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Cell and Molec exam 4 > Cell and Molec exam 4 > Flashcards

Cell and Molec exam 4 Flashcards

1
Q

Why do cells need to have signaling molecules?

A

Help mediate cell proliferation and survival, cell response to nutrients, and organization and cooperation of cells and tissues

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2
Q

5 types of extracellular signals

A

amines
peptides and proteins
steroids
fatty acids (eicosanoids)
gases

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3
Q

Many signaling molecules are ___

A

small peptides or proteins

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4
Q

They then are trafficked through the _____ and then secreted

A

ER and golgi,

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4
Q

These signaling molecules are encoded by genes, transcribed, and translated into _____

A

peptides or proteins

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5
Q

Function of elicosanoids

A

regulating inflammation, vasodilation, smooth muscle contraction, etc.

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6
Q

Steroids bind ___ hormone receptors, which can activate expression of various genes.

A

nuclear hormones

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7
Q

Gases can act like signalling molecules

A

Have no effect on neurotransmission but can act as a vasodilator

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8
Q

Juxtacrine signals are mediated by interactions between

A

two transmembrane proteins.
The ligand is something that never leaves from the cell that produces it.

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9
Q

Paracrine cells

A

signal acts on neighbors

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10
Q

Autocrine signals

A

Are self stimulatory

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11
Q

Endocrine signals are released at a distance and travel to target tissues

A

released from glands
can be released from cells that are not in glands
travel to target cells via circulatory systems

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12
Q

Cell surface receptors

A

G protein-linked receptors
Receptors that contain enzymes, or that directly recruit enzymes
receptors that are ligand-gated ion channels

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13
Q

Different receptors can result in different responses to the ____ ligand

A

same
- can do this because of different receptors, different downstream signaling proteins, or different concentrations or duration of molecules

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14
Q

What influences receptor-ligand interactions

A

specificity
affinity
saturation
physiological response

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15
Q

Binding assays

A

reveals receptor number and affinity

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16
Q

Agonist

A

exerts its effects by direct alteration of the functional properties of the receptor with which it interacts (binds receptor and mimics effects of hormone).

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17
Q

Antagonist

A

Agent that exerts its effects by inhibiting the action of a specific agonist (often, though not always, acts by competing with agonist for binding site).

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18
Q

ways signal transduction can happen

A

Allostery
covalent modification
induced proximity

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19
Q

Cross talk

A

Signals from different receptors are intergrated

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20
Q

Hormone

A

chemicals that coordinate different functions in your body by carrying messages through your blood to your organs, skin, muscles and other tissues. Are signaling molecules.

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21
Q

neurotransmitter

A

A neurotransmitter is a signaling molecule secreted by a neuron to affect another cell across a synapse. The cell receiving the signal, or target cell, may be another neuron, but could also be a gland or muscle cell.

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22
Q

Neurohormone

A

a hormone (such as vasopressin or norepinephrine) produced by nerve cells and secreted into the circulation.

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23
Q

Ligand

A

A molecule that binds a signal

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24
Q

receptor

A

receptors are chemical structures, composed of protein, that receive and transduce signals that may be integrated into biological systems.

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25
Q

Second messenger

A

are small molecules and ions that relay signals received by cell-surface receptors to effector proteins. They are normally small molecules

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26
Q

Allostery

A

Changing the shape and the ability of proteins to act with other substrates. How GTPases work

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27
Q

Effector

A

A small molecule that selectively binds to a protein to regulate its biological activity can be called an effector.

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28
Q

How generally does an extracellular signaling molecule trigger changes in gene expression?

A

Mostly steroid receptors. Requires the signal to get into the cell either through a transporter or through diffusion of the membrane

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29
Q

How do scaffold proteins lead to increased efficiency of signal transduction?

A

Reduces the amount of time for diffusion and concentrating proteins with second messengers

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30
Q

How is an initial signal (e.g. from epinephrine) amplified?

A
  • The receptor activates Adenylyl Cyclase which produces cAMP (the second messenger)
    • this then activates many different kinases which can produce many different products
    • Have a huge application with a small amount of signal
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31
Q

How can the same ligand (e.g. acetylcholine) produce different responses?

A
  • It can bind to different receptors
    • different concentration gradients
    • Different pathways (different downstream signaling proteins called effectors)
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32
Q

What does the dissociation constant in receptor-ligand interactions refer to?

A
  • How we characterize how tightly the ligand binds
    • Ligands can come on and off the receptors
    • Saturation is when the receptor has a limited number of binding sites. If there is no saturation then it is a non-specific interaction site
  • concentration at which half of the sites are filled. With a low affinity, it will be hard to fill up the sites.
  • baseball analogy
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33
Q

A higher dissociation constant = a _____ affinity between receptor and ligand.

A

lower

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34
Q

Nuclear receptors are …… transcription factors

A

ligand-activated

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35
Q

Nuclear receptors share a … domain structure

A

common

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36
Q

Type I nuclear receptor

A

Nuclear receptor (NR) in inactive complex in the cytoplasm
Hormone binding leads to release of chaperone
Nuclear receptor dimerizes
Nuclear receptor enters nucleus and binds DNA response element (RE)

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37
Q

Type II nuclear receptor

A

Nuclear receptor already “docked” on DNA
Hormone binding leads to release of co-repressors and recruitment of co-activators

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38
Q

Many steroid receptors bind ___

A

steroids

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39
Q

Xenobiotic

A

a chemical substance found within an organism that is not naturally produced by that organism
- are stable in the environment
- toxic
- modified by gut microbes and by human cells

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40
Q

Why do we have receptors

A

Similar to chemicals produced by fungi, bacteria and plants that we might need to detect and detoxify
This diagram shows PXR binding to zenobiotics; the aryl hydrocarbon receptor (AHR) also commonly binds them.

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41
Q

Orphan receptors

A
  • Have similar protein structures to other nuclear receptors.
  • Ligands are not known.
  • Some might be constitutively
    active (no ligand needed).
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42
Q

The receptors are inactive in the cytoplasm.
Ligand-binding changes shape of receptor and…

A

recruits transcriptional activators

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43
Q

Nuclear receptors bind to specific DNA sequences called

A

response elements
- Helices of PPAR-gamma and RXR-alpha contact the major and minor grooves of the DNA helix.

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44
Q

Many steroid receptors binds DNA using a

A

zinc finger

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45
Q

Ligand-bound nuclear receptors can recruit

A

coactivators
-Coactivators like histone acetyl transferases (HAT) are recruited.
- Nucleosomes repositioned/chromatin becomes more accessible
-Other transcription factors also join in (as do other surprising proteins).
-RNA polymerase recruited

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46
Q

Nuclear receptors can also repress gene expression

A

-Block access by binding to DNA and preventing something else binding
-Competition for limiting amounts of co-activators
-Recruiting co-repressors like histone de-acetylases
-Recruiting nucleosome remodeling complexes like SWI/SNF

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47
Q

How to run an experiment to see if your transcription factor bonded to sequence you identified

A

Do CHIP and then sequencing/ pcr

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48
Q

nuclear receptors

A

They are ligand-activated transcription factors. They bind ligand and activate gene expression. Required for steroid hormones. And respond to lot of different chemicals

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49
Q

cytochrome p450s

A

Metabolic enzymes which add OH groups to soluble compounds
response element (RE)

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50
Q

zinc finger

A

Used by many steroid receptors to bind DNA. Is on top of the response element and has an affinity for specific nucleotides- the spacing and the orientation are different

51
Q

Give an example xenobiotic. Why do we have receptors for these?

A
  • Are things that are found in the environment but are not naturally produced by us. Can be made by other things. Common sources are when things are burned, herbicides, plastics
  • Lots of microbes produce similar compounds that can be detected by us
  • If we eat these things they can be detected by us and detoxify them.
  • bpa is an example
52
Q

Xenobiotic receptors often lead to activation of cytochrome P450s, like CYP3A4, enzymes that hydroxylate small molecules. Name a possible beneficial effect of hydroxylation and a potential deleterious effect.

A
  • Help detoxify them from us (benefit) We want to add hydroxyl groups to these compounds so that they become more soluble and that we can pump them out of the cell
  • Adding hydroxyl groups makes them more active and sometimes makes them activate DNA etc.
53
Q

Name 2 reasons a receptor might be classified as an orphan receptor.

A
  1. We don’t know their ligand
    1. Some might not need ligands – might be constitutively active
54
Q

Name 2 important characteristics of response elements that help to confer specificity of receptor binding.

A
  1. orientation
  2. spacing
55
Q

You make a chimeric receptor with the ligand binding domain of GR and the DNA binding domain of ER. This receptor will bind _____ and activate ______responsive genes (glucocorticoid, estrogen).

A

glucocorticoid and activate estrogen

56
Q

Name 1 way nuclear receptors like GR can activate gene expression

A
  • Coactivators like histone acetyl transferase (HAT) are recruited
    • Nucleosomes repositioned/ chromatin becomes more accessible
    • Other transcription factors also join in (as do other surprising proteins)
    • RNA polymerase is recruited
    • GR recruits the complex which leads to the activation of genes
57
Q

Name 1 way nuclear receptors like RXR can repress gene expression.

A
  • Block access by binding to DNA and preventing something else from binding
    • Recruiting co-repressors like histone deacetylases
    • can recruit nucleosome remodeling complexes
  • Depends on the cellular context and what receptors are activated whether they activate or inactivate gene expression
58
Q

You are studying the promoter and enhancer regions of a gene. By sequence analysis, you think the region contains three EREs (estrogen response elements). Suggest a possible approach for determining if estrogen regulates the expression of this gene. Suggest a possible approach for determining which (if any) of these three EREs are required for the response to estrogen.

A
  • You can measure gene expression by using ChIP. Can run a PCR to see what genes it is actually interacting with
    • Could do a western blot for the estrogen receptor to see if you actually pulled out. Could also run a komassi stain to see if you have protein in your gel
59
Q

Briefly describe how a ChIP experiment works.

A

A CHIP experiment works by having an immunoprecipitation specific antibody-protein interaction to isolate and quantify a specific protein of interest
- is used to identify the relative abundance of a specific protein or a specific protein modification at a certain region in the genome.

60
Q

Basic structure of G proteins

A

Seven transmembrane α-helices
Three extracellular and three intracellular loops
An extracellular amino-terminal segment
The carboxy-terminal tail

61
Q

Diversity of physiological responses to GPCR stimulation

A

Different extracellular signals can activate GPCRs.

This activates the signal transduction pathways, and in turn, causes alteration incellular responses.

Hence, GPCR stimulation can cause a variety of physiological responses to occur in the body.

multipleGPCRs often recognize thesame ligand

62
Q

Receptor activation of heterotrimeric G-proteins.

A

Upon ligand binding to the receptor inactive G protein heterotrimers dissociate into separate, active Gα and Gβγ subunits.

63
Q

Gαs

A
  • activates adenylyl cyclase, which in turn stimulates cAMP production.
  • Increase in cAMP in turn activates protein kinase A (PKA).
    PKA is a serine/threonine kinase that phosphorylates many different substrates, including other kinases and transcription factors.
64
Q

Gαi

A

inhibits adenylyl cyclase activity

65
Q

Gαq

A

activates phospholipase C β (PLCβ), which produces IP3 and DAG from the hydrolysis of PIP2.
- which breaks down PIP2 into two different second messengers, IP3 and DAG

66
Q

Gα12/13

A

activates Rho guanine nucleotide exchange factor (RhoGEF), which activates Rho GTPases.

67
Q

Gβγ heterodimers

A

regulate K+, Ca2+channels activity
recruit proteins to the plasma membrane as a scaffold, including PI3K, P-Rex-1, and β-adrenergic receptor kinase.

68
Q

Regulation of systemic functions by signaling through G protein pathways

A

-Many extracellular agents, such as hormones, neurotransmitters, chemokines , and local mediators signal to the 4 main G protein families to regulate cellular functions such as metabolic enzymes, ion channels.
- Modulation of the activities of the cellular machines in turn gives rise to altered cellular functions such as changes in glucose metabolism in liver and muscle or altered activities of pacemaker cells in the heart.
-contribute to the regulation of large-scale systems such as organismal homeostasis and learning and memory.

69
Q

Protein kinase A (PKA)

A

-Protein kinase A (PKA) regulates a diverse set of biological functions downstream of cyclic AMP (cAMP).
-It is a tetramer consisting of two catalytic subunits (PKA-C) and two regulatory subunits (PKA-R).
-The two PKA-C and two PKA-R subunits are bound together in the inactive state of the enzyme.
-When cAMP binds the PKA-R subunits, the PKA-C subunits are released and interact with downstream effectors.
- Kinases can also affect transcription, by phosphorylating transcription factors

70
Q

The effects of kinases are terminated by _____
(remove phosphate from target proteins)

A

phosphatases

71
Q

Different extracellular agents can activate the ___ receptor, regulate the ___ pathway to bring about changes in different effectors!!!

A

same
- glycogen and epinephrin

72
Q

Why is the signaling mechanisms so complicated?

A
  • signalling amplification
  • timing
  • cross talk
73
Q

Crosstalk between GPCR and RTK

A
  • The transactivation of GPCRs by RTK agonists can occur in a ligand-independent manner and requires the formation of GPCR–RTK complexes.
  • RTK stimulation triggers GPCR transactivation through the formation of a molecular protein complex.
  • This event is crucial for β-arrestin recruitment, which, in turns, promotes the internalization of the RTK/GPCR complex and intracellular signaling cascades.
74
Q

How to turn off G protein signaling

A
  • Second messenger is degraded by cyclic nucleotide phosphodiesterase
  • G protein inactivates itself (GTP hydrolyzed to GDP by GTPases)
    True of all G proteins, not just heterotrimeric Gs
    -Substrates of protein kinase A are dephosphorylated by phosphatases
  • Receptor is phosphorylated and internalized
75
Q

Turning off GPCR signaling

A

Short-term desensitization
– occurs in minutes
- Requires G-protein coupled receptor kinase (GRK) and β-arrestin

Long-term desensitization
Occurs over hours to days
- Internalizes receptor for recycling or degradation by lysosomes

76
Q

Turning off GPCR signaling – short-term

A
  • GPCR phosphorylated by GRKs
  • The phosphorylated GPCR recruits β-arrestin
  • Binding of β-arrestin to GPCR prevents the dissociated G proteins from interacting with the arrestin-GPCR complex
  • This inhibits further downstream sinaling
    -Arrestin binding targets GPCR for clathrin coated pits in cell membrane for internalization
77
Q

How are the following steps in GPCR signaling TERMINATED?

A

Receptor activation – GRK phosphorylation of GPCR, transactivation of GPCR by RTK, degradation by arrestin and clathrin coated pits
Activation of heterotrimeric G-protein – hydrolysis of GTP
Calcium release – activation of sarcoplasmic reticulum to take in Ca2+, inhibit PLC-beta, inhibit Gq
Cyclic AMP - phosphodiesterase
Phosphorylated proteins - phosphatases

78
Q

Second Messenger

A

molecules that bring signals downstream of the signal cascade
heterotrimeric G protein

79
Q

epinephrine (aka adrenaline)

A

small molecule that increases blood glucose level

80
Q

Be familiar with the general mechanism by which GPCRs work:

A

ligand binding, association with heterotrimeric G protein, GEF activity activates G alpha, Galpha separates from Gbeta and Ggamma subunits, Galpha activates effector, Gbeta+Ggamma can also activate effectors, signal is amplified, various signaling cassettes (sets of proteins working in series) can be activated.

81
Q

Give two examples (from this lecture) where phosphorylation activates the target protein, and two examples where phosphorylation inactivates the target protein (hint: turning off GPCR signaling).

A

a. Inactivation:
i. Substrates of protein kinases A are dephosphorylated by phosphatases
ii. A receptor is phosphorylated and internalized
b. Activation:
i. For gene expression, CREB is phosphorylated to stimulate gene transcription
ii. PKA phosphorylates other kinases to lead to different things being produced

82
Q

Name two ways the original signal detected by the GPCR is amplified.

A

Can activate multiple G proteins
Can phosphorylate multiple cellar proteins

83
Q

How are the following steps in GPCR signaling stopped:

A

i. Receptor activation – GRK phosphorylation of GPCR, transactivation of GPCR by RTK, degradation by arrestin and clathrin-coated pits
ii. Ca2+ release – inhibit PLC-beta and Gq, and activation of sarcoplasmic reticulum to take in CA+2
iii. PKA activity- phosphodiesterase

84
Q

How growth factor signaling generally works

A

Ligand binding
Receptor dimerization
Receptor phosphorylation
Binding of adaptor proteins
Signaling cascade of kinases
Alteration of transcription factors or other effectors

85
Q

Intracellular actions of receptor tyrosine kinases

A

Binding of growth factors to their receptors leads
to receptor dimerization and autophosphorylation

86
Q

Receptor phosphorylation generates multiple binding sites

A

Can do this by
1. localizing protein that will pass the signal to downstream effectors
2. Localizing proteins near the plasma membrane (scaffolding)

87
Q

Proteins containing ____ domains can bind to phospho-tyrosine

A

SH2

88
Q

An SH2-domain-containing protein commonly activated by growth factor receptors is ____

A

Grb2
- Grb2 activates SOS
- SOS is an activator for Ras
- activated RAS begins a kinase chain
- Binds to phosphotyrosine and the signal can be traveled down into the cell

89
Q

MAP kinase cascade

A
  • Raf (kinase)
  • MEK (kinase)
  • ERK (kinase) -> ERK phosphorylates and activates transcription factors that
    regulate, among other things, the initiation of cell division
90
Q

Receptor tyrosine kinases can stimulate _____

A

other pathways – it is not just about activating MAPK!

91
Q

Some receptors don’t contain their own tyrosine kinase, but instead _____

A

recruit and activate cytosolic tyrosine kinases, or other enzymes

92
Q

Turing off RTK signaling

A

Usually by de-phosphorylation
Or in the case of Ras by hydrolysis of GTP
Inhibitory proteins: phosphatase, GAP, or proteins like 14-3-3 that
Bind and sequester phosphorylated proteins

93
Q

Common methods for studying signaling pathways:

A

Phospho-specific antibodies to detect active states of signaling proteins (example: Active ERK)

Chemical inhibitors that block specific enzymes in the pathway (example: blocking the receptor)

Kinase assays (in vitro interaction of kinase and substrate)

Genetics

94
Q

Basic concept of a kinase assay

A

substrate + ATP = ADP + substrate
- Substrate can be protein, peptide, lipid, or sugar depending on the kinase.

95
Q

________are small molecules that block the action of kinases – often by competitively blocking the binding of ATP

A

Kinase inhibitors

96
Q

Kinase assay

A

Treat cells with various concentrations of compound.
Purify kinase.
Add substrate.
Add radiolabeled ATP.
Measure labeled substrate.
- A kinase assay works by simply measuring the activity of the kinase.

97
Q

autophosphorylation

A

Autophosphorylation is a type of post-translational modification of proteins. It is generally defined as the phosphorylation of the kinase by itself.

98
Q

adaptor

A

An adaptor molecule is a double-stranded, chemically synthesized oligonucleotide that is used for the ligation of DNA. The adaptors have one sticky and one blunt end. The blunt end is ligated with the blunt end of the target DNA producing a DNA fragment with sticky ends.

99
Q

phospho-specific antibody

A

detect only the phosphorylated forms of proteins in a complex protein mixture within cells.

100
Q

How do adaptor proteins distinguish between phosphorylated tyrosines?

A
  • different amino acids around the tyrosines
101
Q

Why is it advantageous to have many of the proteins involved in RTK signaling localized to the plasma membrane?

A
  • it gives multiple advantages to regulate them
    • Localized proteins that will pass signal downstream effectors (activating signaling)
    • Localizing proteins near the plasma membrane (scaffolding) GAP inhibit GTPases like Pho, Ras (these are peripheral membrane proteins)
102
Q

Suggest an experiment to determine if your chosen growth factor activates (leads to phosphorylation of) ERK1,2.

A
  1. phosphospecific antibodies w/ western blot. This lets us know if it is activated or not
103
Q

Wnt

A

Wnt signaling regulates embryonic development, cell differentiation, proliferation, and adult stem cell homeostasis
- often dysregular in Cancer

104
Q

Wnt signals ___

A

EMT
- During EMT, cells lose cell-cell junction connections and polarity
- In epithelial cells, beta-catenin is primarily in the adherens junctions, in mesenchymal cells it is primarily in the
Nucleus where it acts as a transcription factor and induces expression of genes

105
Q

Planar cell polarity refers _____

A

to the coordinated alignment of a sheet of cells
-Components of the Wnt signaling pathway also regulate planar cell polarity, like these genes which regulate the alignment of “hairs” on the fly wing.

106
Q

The Wnt/Ca++ pathway triggers the release of Ca++ by stimulating _______

A

phospholipase C

  • The relative balance of these factors determines the cell’s response.
107
Q

The Wnt/Ca++ pathway

A
  • Ligand Wnt
  • Receptor Fz
  • GTPase Gprotein *probably Rho
    CDC42
  • Kinase PKC PKG CAMKII TAK1 NLK1
  • Other enzymes PDE phosphodiesterase; PLC phospholipase
108
Q

Basics of canonical Wnt signaling (no Wnt)

A

No Wnt situation:
Beta catenin is supposed to be in the adherens junctions, or very low level. Any cytoplasmic beta catenin is targeted for degradation by the destruction complex and degraded by the proteasome

109
Q

Basics of canonical Wnt signaling (Yes Wnt)

A

Wnt present situation:
LRP is phosphorylated by the destruction complex. The destruction complex is localized to the receptor and inhibited.
Beta catenin levels build up, beta catenin goes in the nucleus, displaces a repressive complex and activates gene expression

110
Q

Structure of the Wnt

A
  • Wnts ‘pinch’ the Fz receptor using their thumb and index finger
  • big for signalling molecules
111
Q

Frizzled and LRP5/work together to activate _____

A
  • Wnt signaling
    -When these two combine, the destruction complex is inhibited allowing beta catenin levels to increase
112
Q

When Wnt is absent

A
  • When Wnt is absent, the destruction complex is active.
  • Axin is the scaffold.
  • GSK3 and CK1 phosphorylate beta catenin.
  • Phosphorylated beta catenin is “marked for destruction” by ubiquitin ligases (E3)
  • Beta catenin is then degraded.
113
Q

biomolecular condensates

A
  • Liquid-like goo-balls of proteins, lipids and RNAs
  • Can flow, merge and separate
  • Not membrane bound
  • Proteins can join and leave
    ‘phase separate’, like oil in water
114
Q

Functions of biological condensates

A

Enhancing activity by concentrating enzymes and substrates
Inhibiting activity by sequestration
Influencing protein folding
Facilitating specific subcellular localization

115
Q

Intrinsically disordered regions

A
  • seem important in the formation of lipid droplets
  • Many proteins have disordered regions
  • Some are induced to fold by binding partners
  • Others remain (and function) as disordered regions, helping to cluster other proteins, lipids, RNAs, etc
116
Q

Axin, APC, beta catenin, GSK intertwine in _____

A

condensates.

117
Q

Beta catenin

A

is normally found in adherens junctions (Helps to connect cadherin to actin cytoskeleton through binding alpha catenin)
- uses the same binding site to interact with different proteins.
-Can bind axin, e-cadherin, APC, and TCF/LEF

118
Q

DVL

A

Dishevelled
- becomes active when Wnt binds to frizzled and LRP
- DVL blocks the action of the “Destruction Complex” containing Axin/APC/CK-1/GSK-3

119
Q

Genes activated by beta catenin

A
  • depend on which partner transcription factors it binds
  • Beta-catenin doesn’t bind DNA
    Directly it always works with partner proteins to activate genes
    -Depending on the cell type, different partners are available and different genes will be induced
120
Q

The ligand

A

is what is binding

121
Q

GSK3

A

phosphorizes B Catain

122
Q

Axin

A

is a scaffold

123
Q

Define proteolysis.

A

The breakdown of proteins or peptides into amino acids by the action of enzymes

124
Q

What would be the result of a double knock-out of DSH and APC? Of GSK3 and β-catenin?

A

a. There would be no destruction complex
b. DSH is upstream of actin and the beta catin will build up

125
Q
A

Cell and Molec exam 4 (1 decks)

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