Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cell Bio > Review exam 2020 > Flashcards

Review exam 2020 Flashcards

1
Q

interermediate filament protein that are responsible for connecting chromatin to the nuclear membrane.

A

Lamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

During interphase, when the nuclear envelope is intact, lamins are in the _____ state

A

dephosphorylated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Early in mitosis, lamins are _____ by a kinase causing the chromatin-nuclear membrane connection to _____, thus beginning the process of nuclear membrane disassembly and chromosome condensation.

A

phosphorylated

disassemble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Late in mitosis, a ______ returns lamins to the ______ state, thus permitting nuclear membrane assembly and chromosome decondensation to occur.

A

phosphatase

dephosphorylated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Laminopathies (2)

A

progeria

Restrictive dermatopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Problem in progeria

A

lamin is hyperphosphorilated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Nuclear transport disease

A

Huntington’s Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

SINES

A

block action of exporting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Exportins. Specific function of exporting 1

A

export stuff out of nucleus. Exportin 1 exports tumor suppressors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Signal recognized by exportin

A

Nuclear Export signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cells overexposes exporting-1?

A

Cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Signal required for import into nucleus

A

Nuclear localization signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cargo smaller than 5-10kd enter nucleus via ____ through nuclear pores. Larger cargo is actively transported through nuclear pores and guided by ____

A

diffusion

chaperones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nucelar mechanism of why Huntington’s happens

A

The mutant huntintin protein is susceptible to proteolysis, and small (<5kD) fragments of the mutant protein ends up in the nucleus because they are able to diffuse through the nuclear pores.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Membranes are bout ___% lipid, ___% protein and _____ amount of carb.

A

50,50, small

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 classes of membrane lipids (in order of abundance)

A

Phospholipids
Sphingolipids
Cholesterol
Eicosanoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Lipids are ______ distributed in the membrane. Outer leaflet more ____ than inner leaflet

A

asymmetrically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

3 eicosanoid

A

Prostaglandins
Tromboxanes
Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Function of prostaglandins (eicosanoid)

A

regulation of vascular tone, smooth muscle contractility, and uterine contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Function of Tromboxanes (eicosanoid)

A

induces platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Function of Leukotrienes

A

induce vasodilation and bronchoconstriction in asthma and anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Two key properties of Membrane lipids

A

Fusogenicity and fluidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HIV and Measles take advantage of ____ property of phospholipids

A

fusogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Contrary to phospholipids, sphingolipids have no _____ properties

A

fusogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Kinky, (fusogenic) property of phospholipid can lead to _____

A

disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3 diseases resulting from sphingolipid metabolism (aka Lysosomal storage diseases), and what is unique about these diseases

A

Tay-Sach’s (prevalent in certain ethnic groups)
Gaucher (first to be treated successfully with recombinant enzyme replacement therapy)
Fabry (same as Gaucher)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Factors affecting membrane fluidity

4

A
  1. Double Bonds
  2. Acyl chain length
  3. Temperature
  4. Cholesterol (more cool=more fluid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Mechanism of mycoplasma

A

The mycoplasma attach to the base of respiratory epithelial cell cilia and extract the cholesterol from the membrane surrounding the cilia to use for their own metabolic purposes. Removing the cholesterol results in a much more fluid membrane that does not permit the cilia to move rhythmically, or “beat”. Mucous cannot be moved out of the respiratory tract and the mycoplasma are thus able to proliferate, leading to pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Sphingolipid-rich Microenvironments
in the Membrane That Move Rapidly Within a Leaflet. Are major functional organizers of the membrane, bringing lipids and proteins together.

A

Lipid rafts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lipid rafts are critical for (3)

A

1) concentrating ligand-receptor complexes into coated pit regions of the Plasma Membrane for Receptor mediated endocytosis
2) important in bringing together the components of signal transduction pathways
3) mobilizing matrix-modifying enzymes at the leading edge of migrating cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Functions of carbohydrates in cell surface

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

the role of the carbohydrates on membrane glycoproteins in determining blood types

A

self-recognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

interaction of coccidial parasites with cell surface carbohydrates

A

coccidiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

toxoplasmosis is a type of ______, transmitted via ______, and can cause severe ________

A

coccidiosis, transmitted via cat feces, and can cause severe birth defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

if it’s a bacteria or bigger it gets into cells via _______

A

phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

if it’s a virus or smaller it goes into cells via _______

A

Receptor mediated endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

proteins called _____ are involved in concentrating ligand-receptor complexes into specialized regions of the membrane called ________ pits.

A

Clathrin, clathrin-coated pits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

______ are often used to ferry the ligand-receptor complexes to the coated pits

A

Lipid rafts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

The _______ becomes activated in the membrane of endocytic vesicles, thus lowering the pH of the vesicle interior.

A

H+-ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Phagocytosis is an ______-based process.

A

actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Basically, _______ receptors on the plasma membrane recognize IgGs that have coated the particle to be ingested via phagocytosis

A

Fc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Important diseases that involve altered transport (11)

A

Cystic Fibrosis (chloride anion transport via the CFTR, an ABC-class ATPase transporter)

infantile hypoglycemia

drug resistance in cancer chemotherapy

Familial Hypercholesterolemia
rabies
influenza
Legionnaire Disease
streptococcal infections
Leishmania
tuberculosis
leprosy
Tangier Diseae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cause of Cystic Fibrosis

A

chloride anion transport via the CFTR, an ABC-class ATPase transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Cause of infantile hypoglycemia

A

ABC-type ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Cause of drug resistance in cancer chemotherapy

A

ABC-type ATPase

46
Q

Cause of Familial Hypercholesterolemia

A

receptor-mediated endocytosis and due to a defect in the LDL receptor

47
Q

Cause of rabies

A

receptor-mediated endocytosis

48
Q

Cause of influenza

A

receptor-mediated endocytosis

49
Q

Cause of Legionnaire Disease

A

streptococcal infections

50
Q

Cause of Leishmania

A

phagocytosis

51
Q

Cause of tuberculosis

A

phagocytosis

52
Q

Cause of leprosy

A

phagocytosis

53
Q

Symptoms of Tangier Disease

A

coronary heart disease (CHD)
neurological problems
swollen, bright orange tonsils

54
Q

Implications of studying Tangier Disease

A

Revealed process of reverse cholesterol transport (i.e., how cholesterol gets out of cells).

Profound implications and understanding of CHD.Analyzing the genome of affected individuals enabled researchers to first determine which chromosome was involved, and then to isolate the Tangier gene. When the Tangier gene was sequenced, it turned out to be a member of the ATP-Binding Cassette (ABC) family of transporters.

55
Q

Most striking biochemical change in Tangier disease patients is markedly reduced ________.

A

of High Density Lipoprotein (HDL; also known popularly as “good cholesterol”).

56
Q

Biochemical pathway of Tangier Disease

A

If the Tangier ABC transporter is
defective, cholesterol is not transported out of the cells into the plasma and this causes the “empty” HDL to be cleared from the plasma into lymph glands, thus explaining the reduced HDL levels in the plasma and the buildup of cholesterol in the blood vessel wall

57
Q

Low levels of ____ are found in 55% of Coronary Heart Disease Patients

A

HDL (High density lipoproteins)

58
Q

the first 20-25 aa translated of a protein determine if _____

A

if the protein continues to be translated in the cytoplasm or contains the hydrophobic “Signal Peptide” that will cause the ribosome/nascent protein complex to relocate to the ER to finish translation of the protei

59
Q

Possible Fates of Proteins Translated in Cytosol

A
  1. Nucleus
  2. Mitochondria
  3. Cytoplasm
  4. Peroxisomes
60
Q

Possible Fates of Proteins Translated in ER

A
  1. ER
  2. Plasma membrane
  3. Secretory Vesicles
  4. Lysosomes
  5. Golgi
61
Q

Diseases of Peroxisomal Targeting (2)

A
  1. Neonatal Adrenoleukodystrophy

2. Zellweger Syndrome

62
Q

Diseases of Nuclear Targeting (1)

A

Huntington

63
Q

Lysosome Storage Diseases (4)

A
  1. Gaucher,
  2. Fabry
  3. Tay-Sachs
  4. Mucopolyasaccharide
64
Q

Several LSDs (lysosomal storage disease) are now being treated with either _________ or ______ therapies

A

enzyme replacement or enzyme enhancement therapies.

65
Q

______ is the tripeptide sequence that targets proteins to the peroxisome

A

S-K-L

66
Q

short (typically 5-6) basic aa sequences are the _________

A

Nuclear Localization Signals (NLS)

67
Q

3) a long-ish (about 75 aa) sequence near the N-terminal end of the protein directs proteins to ________

A

mitochondria

68
Q

defects in KDEL lead to _______

A

dilated cardiomyopathies

69
Q

Subunit of Microtubules

A

tubulin

70
Q

Subunit of microfilaments

A

actin

71
Q

Subunit of intermediate filament (6)

A
  1. lamins
  2. keratin
  3. desmin
  4. neurofilamin
  5. vimentin
  6. GFAP
72
Q

Accessory proteins of microtubules

A

Tau

73
Q

Hyperstable structures of microtubules (2)

A
  1. axonemes (cilia and flagella)

2. centrioles

74
Q

Hyperstable structures of microfilaments (2)

A
  1. sarcomere (muscle)

2. microvilli

75
Q

Hyperstable structures of intermediate filaments

A
  1. desmosome

2. hemi-desmosome

76
Q

Motors of microtubules

A
  1. dynein (retrograde)

2. kinesin (orthograde)

77
Q

motor of microfilament

A

myosin

78
Q

motor of intermediate filament

A

None

79
Q

Functions of microtubules

A
  1. cilia/flagella functions
  2. mitotic spindle
  3. organelle/cargo transport
80
Q

functions of microfilaments

A
  1. phagocytosis
  2. cytokinesis
  3. cell motility
81
Q

Function of intermediate filaments

A

mechanical integrity

82
Q

Drugs for microtubules

A
  1. taxol

2. vinca alkaloids (colchicine, vinblastine)

83
Q

Medical significance of microtubules (diseases) (2)

A
  1. Kartageners (Primary Ciliary Dyskinesia, Immotile Cilia Syndrome)
  2. cancer chemotherapy dementias (Tau-opathies)
84
Q

Medical significance of microfilaments (3)

A
  1. Hereditary Spherocytosis
  2. Listeria infection
  3. Smallpox/Vaccinia
85
Q

Medical significance of intermediate filaments

A
  1. laminopathies
  2. blistering diseases
  3. cancer diagnosis
86
Q

Viruses ______, _____, and bacterium _____ are special examples of pathogens that hijack the actin machinery of the host cell to propel themselves from one cell into another without being exposed to the immune system

A

Viruses smallpox and vaccinia

Bacterium Listeria

87
Q

Problem in Kartageners syndrome

A

microtubules are lacking cilia

88
Q

An increase in the size or volume of a cell. Not an altered proliferative state. Examples include muscle cells of a bodybuilder, adipose cells during fat accumulation, oocytes during maturation.

A

Hypertrophy

89
Q

Irreversible proliferation: proliferation continues in the absence of an external stimulus.

A

Neoplasia

90
Q

Regeneration

A

1-for-1 replacement of lost cells by the same cell type

e.g. Endothelial cell regeneration following vascular surgery; liver cell regeneration following partial hepatectomy or live-donor liver transplants (in the donor, not the recipient).

91
Q

Hyperplasia

A

increase in the number of cells in a tissue; cells are fully differentiated. Can be physiological (helpful) or pathological (harmful).

e.g. Hematopoietic cells in bone marrow following severe blood loss or changes in altitude (helpful); thyroid cells in Grave’s Disease (hyperthyroidism; harmful); smooth muscle cells in the arterial wall in atherosclerosis or following vascular surgery (termed restenosis; occurs following angioplasty, coronary artery bypass graft, arterio-venous shunts, etc.; harmful)

92
Q

Metaplasia

A

adaptive substitution of one cell type for another

e.g. Replacement of ciliated columnar epithelium by stratified squamous epithelium in response to chronic inflammation (e.g., chronic PID) or other injurious stimuli (e.g., smoking).

93
Q

Dysplasia and 2 examples

A 
activated metabolic pathways for proliferation; loss of orientation in a tissue.
Abnormal appearance (pleiotropy, disorientation within tissue, high mitotic rate) of cells

examples:

  1. Pap Smear in women
    dysplastic moles removed from skin
94
Q

2 Types of Neoplasia (and examples)

A

Benign –loss of proliferation control only; “benign” tumors, like fibroids

Malignant – loss of both proliferation and positional controls; metastatic tumors; “cancer”

95
Q

Regeneration, Hyperplasia, Metaplasia and Dysplasia

A

Altered proliferative states of cells that are reversible (or at least stoppable): proliferation stops when the stimulus that provoked it is removed.

96
Q

3 steps of apoptosis

A
  1. Induction
  2. Modulation
  3. Execution
97
Q

3 categories of apoptosis inducers

A

Physiologic, damage related, therapy associated

98
Q

2 major pathways of apoptosis induction

A

Intrinsic and extrinsic

99
Q

Modulation of apoptosis only happens in ____induction pathway and is done by ____proteins

A

intrinsic, Bcl proteins

100
Q

Execution of apoptosis is done by ___A__ followed by ___B___. ___A___ are directly responsible for blebbing

A

Caspases (particularly Caspase-3), followed by endonuclease.

Caspase 3 is responsible for blebbing

101
Q

Physiologic inducers of Apoptosis

A
  1. TNF-alpha
  2. FasL
  3. growth/survival factor withdrawal
  4. glucocorticoids
102
Q

Damage-related inducers of Apoptosis

A
  1. Viral infection
  2. Heat shock
  3. Toxins
  4. Tumor suppressors
  5. Oxidants/free radicals
103
Q

Therapy associated inducers of apoptosis

A
  1. UV/gamma radiation

2. chemotherapeutic drugs

104
Q

_____ reduce neuronal damage after stroke

A

Apoptosis inhibitors

105
Q

During apoptosis, caspases activate specific endonucleases that cleavecleave the DNA in the ______ between the nucleosomes

A

the linker regions between the nucleosomes

106
Q

Dysregulated apoptosis—either too much or too little—is the hallmark of 5 conditions:

A
  1. Syndactyly and polydactyly
  2. Expansion of many cancers
  3. The cachexia (“wasting”) seen in some late-stage cancer patients
  4. Polycystic Kidney Disease
  5. Hashimoto’s (autoimmune form of hypothyroidism)
107
Q

Clinical Significance of Cell Birth and Death

A
  1. Liver regeneration following partial hepatectomy
  2. Restenosis following vascular surgery
  3. Grave’s Disease (hyperthyroidism)
  4. Bone marrow replenishment following blood loss
  5. Chronic pelvic inflammatory disease
  6. Pulmonary function in smokers
  7. Pap smear
  8. Fibroids
  9. Cancer
  10. Polydactyly and Syndactty
  11. Polycystic Kidney Disease
  12. Hashimoto’s (hypothyroidism)
  13. Burkitt’s Lymphoma
108
Q

Hashimoto Disease

A

Most common form of hypothyroidism. Represents too much apoptosis in thyroid gland.

109
Q

Intrinsic (mitochondrial) pathway of apoptosis

A

Withdrawal of growth factors, hormones —->stimulates mitochondria membrane modulation of apoptosis (by Bcl-2)–>mitochondrial leakage of cytochrome-c, that initiates caspase cascade–> initiator caspases are activated–> activator caspases activted–> 1) endonuclease activation (degrades DNA)and breakdown of cytoskeleton

110
Q

Therapeutic uses of apoptosis (2, first has 2 specific conditions second has 3 specific diseased)

A
  1. may be useful in limiting the damage caused by strokes or heart attacks
  2. Other diseases or pathologies in which modulating apoptosis is a potential therapy include cancer, restenosis following vascular surgery, and autoimmune diseases like Hashimoto’s
111
Q

Extrinsic (death receptor-initiated) pathway

A

Receptor-ligand interactions (FAS & TNF receptor)–> Adapter proteins activated–>initiator caspases activated–>activator caspases activted–> 1) endonuclease activation (degrades DNA)and breakdown of cytoskeleton

Cell Bio (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions