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MCB Proteins > MCB Block 3 > Flashcards

MCB Block 3 Flashcards

1
Q

What are liposome used for?

A

Drug delivery

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2
Q

What do GPI do?

A

Attach protein to the PM.

Found at lipid rafts

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3
Q

RBC Transmembrane proteins

A

Band 3 and Glycophorin

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4
Q

RBC Linking Proteins

A

Protein 4.1 and Ankyrin

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5
Q

What is specrtin and where is it found?

A

Alpha/beta F-Actin. Linked to junctional complex within RBC

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6
Q

Function of Nucleolus?

A

rRNA synthesis and Ribosome assembly

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7
Q

What are nucleoporins made up of?

A

Glycoproteins of NPC

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8
Q

What is inner membrane of nuclues supported by

A

Lamin intermediate Filaments. Maintains cell shape and protects membrane.

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9
Q

What is the sig. seq. to go into the nucleus.

A

NLS

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10
Q

What is the sig. seq to leave the nucleus

A

NES

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11
Q

What G protein family is used for transport in and out of the nucleus?

A

RAN GTPase
GEF- GDP to GTP
GAP - GTP to GDP

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12
Q

What do Lamin A, B, and C form during phosphorylation of CDK1

A

Lamin B: Gene, anchored to inner membrane

Lamin A/C: Splice variants, forms free heterodimers

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13
Q

What are the Cajal bodies and Gems? (subnuclear structure)

A

Maturation of snoRNA and snRNA

Contain the survival of motor neurons protein (SMN)

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14
Q

Substructures of the nucleolus

A

Fibrillar center
Dense fib component/ PARS FIBROSA
Granular component/ PARS GRANULOSA

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15
Q

Fibrillar center

A

Transcriptionally INACTIVE DNA

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16
Q

Pars Fibrosa

A

rRNA being transcribed, then modified by snoRNPS

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17
Q

Pars Gransulosa

A

rRNAs being assembly with ribosomal proteins

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18
Q

Function of the smooth er

A

Steroid hormone synthesis, detox, membrane lipid synthesis

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19
Q

Function of the rough er

A

Lipid and protein production, modification and intracell trafficing

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20
Q

If there is no ER signal, where will the protein end up?

A

It will be made by a free ribosome and be discharged in the cytosol post translationally

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21
Q

Which amino acids are N-linked glycosylated?

A

Asparagine

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22
Q

Which amino acids are O-linked glycosylated?

A

Ser/Thr

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23
Q

What GTPase are used for vesicle formation?

A

ARF/SAR GTP
ARF= COP 1
SAR = COP 2

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24
Q

ARF/SAR GEF vs GAP

A

GEF: Promotes coat protein assembly. GDP to GTP

GAP: Promotes coat disassembly. GTP to GDP

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25
Q

Function of Golgi app?

A

Major site of carbohydrate synthesis (GAGs)
Addition of oligosac to proteins and lipids.
Acquire specificity

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26
Q

Regulated exocytosis

A

Vesicles wait for external signals, usually an increase int he cytosolic calcium

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27
Q

Transcytosis

A

Endo + exocytosis across epithelium.

pH Determines direction (usually from low to high)

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28
Q

Which GTPase is used in vesicle fusion?

A 
RAB, GTP and GDP
RAB GTP (on the vesicle)
Rab effector = tethering protein, on the target membrane
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29
Q

V-Snare, T-Snare, and extra protein used in nuerons?

A

SynaptobreVin
SynTaxin
Synaptotagmins (Ca2+sensor) (interacts with T-Snare)

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30
Q

What is the final stage of vesicle fusion? What protein is involved?

A

allowing membrane fusion
NSF assist in dissociation
of synaptobrevin from syntaxin, allowing membrane fusion

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31
Q

2 coats used for receptor mediated endocytosis?

A

Clatherin (for lysosome) and Caveolin coats

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32
Q

What proteins are needed for receptor mediated endosytosis?

A

Adaptins to bind to the receptor, which allows Clatherin coat to form then Dynamin helps the vesicle pinch off.

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33
Q

What are opsonins?

A

Opsonins are anything that is engulfed by a phagosome

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34
Q

Caveolin coat

A

Form from lipid rafts
Invaginations in PM

Coat of calveolin protein (integral membrane protein)
Have SPIKES on COAT

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35
Q

What is the tag called for lysosomes?

A

M6P. Tagged at the Cis-golgi by GlcNAC Phosphotransferase

M6p receptor is in TRANS golgi

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36
Q

Early Endosome + Primary Lysosome = …

A

Late enosome

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37
Q

Late Endosome + Maturation = ….

A

Secondary Lysosome

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38
Q

Endosome + Lysosome –> Endolyosome + Maturation = …..

A

Secondary lysosome

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39
Q

What type of pump is found on lysosome?

A

V-Type ATPase: Pumps H+ into lysosome.

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40
Q

Autophagy

A

Break down of old or unneeded proteins

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41
Q

Multivesicular Bodies

A

Maturation of early endosomes containing endocytic vesicles to late endosomes occurs.

MVBs shed vesicles to recycle material back to PM

Proteins destined for MVB receive mono-ubiquitin tag (down regulation of receptors

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42
Q

If lysosome can’t degrade material, what happens to that material?

A

Residual body that can be exocytosed or remains as lipofuscin (pigmented lipids)

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43
Q

Peroxisomes function

A

Carry out Oxidative Reactions that generate H2O2 for oxidative purposes.
Catalase destroys the H2O2 to detoxify the cell.

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44
Q

Peroxin tag?

A

SKL. (Ser-Lys-Leu)

Peroxisome are made on free ribosome in cytosol

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45
Q

3 peroxisome synthesises

A

Plasmalogen (Myline;schwann)
Bile acid
Lipid Biosynthesis

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46
Q

3 peroxisome degradations

A

VLCFA Beta oxidation
Purine Catabolism (degrade Uric acid using Xanthine Oxidase)
H202

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47
Q

Oxidase of peroxisome

A

Synthesis H2O2

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48
Q

Catalases of peroxisome

A

Eliminate the H2O2 into H2o and O2

49
Q

What do peroxisomes contain within? What gene encodes them?

A

Peroxisomal enzymes aka Peroxins. Encoded by PEX.

50
Q

What do peroxins form?

A

Channels within membrane

51
Q

Where is the only place VLCFA degradation can occur?

A

In peroxisomes. Broken down until get down to 10 carbons.. Then can move to mitochondria to be transformed into Acetyl CoA.

52
Q

Where is cardiolipin found

A

On the inner membrane of the mitochondria and it is thought to contribute to the impermeability of the membrane

53
Q

Where is cardiolipin synthesized? Structure?

A

Outer mito membrane

4 FA Tails

54
Q

Where does Glycolysis, TCA cycle, and ETC occur?

A 
Gly= cytoplasm
TCA= Mito matrix
ETC= matrix ( even though the ETC is on the inner membrane itself)
55
Q

Where can you find brown adipose? What do you find in there?

A

In mitochondria.

Find uncoupling proteins Thermogenin on the inner membrane.

56
Q

Thermogenin

A

A channel on the inner membrane of the mitochondria that allows protons to “leak” from cytoplasm to matrix. DOESNT use ATP SYNTHASE.
Instead releases energy as HEAT

57
Q

Reactive Oxygen Species

A

Produced during oxidative phosphorylation. Can inactivate electron acceptors and damage RNA, DNA.

58
Q

2 proteins that work against generation of superoxides (ROS)

A

GPX and SOD2. THey convert the ROS into water

glu peroxidase, and superoxide dismutase

59
Q

Apoptosis Enzymes

A

Bax, Bad, BCL-2

60
Q

BAD enzyme

A

Dimerizes with BCL-2 and prevents BCL2 from dimerizing with BAX

61
Q

BAX Enzyme

A

Forms pores on outermembrane of mito

62
Q

BCL-2 Enzyme

A

Anti-apoptotic. Dimerizes with Bax and prevents it from forming a pore.

63
Q

Intrinsic pathway for cell death

A

p53 will get activated and it will go on to activate Bax –> make pores in the outer membrane of mitochondria –> cytochrome c form a complex (apoptosome) that will activate capsases 9 –> activate caspase 3/7 –> Apoptosis

64
Q

Extrinsic pathway for cell death

A

Death ligand bind to death receptor outside the mitochondria

Activate procaspase 8 –> caspase 8 –> activates caspase 3/7 –> apoptosis

65
Q

Protein import into the mito

A

Protein has Mito sig. seq. Binds to HSP70+ in the cytosol to prevent folding of protein.
TOM and TIM recognize sig. seq.
HSP70+ binds to TOM
HSP70+ binds to TIM (but tim needs an electrochemical gradient)

HSP70 brings in the protein (function like Bip)

Matrix Protease removes Mitochondrial Signal Sequence

HSP60 + ATP can help the protein fold inside of the matrix if it does not fold spontaneously.

66
Q

TOM and TIM of Mito

A

Tom: Translocase of Outer Membrane

Tim: Translocase of Inner Membrane

67
Q

HSP 60+ of mito

A

can help the protein fold inside of the matrix if it does not fold spontaneously.

68
Q

Mito GENOME H and L Loop

A

H loop is all coding execpt for D-Loop.
(12 mRNA)

L codes for 1 mrna and several tRNA

69
Q

How many genes does Mito genome make

A

33 genes all together
13 protein coding genes
22 tRNA
2 rRNA

70
Q

DNA Poly and helicase in mito

A

Gamma and Twinkle

71
Q

DNA Poly Gamma and the alpha subunit

A

encoded by nuclear DNA.

PLOG encodes for alpha subunit of the gamma.

72
Q

HIV Patients treated with AZT

A

DNA polymerase δ is not inhibited because the nucleotide entry channel in this polymerase does not accept the AZT derivative, so nuclear DNA replication is not affected

DNA polymerase γ is inhibited by the AZT derivative causing depletion of mitochondrial DNA, explaining the myopathy as a side effect of AZT therapy

73
Q

AZT

A

AZT is a drug that stops Reverse Transcription from occurring in the HIV Virus.

74
Q

Processesing of mito MRNA

A

Polyadenylated by not capped

75
Q

Mito Trnx

A

2 promoters in control region (D-loop) HSP/LSP. Transcribed at same rate.

RNA endonuclease cuts into tRNA,rRNA, mRNA.
NO INTRONS
Recomb not evident

76
Q

Mito TrnsL

A

Starts with N-Formyl Methionine

22 tRNA in mito translation

77
Q

Why does the accumulation of mito occur faster compared to nuclear DNA

A

occurs 10 fold faster because of the formation of oxidative radicles

78
Q

3 types of mutations in Mito

What do they affect?

A

1) Deletion/dup
2) point mutation in tRNA (prot. syn)
3) Missense mutation in coding region that impairs ox. phos.

Directly or indirectly effect oxid phos and atp production.
Cause lactic acidosis and ragged red muscle fibers (cause more mito to form b/c think theres energy deficiency)

79
Q

How can you detect giant deletions in mitochondrial genome

A

Use Southern blot or PCR.

Alway find in heteroplasmic state

80
Q

Two types of intracellular signaling proteins

A

Kinases (tyrosine kinases, serine/threonine kinases)

GTP-bindng proteins (G-proteins)

81
Q

2 signaling pathways of GPCR

A

1) cAMP as 2nd messenger
Effector: Adenyl cyclase
uses Gi and Gs

2) DAG and IP3 as 2nd messenger
Effector: PLC
Uses Gq

82
Q

Adenyl Cylcase Path

A

Adynl activated –> Converts ATP to cAMP –> Activates PKA by bing to its regulatory proteins –> The catyltic PKA enters nucleus –> Bind to CREB –> Bind to CRE –> Gene regulation

PKA = Adenyl Cyclase

83
Q

PLC Path

A

PLC activated –> breaks down inositol phospholipid into IP3 and DAG –> IP3 opens calcium channel on endo reticulum –> Ca binds to DAG to activate PKC Ser/Thr

PKC = PLC

84
Q

Tyrosin Kinase Receptor pathways

A

PLC and PI3K and GRB2

85
Q

PI3K Pathway

A

RTK phos PI3 Kinase –> phos PIP2 –> Phos PIP3 activate PKB/AKT –> AKT phos BAD by freeing the apoptosis inhibitory protein leading to the inhibition of apoptosis

86
Q

Cell survival inhibitions

A

PKB inhibits BAD
BAD inhibits BCL-2 by heterodimerizing with it.
BCL-2 inhibits BAX
BAX forms pores… Active Bad = active Bax

87
Q

Ras-MAPK Path

A

GRB2 SH2 domain binds to phos Thyrosin on activated RTK.
SH3 domain of GRB2 attracts RAS-GEF SOS. This activate Ras protein with GTP.
Ras –> Raf –> Mek –> Erk (MAPK)

88
Q

Cytokine Path JAK/STAT

No TK activity

A

No enzymatic activity.
2 monomer receptors come close –> JAK tyrosine phos each other –> Phos binding site –>STAT binds to site –> Phos STAT –> Dimerize STAT –> Enter nucleus

89
Q

What element is essential for DNA binding

A

ZN2+. Receptors bind to these

90
Q

Microtubule energy

A

GTP and GDP. Growth on + end.

Hydrolyze the beta tubule

91
Q

Where does catastrophe occur and dynamic instability occur?

A

Microtubules. If hydrolysis catches up with dimer addition

92
Q

Singlets, doublets, triplets

A

1: carrying, chromosomes
2: Cillia/flagella/Axoneme
3: MTOC (Centriole and Basal bodies)

93
Q

Axoneme structure

A

made up using 9 microtubules doublets and 2 singlets in middle

94
Q

Centriole structure

A

9 MT triples

95
Q

Centrosome

A

2 centrioles

96
Q

Gamma tubulin

A

Associated with centrosome through the pericentriolar.

Where singlet MT extend through from MTOC

97
Q

MAPS

A

Protect from MT disassembly. Example TAU. Inhibit tubulin dissociation.
Make MT more stable which causes less catastrophes and makes them less dynamic

98
Q

Kinetichore

A

Shorten as the cell goes from Metaphase to Anaphase.

Dynein pulls the Chromatids in towards the centrosome

99
Q

Polar

A

Grow as the cell goes from Metaphase to Anaphase

Kinesin: walks towards the + end, pushing the centrosomes apart

100
Q

Basal body =

A

MTOC ; 9 triplets

2/3 MTs from each Triplet form Doublets that protrude into the Axoneme for cilia

101
Q

Actin Cross linking proteins

A

Parallel bundles = A-Actinin
Fimbrin, & Vilin

Webs/gels= Spectrin and filamin

102
Q

A Actinin

A

Loost packing, STRESS FIEBRS, contractile, cytokenesis

103
Q

Fimbrin

A

Tight packing of bundles, MICROVILLI, LAMMELPODIA, non-contractile

104
Q

Fimbrin and Villin

A

Crosslink acting to increase SA for absorption.

Non-contractile

105
Q

Where do you find stereocilia

A

Mechanoreceptors of hair cells in the inner ear

Epididymis absorptions

106
Q

Filamin

A

3D crosslink of actin under the Plasma Membrane for support

107
Q

Spectrin

A

Actin cross link protein in RBC

108
Q

Dystrophon

A

Anchors actin cytoskel to the sarcolemma in skeletal muscles

109
Q

Vinculin & Talin

A

Attach actin cytoskel to membranes in focal adhesions

110
Q

Cadherins

A

Cell to cell contacts mediated by this protein

111
Q

3 types of cytoplasmic IF

A

Keratin (Epithelia), Neurofilaments(Nerve cells), vimentin (CT, Muscle, neuroglial cells)

112
Q

Nuclear Lamins

A

Nuclear filament found in all animal cells

113
Q

Keratin IF Defects

A

Epidermolysis Bullosa simplex, Hyperkeratosis, Plantopalmar keratoderm

114
Q

Epidermolysis Bullosa Simplex

A

Auto Dom Defect in Basal layer
Keratin 5,14.
Rupture cells in epidermis basal layer
Wearing shoes causes blisters above basement membrane. Fragile skin

115
Q

Epidermolytic Hyperkeratosis

A

Keratin 1, 10 Defect in suprabasal layer
Excess proliferation
Prone to infection
Hyperproliferation, Thickened skin, chronic wounding

116
Q

Epidermolytic Plantopalmar Keratoderma

A

Keratin 9 defect in cornified layer
palms of hand and soles of feet
Everything above basal layer is ripped off

117
Q

Desmin

A

IF that lines up the myofibrils so they’re packed together for their strength

118
Q

Lamins

A

Lines inner surface of Nuclear envelope

Structural stability of nucleus, protects the DNA

MCB Proteins (1 decks)

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