolism, aka an _______

Back 27

- sphingolipid

- LSD

Front 28

what are 4 diseases of sphingolipid metabolism (LSDs)

Back 28

- Gaucher's
- Tay-Sach's
- Fabry's
- Niemann-Pick

Front 29

is the membrane more fluid with shorter or longer acyl length? fewer or more double bonds? higher or lower temp? more or less cholesterol?

Back 29

- shorter

- more double bonds

- higher

- less cholesterol

Front 30

what happens in walking mycoplasma pneumonia?

Back 30

- mycoplasma extract cholesterol from membrane so membrane becomes very fluid

Front 31

what do lipid rafts do?

Back 31

1) signal transduction
2) endocytosis
3) rapid re-organization of membrane for ECM modification & motility

Front 32

what amino acids help make a protein transmembrane?

Back 32

- 20-25 hydrophobic amino acids (nonpolar)

Front 33

what happens in hereditary spherocytosis?

Back 33

- normally connected Integral membrane proteins (ex band 3) w/ spectrin cables that run below cytoplasm side using ankyrin

- if have defect can't have membrane-cytoskeletal interactions resulting in weird shape red blood cells

- causes anemia & hepatosplenomegaly

Front 34

what are glycoproteins important for?

Back 34

1) blood-type antigens
2) pathogen recognition
3) resevoir for cytokines/growth factors

Front 35

how does coccidia work?

Back 35

- recognizes specific carbohydrates on intestinal cell surface

Front 36

how does taxoplasmosis work?

Back 36

- recognize certain glycoproteins expressed on cells

Front 37

channel-mediated & carrier-mediated are examples of _______ transport. The glucose permease is a good example of this (________ diffusion)

Back 37

- passive

- aka facilitated transport

Front 38

the sodium glucose transporter is a good example of _______ transport. how does it work? Band 3 anion exchanger is a good example of ________.

Back 38

- coupled

- harvests energy from sodium gradient to push glucose against its concentration gradient

- antiport

Front 39

how do you take glucose from the intestine into blood cells?

Back 39

- low glucose in gut (bc of volume) after you eat --> bring glucose into cell (where [ ] high w/ sodium glucose cotransporter)

- then glucose can passively diffuse into blood & use sodium potassium pump to go out of cell

- the overall process is active

Front 40

what are the 3 diseases of defective ABC transporters?

Back 40

1) cystic fibrosis (CF transmembrane receptor)

2) hypoglycemia in infancy (sulfonylurea receptor)

3)drug resistance (p-glycoprotein/MDR)

Front 41

Rare genetic disorder characterized by severe HDL deficiency in plasma

Back 41

tangier disease

Front 42

Hallmark of _________ is accumulation of cholesteryl ester (CE) in various tissues, leading to severe CVD

Back 42

- Tangier Disease

Front 43

what happens in tangier disease?

Back 43

- ABC1 transporter (ATPase) is defective

- prevents efflux of CE from cells --> therefore no need for HDL so it gets cleared from plasma

Front 44

some of excess damage in stroke is due to ________

Back 44

- pinocytosis

Front 45

pneumonoultramicroscopicsilicovalcanonesosis

Back 45

- when phagocytosis of asbestos particles happens b/c cannot digest

- turns into mesothelioma

Front 46

what are the diseases of the dark side of phagocytosis (in an actin mediated process)?

Back 46

- Legionnaire's
- Leprosy
-Leishmaniasis
- TB
- Taxoplasmosis/coccidiosis
- Streptococcus

Front 47

clathrin-coated pits & vescles are associated with what?

Back 47

- RME

Front 48

familial hypercholesterolemia is a disease of what?

Back 48

- dark side of RME

- problem with LDL receptor

Front 49

maternal IgG getting into baby bloodstream is a good example of what? explain the pH changes

Back 49

- RME

- receptor is stable at low pH therefore does not dissociate in endosome & dissociates when it gets to blood which is regular pH

Front 50

influenza & rabies virus get into cell via _____

Back 50

RME

- fusing with endosome released the viral genome into cell

Front 51

Housekeeping (constitutive) genes

Back 51

Genes expressed in all cells because they provide basic functions needed for sustenance of all cells.

Front 52

is a nucleosome DNase accessible?

Back 52

- no

Front 53

_______ is transcriptionally inactive and not accessible to limiting amounts of DNase I. _________ transcriptionally active and accessible to limiting amounts of DNase I. ___________ sections of chromatin (usually in control regions) that are very sensitive to DNase I.

Back 53

- heterochromatin

- euchromatin

- hypersensitive sites

Front 54

locus control regions? how were they mapped?

Back 54

- regulate chromatin organization over large regions

- by observing DNase sensitivity, there was a region before gene that became highly sensitive to DNase

Front 55

Protein complexes like ______ can alter chromatin structure. what do they do?

Back 55

- SWI-SNF

- thought to increase mobility of nucleosomes

Front 56

what residues get acetylated? what does this do?

Back 56

- lysines on histones are acetylated which leads to unfolding of chromatin

- many transcriptional activators possess histone acetylransferase activity

- repressors usually have histone deacetylases

Front 57

methyl groups (ie hypermethylation) is used to ______ a gene. Conversely, gene activity is associated with _________. CpG methylation is a key mediator of ________ and other epigenetic effects. Which residues get methylated?

Back 57

- silence

- hypomethylation

- X-inactivation

- C's

Front 58

what are the 4 factors a gene needs to prepare for expression?

Back 58

1) LCR
2) SWI-SNF (nucleosome remodeling complexes)
3) histone acetylation
4) changes in methylation

Front 59

In mammals, DNA _______ adds a methyl group to the fifth carbon atom of some, but not all, cytosine residues in CpG dinucleotides. This is a problem often b/c Deamination of 5-methyl cytosine produces ________; a change that is not “noted” by the repair machinery.

Back 59

- methyltransferase

- thymine

Front 60

_______: They are long stretches of DNA in the promoter regions of genes that are actively transcribed in all cell types. they almost always have or do not have methylation regardless of if gene is being expressed?

Back 60

- CpG Islands

- almost always lack methylation regardless of whether gene is being expressed

Front 61

p53 is a ________ because it has DNA binding domains that help bind to enhancer regions

Back 61

- transcriptional activator

Front 62

how are heat-shock genes activated? what is this an example of?

Back 62

- even if TFIID bound, in the absence of heat shock gene is still off

- upon heat shock the (HSF = heat shock factors) bind the gene & it is turned on

- inducible gene expression

Front 63

how do steroid hormones work? do they bond enhancer elements or promoter regions?

Back 63

- diffuse into cell & bind specific steroid receptor inhibitor complexes displacing the inhibitor

- the hormone-receptor complex goes into nucleus & binds intracellular steroid receptors (DNA-binding molecules)

- binding sites on DNA are termed response elements (enhancer elements)

Front 64

steroid hormones diffuse through membrane & bind to specific ___________. When bound to hormone, these receptors are site-specific DNA binding molecules.The binding sites on DNA for the hormone-steroid receptor complex are termed _____________

Back 64

- intracellular steroid receptors

- response (or enhancer) elements

Front 65

In the presence of glucose, the transcription factor _____ is activated and sent to the nucleus & promoter region (maybe enhancer region) to turn on the _______ gene

Back 65

- PDX1

- insulin

Front 66

what do the following transcription factors regulate? Isl-1, MyoD, Oct-2

Back 66

1) Isl-1: islet cells of pancreas --> insulin

2) MyoD: skeletal muscle --> myosin

3) Oct-2: B-cells --> immunoglobulin heavy & light chains

Front 67

Powerful technique used to determine differences in the mRNA population between two cell types.

Back 67

DNA Microarrays

Front 68

how do you extract mRNA from a cells? how do DNA microarrays work?

Back 68

- poly dT column

- make disease cells red & WT green - if they have equal amounts

- if particular mRNA is present at abnormal levels in one cell type you will see either more green or more red

Front 69

how do antisense oligonucleotides work?

Back 69

- complementary binding of RNA will stop transcribing from the ribosome

Front 70

how does siRNA work?

Back 70

- targeted destruction of particular mRNAs via complementarity to dsRNA

Front 71

once siRNA is injected into cell, __________ complex forms. Then there is target mRNA recognition by complementary base pairing & degradation. This is done by the ____ complex.

Back 71

- ribonucleoprotein complex

- RISC complex = RNA-induced silencing complex

Front 72

_________ are found either free in the cytoplasm or associated with
the endoplasmic reticulum.

Back 72

- Ribosomes

Front 73

inbetween the 5' cap & coding region & poly A tail there are ___________ regions

Back 73

- untranslated regions (5' & 3' UTRs)

Front 74

3 pair base code can specify _____ amino acids. These groups of 3 bases are called _______. For most amino acids, there is more than one code word (aka the code is ________).

Back 74

- 64

- codons

- degenerate

Front 75

The acceptor sequence 5' CCA-OH on the tRNA is added ________.

Back 75

- post transcriptionally

Front 76

before amino acid is incorporated into protein chain, it's attached to carboxyl end to 3' of right tRNA molecule to: covalently link the aa to the tRNA with the right _________ and attachment ______ the aa

Back 76

- anticodon

- activates (ie generates high energy linkage @ carboxyl end)

Front 77

For any given amino acid, the activation & transfer steps are catalyzed by the same ___________. There is a ______ for every amino acid.

Back 77

- aminoacyl-tRNA synthetase

- synthetase

Front 78

how do you activate the amino acid using the particular aminoacyl tRNA synthetase? (2 steps)

Back 78

1) take amino acid + ATP --> aminoacyl-AMP

2) aminoacyl-AMP + tRNA --> aminoacyl-tRNA +AMP

Front 79

what would be the anticodon for 5' AUG 3'?

Back 79

- 5' CAU 3'

Front 80

what is the wobble hypothesis?

Back 80

- more relaxed bonding takes place b/w 3' base of codon & 5' base of anti-codon

- arrangement allows for single tRNA to recognize several codons

Front 81

what 3 things need to assemble for the early steps in protein synthesis? what happens once they find AUG? what site do they assemble in?

Back 81

at AUG...
1) cap binding protein
2) eIF2-GTP-Met-tRNA
3) 40s subunit & additional eIFs (eIF4) --> this helps 40s subunit to assemble

- once find AUG, GTP is hydrolyzed to GDP and release eIF2--> bring in 60s

- assemble in P site, A site is empty at this point

Front 82

The ___ site accommodates the incoming amino acyl-tRNA.
The ____ site contains the peptidyl-tRNA complex (the tRNA still linked to all the amino acids added to the chain so far).
The ___ site is for empty tRNA that has been used.

Back 82

- A

- P

- E

Front 83

__________ are required to position subsequent amino acyl-tRNAs on the ribosome. The hydrolysis of ____ furnishes the energy for the translocation
step.

Back 83

- Elongation factors (EF)

- GTP

Front 84

EF1

Back 84

- catalyzed GTP-dependent binding of aminoacyl-tRNA to ribosomes

- regulates fidelity/rate of polypeptide elongation during translation

Front 85

The soluble protein ____ is required for aminoacyl-tRNA binding in A site during chain elongation. This forms a ________ complex with aminoacyl-tRNA & GTP. The binding is followed by GTP hydrolysis and release of the factor.

Back 85

- EF1

- ternary complex

Front 86

____ is needed for translocation from the A --> P site in ribosome. This is a ____ dependent process.

Back 86

- eEF2

- GTP

Front 87

What site in the ribosome is the peptide bond formed on the growing protein? who catalyzes this peptide bond formation? why is this interesting?

Back 87

- A site

- peptidyl transferase (this is actually an enzymatic part of the ribosome) --> aka a ribozyme

Front 88

Three triplets (UAA, UAG and UGA) function as _______signals. A ________ binds to the stop codon and causes termination.

Back 88

- termination

- termination factor

Front 89

what's the difference b/w mRNA in prokaryotes vs eukaryotes?

Back 89

- monocystronic in eukaryotes

- polycystronic in prokaryotes

Front 90

the ________ sequence in prokaryotes helps to specify which AUG codes for a gene. what is it?

Back 90

- Shine-Dalgarno sequence

- region in 3' of 16s ribosomal RNA that is copmlementary to translation initiation sites

Front 91

What are the 4 diseases of ABC ATPase transporters?

Back 91

1) CF
2) hypoglycemia in infancy
3) MDR
4) Tangier disease

Front 92

What are the 3 diseases of RME?

Back 92

- Familial hypercholesterolemia

- Rabies, Influenza

Front 93

What are the 7 diseases of phagocytosis?

Back 93

1) listeria
2) legionnaires
3) Leishmaniasis
4) Leprosy
5) Taxo/coccidiosis
6) TB
7) Streptococcus

Front 94

Protein synthesis begins in the __________. what tells the protein to move to the ER to continue synthesis?

Back 94

- cytoplasm

- first two dozen (24) aa at N-terminal are hydrophobic

Front 95

If a protein is made in the cytoplasm, what are the 4 fates? what is default?

Back 95

1) cytoplasm
2) Mito
3) Nucleus
4) Peroxisome

- default is stay in cytoplasm

Front 96

If a protein is made in the ER, what are the 5 fates? what is default?

Back 96

1) Golgi
2) ER
3) Lysosomes
4) Secretory vesicles
5) Plasma membrane

- default is be secreted

Front 97

what is the signal to get to the mitochondria?

Back 97

- 75 long amino acid stretch (complicated)

Front 98

To target the peroxisome the sequence is ____. To target the ER the sequence is ______.

Back 98

- SKL

- KDEL

Front 99

what induces chaperone proteins?

Back 99

- inducible by conditions that cause unfolding of newly made proteins (high temp, toxins)

- bind unfolded, misfolded & aggregated proteins & chaperone them to the proteasome for degradation

Front 100

__________ Bind unfolded, mis-folded, and aggregated proteins; chaperone them to __________ for degradation

Back 100

- chaperone proteins

- proteasomes

Front 101

what are two diseases of defective peroxisomal targeting?

Back 101

- Zellweger syndrome

- Neonatal Adrenoleukodystrophy

Front 102

Zellweger is a disease of ________.

Back 102

- defective peroxisomal targeting

Front 103

Neonatal Adrenoleukodystrophy is a disease of ________.

Back 103

- defective peroxisomal targeting

Front 104

the inside of the ER is equivalent to what? why is this important for transmembrane proteins?

Back 104

- the outside of the cell

- transmembrane proteins that face inside the ER & are secreted end up on the face of the cell

Front 105

What are the order of events in the ER & Golgi?

Back 105

1) ER: translation sorting sugar addition

2) Cis golgi: PO4 & sort
3) trim + sort
4) trim + add + sort
5) add + sort
6) process + sort
7) send vesicles

Front 106

lysosomal enzymes work best as ____ pH

Back 106

- low

Front 107

What is the label added to the protein to specify it as a lysosomal protein? why is this a special label?

Back 107

- mannose-6-phosphate added by M6P kinase

- only label that isn't an amino acid sequence of some sort

Front 108

how do you build a lysosome? why is the M6P receptor important?

Back 108

- add Mannose-6-phosphate label

- acidify & fuse with others --> low pH causes M6P to dissociate and go back to golgi and label more

- M6P receptors are important on the membrane b/c they go pick up all the lost proteins

Front 109

I - cell disease

Back 109

- either don't have M6P receptor or can't put M6P on

- LSD

Front 110

Mucopolysaccharidoses I-IV, pompe's, GMI gangliosidoses, Hurler's, Pseudo-Hurler's, beta-galactosidase deficiencies & sulfatase deficiences are all what?

Back 110

- LSD

Front 111

what is the subunit(s) of microtubules? microfilaments? intermediate filaments?

Back 111

- tubulin

- actin

- lamins, keratin, neurofilamin, vimentin, desmin, GFAP

Front 112

are microtubules polarized? microfilaments? intermediate filaments?

Back 112

- yes

- yes

- yes

Front 113

what are the accessory proteins to MTs?

Back 113

- MAPs, Tau

Front 114

what are the 3 hyperstable structures of microtubules? 2 of microfilaments? 2 of intermediate filaments?

Back 114

- cilia, flagella, centrioles (centromeres)

- sarcomere, microvilli

- desmosomes & hemidesmosomes

Front 115

what are the motors (ATPases) of microtubules? microfilaments? intermediate filaments?

Back 115

- kenesin (orthograde), dyenin (retrograde)

- myosin

- none

Front 116

what are the 3 functions of microtubules? 5 of microfilaments? 1 of intermediate filaments?

Back 116

- mitotic spindle, organelle/cargo transport, cilia/flagella

- phagocytosis, cytokenesis, cell motility, force generation (muscle), membrane stabilization

- mechanical integrity (nucleus, cell-cell, cell-matrix)

Front 117

hereditary spherocytosis is due to a defect in ______filaments

Back 117

- microfilaments

Front 118

listeria infection is due to hijacking of _________

Back 118

- actin (microfilaments)

Front 119

vaccinia (small pox) is due to hijacking of _________

Back 119

- actin (microfilaments)

Front 120

_______ are the specialized MT-based structures in cilia & flagella

Back 120

- axonemes

Front 121

basal bodies are another specialized _________ structure

Back 121

- axoneme (9-triplet conformation of MTs)

Front 122

_______ Often Anchor Other Axonemes, Especially Cilia

Back 122

-Basal Bodies

Front 123

______ arms are the motor for most/many MT functions

Back 123

- dynein

Front 124

Kartagener's (immotile cilia) syndrome

Back 124

- affected individuals lack dynein arms

- ends up in ciliary/flagellar dyskinesis

Front 125

taxol

Back 125

- binds and stabilizes microtubules (stops depolymerizaiton)

Front 126

cholchicine, colcemid

Back 126

- binds & prevents MTs from polymerizing

Front 127

vinblastine, vincristine

Back 127

- binds & prevents MTs from polymerizing

Front 128

Dementia (Tauopathy)

Back 128

- Tau proteins can't bind to MTs & MTs don't function

- they usually regulate length, but when have defective protein get accumulation

Front 129

stress fibers are an _____ based structure

Back 129

- actin

Front 130

which actin is at the front of migrating cells? which is inside the cell?

Back 130

- beta at the forefront

- alpha in the cell

Front 131

actin pairs with _____ to generate force in muscles

Back 131

- myosin

Front 132

cytokinesis is an ______-based structure

Back 132

- actin

Front 133

platelet aggregation is ________-dependent

Back 133

- actin

Front 134

phagocytosis is an _______-mediated process

Back 134

- actin

Front 135

microvilli are specialized _______ structures

Back 135

- actin

Front 136

hereditary spherocytosis is a disease of defective _____

Back 136

- actin or actin like structures

- cytoskeleton/membrane interactions

Front 137

basic structure of _________ is like a twisted rope

Back 137

- intermediate filament

Front 138

where is the IF vimentin found? Desmin?

Back 138

- endothelial cells

- smooth, striated, cardiac muscle cells

Front 139

IFs are Cell-Type Specific, Except for ______

Back 139

- lamins

Front 140

______ are specialized IF structures inbetween cells. ______ is a specialized IF structure that anchors skin cells

Back 140

- desmosomes

- hemidesmosome

Front 141

blistering diseases is due to defects in what?

Back 141

- IF

Front 142

REGENERATION, HYPERPLASIA, METAPLASIA, and DYSPLASIA

Back 142

Altered proliferative states of cells that are reversible: proliferation stops when the stimulus that provoked it is removed.

Front 143

NEOPLASIA

Back 143

Irreversible proliferation of cells: proliferation continues even in the absence of an external stimulus

Front 144

endothelial cells re-form lumenal lining after balloon angioplasty

Back 144

- regeneration

- 1 for 1 replacement of cell type

Front 145

regeneration

Back 145

one-for-one replacement of cells

- new cells replace old

Front 146

restenosis following vascular surgery is an example of _________

Back 146

- hyperplasia

Front 147

hyperplasia

Back 147

- increase in # of cells, all cells are fully differentiated & functioning

Front 148

Grave's disease is an example of _________

Back 148

- hyperplasia

Front 149

erythrocyte hyperplasia in bone marrow following blood loss is an example of _________

Back 149

- hyperplasia

Front 150

metaplasia, it is always _________

Back 150

- adaptive substitution of one cell type by another

- pathologic

Front 151

endovercial epithelial cells get changed from columnar to stratified squamous because of chronic inflammation, is an example of _________

Back 151

- metaplasia

Front 152

dysplasia

Back 152

- changes in mitotic rates, loss of positional control, pleiotropy

- often a precursor to cancer

- increase in number & pleiotropic

Front 153

abnormal cells in a pap smear is an example of _________

Back 153

- dysplasia

Front 154

benign neoplasia

Back 154

- irreversible

- loss of proliferative control (not positional yet)

- will form a benign tumor

Front 155

uterine fibroids is an example of _________

Back 155

- benign neoplasm

Front 156

cancer is an example of _________

Back 156

- malignant neoplasia

Front 157

malignant neoplasia

Back 157

- loss both positional & proliferative control (can begin invading other areas)