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MtC > Block 1 > Flashcards

Block 1 Flashcards

1
Q

3 filament types and their thicknesses

A
  • Actin: 5-9nm,
  • Intermediate filaments: 10nm
  • Microtubules: 25nm
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2
Q

2 motor proteins, and the directions go

A
  • Kinesin: towards + end, anterograde movement

* Dynein: towards - end, retrograde movement

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3
Q

Types of tubulin subunits

A 
alpha/beta dimers
gamma tubulin (minus end cap)
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4
Q

List intermediate filament proteins

A 
Nuclear lamins
Vimentin
Desmin
Keratin
Neurofilaments
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5
Q

F actin and G actin

A 
F actin (filamentous) polymerizes from G actin (globular).
Subunit binding and ATP hydrolysis are not a coupled process.
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6
Q

Emery-Dreifuss muscular dystrophy

What is the cause

A

Mutation in lamins A/C

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7
Q

Epidermolysis bullosa simplex

What is the cause

A

Mutations in keratin. Skin easily blisters.

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8
Q

Structure of intermediate filaments

A

Monomers form dimers.

Dimers bind into antiparallel tetramers.

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9
Q

Action of phalloidins and cytochalasins

A

• Phalloidins lock F actin units together.
• Cytochalasin inhibits polymerization.
(Both are from mushrooms)

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10
Q

Actin concentration in cells, and critical concentration.

A

Actin is > 1mM, and critical concentration is 0.1µM.

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11
Q

What is an actin comet

A

When a mycobacterium utilizes cellular actin polymerization to move around the cell.

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12
Q

4 classes of actin binding proteins

A
  1. Regulation (thymosin beta4, profilin, tropomodulin, capping protein).
  2. Severing (ADF/cofilin, gelsolin).
  3. Cross-linking (spectrin, dystrophin, fimbrin, filamin, actin-actinin).
  4. Motor (myosin)
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13
Q

Myosin I vs. Myosin II

A
  • Myosin I binds to membranes (with the head directed towards cytoplasm)
  • Myosin II forms thick filaments
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14
Q

Amoeboid movement pathway

Dendritic nucleation model

A

Actin polymerizes with Arp2/3 branch points, with lamellopodia forming at Wiskitt-Aldrich protein on cell wall.

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15
Q

RBC ghosts consist mostly of

A

Spectrin, actin, ankyrin, band 4.1, glycophorin, and anion exchanger

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16
Q

Hereditary spherocytosis

What it is and what causes it

A

RBC lose their shape and become fragile. Caused by mutations in spectrin, ankyrin or band 4.1

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17
Q

Symptoms of immotile cilia syndrome (ICS)

A
  • infertility (because their sperm are immotile)
  • chronic sinusitis and bronchitis (because cilia in their respiratory tracts cannot effectively move mucous toward the pharynx).
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18
Q

Axoneme structure

A

9 + 2

9 MT doublets (13 + 11 protofilaments), and 2 normal MTs

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19
Q

Membrane ER is continuous with

A

Nuclear membrane

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20
Q

4 post-translational processes that take place in ER

A
  • Glycosylation
  • Disulphide bonds
  • Folding
  • Subunit assembly
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21
Q

Location where steroids are made. Cellular structure that is visually developed in high-demand synthesis.

A

Mitochondria inner surface

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22
Q

Mechanisms of taxol and vinblastine

A
  • Taxol inhibits MT depolymerization

* Vinblastine detaches MT minus ends

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23
Q

Types of proteins synthesized by ER-bound ribosomes

A

• Transmembrane proteins
• Secretory proteins
• Lysosome proteins
(These all go to the Golgi next)

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24
Q

Types of proteins synthesized by cytosolic ribosomes

A

• Mitochondrial proteins
• Nuclear proteins
• Peroxisome proteins
(These all go directly)

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25
Q

Signal Recognition Peptide (SRP) pathway

A

SRP on nascent peptide directs cytosolic ribosome to ER surface. Peptide is fed through peptide translocation complex, which is GTP-dependent.

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26
Q

Features of the SRP

A

Usually at N-terminus, hydrophilic, net positive charge, 13-48aa (no consensus sequence), contains an alpha helix, becomes non-polar at carboxyl end of sequence. Similar structure in all SRPs.

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27
Q

Signal peptidase

A

ER transmembrane protein, with catalytic side on lumen side. Cleaves SRP co-translationally.

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28
Q

Stop transfer sequences

A

Hydrophobic sequence that contains an alpha helix. Translocation into ER stops at this sequence, and peptide remains embedded.

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29
Q

Structure and function of Golgi apparatus

A
  • 4-12 cisternae
  • Cis Golgi is close to ER; distinct compartments that modify membrane proteins differentially
  • Trans Golgi network (TGN) is a reticulum where proteins are sorted according to where they will be transported
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30
Q

Regulated secretory pathway vs. Constitutive secretory pathway

A
  • All cells have constitutive secretory pathway; Regulated secretory pathway is only in exocrine, endocrine, and neurons.
  • Secretory granules store proteins for later release.
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31
Q

V-type ATPases

What do they do

A

Pump H+ into the vacuoles: endosomes and lysosomes (pH = 5.0)

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32
Q

Lysosome functions

A
  • Protein disposal
  • Downregulate surface receptors, such as EGFR
  • Releases of endocytosed nutrients
  • Degradation of phagocytosed pathogens
  • Autophagy
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33
Q

Lysosome storage diseases (LSDs)
• Incidence
• Cellular hallmark
• Treatment

A
  • 1 in 5000 live births
  • Enlarged lysosomes (Inclusion bodies)
  • Enzyme replacement therapy (ERT)
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34
Q

How are enzyme replacement therapy (ERT) drugs tagged to ensure they localize to lysosomes

A

They have a mannose-6-phosphate tag

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35
Q 
Mucolipidosis II (I-cell disease) 
What is the cause
A

Lack of GlcNAc phosphotransferase, which normally adds a mannose-6-phosphate to proteins to target them to the lysosome. Pan-deficiency of lysosomal enzymes.

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36
Q

How do ER vesicles target to the Golgi?

A

ER v-SNAREs bind to the Golgi t-SNAREs.

v is for vesicle and t is for target

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37
Q

Tetanus toxin and botulinum toxin

Compare the mechanisms

A

Both are SNARE peptidases
• Tetanus toxin prevents GABA release; spastic paralysis.
• Botulinum prevents ACh release at NMJ; flaccid paralysis.

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38
Q

Receptor-mediated endocytosis pathway

A

Clathrin-coated pits with receptors collect ligand before endocytosing. Clathrin then disengages.

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39
Q

Four types of receptor-mediated endocytosis, with examples

A 
• Ligand degrades / Receptor recycled 
(LDL, peptide hormones, viruses)
• Both degraded. (EGF, Immune complexes)
• Both are recycled. (Transferrin, MHC)
• Both are transported to different side. (Maternal IgG, IgD)
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40
Q

Transferrin pathway

A
  • Apotransferrin scavenges Fe3+, becoming holotransferrin
  • Holotransferrin binds to transferrin receptor
  • Receptor-mediated endocytosis
  • Clathrin dissociates, vesicle fuses to acidified endosome
  • Fe3+ dissociates as Fe2+, and is pumped into cytosol
  • Apotransferrin-bound receptor is exocytosed
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41
Q

Familial hypercholesterolemia (FH)
• Prevalence
• Symptoms
• Cause

A

• 1 in 500 are heterozygotes; 1 in 1,000,000 are homozygotes. Partial dominance.
• Elevated LDL, cholesterol depositions.
• LDL receptor mutations (over 400 documented)
Can interfere with synthesis, transport, binding, clustering, or recycling.

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42
Q

4 types of cell signaling

Terms related to distance

A
  • Contact-dependant
  • Synapse
  • Paracrine
  • Endocrine
43
Q

Nitric oxide pathway

A
  • Autonomic nerves release ACh onto vessels, triggering intracellular Nitric Oxide Synthase (NOS)
  • NOS cleaves arginine into Nitric Oxide (NO)
  • NO diffuses readily, activates guanylyl cyclase
  • Guanylyl cyclase converts GTP into cGMP
  • cGMP triggers smooth muscle relaxation
44
Q 
What do these 4 interaction domains bind to?
What do they stand for?
• SH2
• SH3
• PH
• PTB
A
  • SH2, src homology domain 2, binds to phosphorylated tyrosine
  • SH3, src homology domain 3, binds to proline-rich sequences
  • PH, Pleckstrin homology, binds to charged phosphoinositides
  • PTB, phosphotyrosine binding, binds to phosphorylated tyrosine
45
Q

Signal transduction at the level of the GPCR

A

Ligand-bound GPCR acts as a GEF for bound G-protein (alpha, beta, and gamma subunits). The alpha subunit is the GTPase, which activates the beta/gamma subunits. The GAP to this G-protein is are RGS proteins.

46
Q

Action of these GPCRs:
• Gs
• Gi
• Gq

A
  • Gs activates adenylyl cyclase; opens Ca2+ channels
  • Gi inhibits adenylyl cyclase
  • Gq activates PLC-ß
47
Q

cAMP
How is it produced and degraded?
What does it activate?

A

cAMP is formed by adenylate cyclase.
cAMP is degraded by cAMP phosphodiesterase.
cAMP activates PKA, which binds to CREB.

48
Q

Mechanism of cholera toxin

A

Catalyzes ADP ribosylation alpha subunit of Gs, which inhibits GTP hydrolysis, causing constitutive activation, over-activation of adenylyl cyclase, and overproduction of cAMP. Efflux of Cl- from gut causes diarrhea.

49
Q

Mechanism of pertussis toxin

A

Catalyzes ADP ribosylation alpha subunit of Gi, which inhibits GDP release, preventing inactivation of adenylyl cyclase, leading to overproduction of cAMP. Causes whooping cough.

50
Q

PLC-ß pathway

A
  • GPRC with Gq activates PLC
  • PLC cleaves membrane PIP2 into IP3 and DAG.
  • IP3 releases Ca2+ from the ER
  • Ca2+ translocates PKC to the cell membrane
  • DAG activates PKC
51
Q

Desensitization of GPCRs

A
  • Phosphorylation by PKA, PKC, or GRKs (GPCR kinases).

* Phosphorylated GPCRs bind to arrestin, which tags them for endocytosis.

52
Q

Five types of enzyme-coupled receptors

A
  • Receptor tyrosine kinases (RTKs)
  • Tyrosine kinase-associated receptors
  • Receptor Ser/Thr kinases
  • Receptor guanylyl kinases
  • Receptor-like tyrosine phosphatases
53
Q

RTK basic structure.

What is the exception in insulin?

A

RTKs have a single transmembrane domain, with an extracellular ligand-binding domain, and intracellular kinase domains. They signal by transautophosphorylation upon dimerization by ligand binding.

The insulin receptor is already a dimer (of dimers), and insulin binding brings the kinase domains closer together.

54
Q

List some proteins that signal by RTKs

A

EGF, IGF1 and IGF2, NGF, PDGF, MCSF, FGF1, VEGF, Ephrins.

55
Q

What is Ras?

What are the three major proteins?

A
  • Ras are GTPases (molecular switches) of RTK signaling.

* The major proteins are K-ras, N-Ras, and H-Ras.

56
Q

Ras pathway

A
  • RTK interacts with Grb2 via phosphorylated SH2 domain
  • Grb2 interacts with Sos (a GEF of Ras) via SH3 domain
  • Sos activates Ras by this localization
  • Ras –> Raf –> MEK –> ERK (MAPK) –> Gene transcription
57
Q

Diseases caused by Ras mutations

A
  • Cardiofaciocutaneous (CFC) syndrome: K-Ras, B-Raf, MEK1/2
  • Noonan syndrome: K-Ras, SHP2 (adaptor between RTK and Ras), SOS1 (Ras-GEF)
  • Costello syndrome: H-Ras
  • LEOPARD syndrome: SHP2
  • Neurofibromatosis type I: NF1 (Ras-GAP)
58
Q

PI3K/AKT pathway

A

• RTKs activate PI3K class 1a
• GPCRs activate PI3K class 1b
• PI3K can add a 3-phosphate to any of the inositols.
• PI(3,4,5)P3 is a lipid docking site, in that PH domains can bind to it.
• PDK1 and AKT both dock; PDK1 phosphorylates AKT
• AKT phosphorylates Bad, which releases an apoptosis-inhibiting protein.
(This is the pathway activated by insulin)

59
Q

JAK/STAT pathway

A
  • Dimerization of cytokine receptors (no kinases activity)
  • Transphosphorylation of bound JAKs
  • JAKs then phosphorylate receptor
  • Receptor recruits STATs
  • JAKs also phosphorylate STATs.
  • STATs bind each other and enter nucleus
60
Q

Receptor Ser/Thr kinases (TGF-ß/SMAD pathway)

A
  • TGF-ß or BMP ligand binds; receptor dimerizes
  • Transphosphorylation (one-way)
  • Binds to SMAD2 or SMAD3, which are phosphorylated
  • SMAD2/3 oligomerizes with SMAD4; enters nucleus
61
Q

Notch pathway

A
  • Notch (transmembrane proteins) bind to delta (transmembrane protein) on another cell
  • Notch is then cleaved by gamma-secretase intracellularly, and Notch fragment goes to nucleus to transcribe Notch responsive genes with Rbpsuh.
62
Q

Acute Lymphoblastic Leukemia (ALL)
• Causes
• Symptoms
• Treatments

A
  • ALL is a lymphoproliferative cancer, caused by translocation events, including the BCR-ABL (Philadelphia chromosome) translocation
  • Elevated lymphs, lymphadenopathy; neutropenia, infections; thrombocytopenia, bleeding; low RBCs, anemia;
  • Treated with methotrexate and mercaptopurine
63
Q

Mercaptopurine
• Mechanism of action
• Pharmacogenetics

A
  • Competes with HGPRT to reduce GMP and AMP salvage.

* Toxicity of mercaptopurine is increased in patients with TPMT insufficiency.

64
Q

Methotrexate

Mechanism of action

A

Inhibits DHFR (DHF –> THF). THF is needed for thymidylate synthase (dUMP –> dTMP)

65
Q

5-fluorouracil (5-FU)
• Mechanism of action
• Pharmacogenetics

A
  • An irreversible inhibitor of thymidylate synthase (dUMP –> dTMP).
  • 8% of population has dihydropyrimidine dehydrogenase (Uracil –> Thymidine) deficiency, which also metabolizes this toxic drug.
66
Q

Vincristine

Mechanism of action

A

Inhibits tubulin dimerization. Anti-mitotic

67
Q

Three elements that regulate a prokaryotic operon

A
  • Regulatory genes that encode regulatory proteins
  • Promoter, binding site for RNA Polymerase
  • Operator, sequence that binds repressor
68
Q

Inducers vs. Repressors

A
  • Repressors bind to operators, prevent transcription

* Inducers bind to repressors, prevent their inhibitor activity

69
Q

In the Lac operon, what is the repressor and what is the inducer?

A
  • The repressor is the LacI protein

* The promoter is allolactose and IPTG

70
Q

What is the role of glucose sensing in the Lac operon

A

Lactose is needed for ß-galactosidase transcription from the Lac operon. Transcription is promoted by cAMP-CBP, which is elevated when glucose levels are low. (Cell preferentially uses glucose).

71
Q

4 major classes of DNA-binding proteins in eukaryotes

A
  • Helix-turn-helix (bind palindrome sequences)
  • Zinc finger (motif can link to select longer sequences)
  • Leucine zipper (1 alpha helix dimerizes to bind DNA)
  • Helix-loop-helix (2 alpha helices dimerize to bind DNA)
72
Q

Ribosome subunit sizes

A
  • Prokaryotes: 70S = 30S + 50S

* Eukaryotes: 80S= 60S + 40S

73
Q

Stop codons

A

UGA (you go away)
UAA (you are away)
UAG (you are gone)

74
Q

tRNA alignment with mRNA. Wobble position.

A

Antiparallel allignment. 3rd position of codon is wobble (1st position of tRNA).

75
Q

Needed to make a a aminoacyl-tRNA

A

tRNA, amino acid, ATP, Mg2+, and the corresponding aminoacyl-tRNA synthetase.

76
Q

Initiation of transcription sequence of prokaryotes

A

• Prokaryotes: AUG start codon pairs with fMet-tRNA. Upstream, Shine-Dalgarno pairs with 16S rRNA.

77
Q

Eukaryotic Protein Synthesis - Initiation

How to make 48S complex

A
  • eIFA1 and eIF3 help keep 60S and 40S dissociated, eIF1 helps to bind ternary complex
  • Ternary complex (eIF2-GTP:met-RNA) binds to 40S along with eIF5B-GTP
  • 43S complex binds eIF4F bound CAP of mRNA to form 48S complex
78
Q

Eukaryotic Protein Synthesis - Initiation

How to make 80S complex from 43S complex

A
  • 48S complex unwinds any helix structure and scans to find first AUG (eIF4 has helicase activity)
  • Once AUG is found, 60S ribosomal subunit binds and releases many initiation factors, and 80S initiation complex is formed.
79
Q

Diptheria Toxin

Mechanism of action

A

Blocks eukaryotic translation by inhibiting translocation; ADP ribosylation of EF2-translocase.

80
Q

Streptomycin

Mechanism of action

A

Inhibits initiation of translation (prokaryotes)

81
Q

Tetracycline

Mechanism of action

A

Binds 30S subunit and prevents binding of aminoacyl-tRNA (prokaryotes)

82
Q

Chloramphenicol

Mechanism of action

A

Inhibits peptidyl transferase activity of 50S subunit (prokaryotes)

83
Q

Erythromycin

Mechanism of action

A

Binds 50S subunit and prevents translocation (prokaryotes)

84
Q

Cyclohexamide

Mechanism of action

A

Inhibits peptidyl transferase activity of 60S subunit (eukaryotes)

85
Q

Puromycin

Mechanism of action

A

Causes premature chain termination by acting as an analog of aminoacyl-tRNA (prokaryotes and eukaryotes).

86
Q

Barth Syndrome

A

Rare disorder that causes infantile death due to deficient cardiolipin synthesis

87
Q

Are the following lipids found mostly on the inner or outer membrane?

A 
Phosphatidyl ethanolamin - inner
Phosphatidyl choline - outer
Sphingomyelin - outer
Phosphatidyl serine - inner
Phosphatidyliositol - inner
Phosphatidic acid - inner
88
Q

What is phosphatidic acid?

What is it synthesized from?

A
  • Glycerol with 2 fatty acids attached. Starting point for synthesis of other lipids.
  • Synthesized from DAG or from glycerol-3-phosphate
89
Q

Neonatal Respiratory Distress Syndrome (RDS)
• Causes
• Symptoms
• Treatment

A
  • Pulmonary surfactant deficiency
  • Alveoli collapse
  • Surfactant supplementation
90
Q

List the surfactant proteins. Which one is the most abundant?

A

SP-A, SP-B, SP-C, SP-D, and DPPC (dipalmitoylphosphatidylcholine), which is the most abundant.

91
Q

Sphingolipid base structure

A

Sphingosine (and not glycerol), which can two hydroxyl groups, binds at C2 to a fatty acid to form ceramide.

92
Q

Tay-Sachs disease
• Cause
• Occurrence
• Symptoms

A
  • Deficiency in Hexoaminidase A, used to break down ganglioside in the lysosome. This is a type of lysosome storage disease (LSD)
  • Incidence of 1:4000 live births among Ashkenazi Jews and 100-fold lower outside this population
  • Retardation and poor motor control. Death by 4.
93
Q

Niemann-Pick disease
• Cause
• Symptoms

A
  • Deficiency in sphingomyelinase, used to break down sphingomyelin into ceramide and PC. This is a type of lysosome storage disease (LSD)
  • Retardation and early death
94
Q

Eicosanoid synthesis

What are the three classes of eicosanoids?

A
  • Linoleic acid is cleaved by phospholipase A2 into converted to arachinodate, which is converted into an eicosanoid.
  • Prostaglandins, leukotrienes, and thromboxanes.
  • COX1/2 converts arachidonate into prostaglandin H2, which is converted to thromboxanes and other protstaglandins.
  • Lipoxygenases convert arachidonate into leukotrienes
95
Q

Inhibitors of eicosanoid synthesis

A

• Corticosteroids, such as prednisone, inhibit COX2 and PLA2.
• NSAIDS, such as ibuprofen and aspirin, inhibit COX1/2. Aspirin is irreversible due to its acetylation
•

96
Q

Statins, such as Lipitor

Mechanism of action

A

Competitively inhibit HMG-CoA reductase, the rate-limiting step of cholesterol de novo synthesis

97
Q

Celebrex and Vioxx

Mechanism of action

A

Specific inhibitors of COX2 (and not COX1)

These had serious adverse events

98
Q

How are sugars activated for glycosylation?

A

sugar 1-phosphate + NTP –> NDP-sugar + PPi

99
Q

Classic Galactosemia
• Cause
• Symptoms
• Treatment

A

• Deficiency in galactose-1-phosphate uridyltransferase (GALT)
• Failure to thrive, hepatomegaly, jaundice, cataracts
* Removal of lactose and galactose from the diet

100
Q

What are glucosaminoglycans?

A

Negatively charged polysaccharides composed of repeating disaccharide units. The disaccharide unit consists of an amino sugar (glucosamine,GlcN or galactosamine,GalN) and an uronic acid (glucuronic acid,GlcA or iduronic acid,IdoA), both of which may be sulfated, thus contributing to the polyanionic properties of the molecule. The addition of carbohydrates occurs in a stepwise fashion in the Golgi. The glycosaminoglycans condroitin sulfate, heparin, heparin sulfate, and dermatan sulfate are attached to proteins via a Xyl-Ser O-linkage. Hyaluronic acid (also called “hyaluronan”), which is not covalently attached to protein and is not sulfated, serves as a scaffolding platform for large numbers of proteoglycans in the extracellular matrix.

101
Q

What are mucins?

A

Mucins are heavily O-glycosylated glycoproteins (GalNAc-Ser/Thr) found in mucous secretions or on the cell surface. Mucins (~20 mucin genes “Muc” in the human genome) are synthesized by many epithelial cells and by goblet cells of the tracheobronchial, gastrointestinal, and genitourinary tracts. Mucins hydrate and protect epithelial cells, but have other functions as well (e.g. fertilization).

102
Q

Lectins bind to what?

A

Carbohydrates of glycoproteins

103
Q

HbA1c
• What it indicates
• How it is formed

A
  • Indicates a history of high blood glucose levels
  • Formed spontaneously by addition of glucose to epsilon amino group of lysine on HbA. Undergoes Amadori rearrangement, then cyclizes. Develops into advanced glycation end products (AGEs).
104
Q

Neuraminidase inhibitors
• What are they called
• Mechanism of action

A
  • oseltamivir (Tamiflu), zanamivir (Relenza).\
  • These inhibit influenza neuraminidase, which normally cleaves sialic acid residues of glycoproteins that would otherwise sequester the virus.

MtC (3 decks)

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