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Biochem > Exam3Lec1Part2CellSignaling > Flashcards

Exam3Lec1Part2CellSignaling Flashcards

1
Q

What are the three basic steps of Cell signaling?

A

reception: target cell senses the substance in its exogenous environment
transduction: conversion of the signal via a cascade of molecular events
response: specific cellular effect attributes to the signaling molecule.

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2
Q

What type of signaling is reception?

A

INTERcellular signaling-contact dependent or contact independet

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3
Q

What type of signling is transduction?

A

INTRAcellular signaling

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4
Q

Transcription of genes reulting in protein expression mediating a biological response

A

Response

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5
Q

Explain the contact dependent (juxtacrine) mode of intracellular signaling of reception

A

It requires cells to make physical contact with one another.

Receptor contact!!

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6
Q

Explain the contact independent mode of intracellular signaling of reception

A

Cells do NOT make physical contact.
* Endocrine: target receptors reached through bloodstteam
* Paracrine: target receptors on nearby cells
* Synpatic: target receptors use an electrical signal
* Autocrine: target receptors on the same cell

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7
Q

Tisses capable of responding to hormones have 2 properties in common. What are they?

A
  1. They possess a receptor having very high affinity for hormone.
  2. The receptor is coupled to a process that regualtes metabolism of the target cells
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8
Q

What is the definition of transduction?

A

A signal from an extracellular substance carried/amplified intracellularly to produce a biological response

signal amplification

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9
Q

What are the secreted molecules (AKA ligands) for Transduction (INTRAcellular signaling)?

A
  • Hormones (peptide and steroid hormones)
  • Neurotransmitters
  • Peptides
  • lipids
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10
Q

What are the receptors for secreted molecules for Transduction (INTRAcellular signaling)?

A

Intracellular: steroid hormones
Cell-Surface: peptide hormones

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11
Q

Explain the general process of how a hydrophobic hormone such as estrogen and androen (steroid hormones) enter a cell via an intracellular receptor

A

The hydrophobic hormone enters the cell and binds to an intracellular receptor. This then travels to the nucelus where it then promotes change

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12
Q

What are the two main steroid hormone receptors for transduction

A

Glucocorticoid and estrogen

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13
Q

Explain how the glucocorticoid receptor works

A

Location : cytosol
Glucocorticoid binds to GC receptor activating HSP. HSP leaves and the receptor and hormone translocates to the nucleus and activates transcription of a gene upon HRE binding to glucocorticod response element on the target cell.

Location: cytosol
response: activate transcription

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14
Q

Explain how the esterogen receptor works

A

Location: nucleus
Estrogen receptor binds to estrogen hormone within the nucleus, and activates transcription .

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15
Q

What are the two types of steroid hormone receptors activities?

A
  1. Slow: last longer
  2. Rapid: simple turn on and off

for slow , the receptor is inside the cell and it then translocated to nucleus with hormone

for fast, the receptor is on the cell surface and it binds to a secondary messenger giving an immediate response

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16
Q

What are the two major subtypes of estrogen receptor and what do they do?

A

These estrogen receptors can be found ALL over the body, different parts of your body have different estrogen receptors.

ERalpha and ERbeta: exert differential effects on growthe and differention in tissues, including bone, colon, uterus, liver, brain, and ,mammary gland

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17
Q

What is the selctive estrogen receptor modulators (SERM)?

A

ER ligands which exhibit antagonistic or agonistic activity depending on the tissue by inducing structural changes that influences dimerization which affecs the receptor’s ability to interact with co-facors, which effects gene expression( can result in gene activation or repression). This all happends upon a SERM binds to a receptor.

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18
Q

What is Tamoxifen?

A

1st SERM used clinically in ERalpha-positve breast cancer

Breast: antagonistic (inhibition)
Uterine: agonistic (activation)

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19
Q

Explain the general process of how hydrophilic hormones (ex: insuslin), growth factors, neurotramsitters, and EGF enter a cell via cell surface receptors

A

Hydropholic hormones bind to cell surface receptors. These receptors are integral membrance proteins. Binding of the hormone to its receptors activates secondary messengers within the cell. This leads to signal transduction. These receptors can be internalized by endocytosis to negatively regulate the hormone action

The ligand binds to the receptor and causes change inside the cell (concentration of 2nd messenger increases)

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20
Q

What are the three domains of cell surface receptors?

A

Extracellular
Transmembrane
Intracellular

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21
Q

All cell surface receptors are what type of receptors?

A

Transmembrane

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22
Q

What are the major classes of Transmembrane receptors?

A
  1. Ligand Gated Ion channels
  2. Enzyme-linked receptors.
  3. Cytokine receptors
  4. GPCR
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23
Q

Explain Ligand Gated Ion channels (simplest receptor)

A

The ligand binds to the receptor and causes a change in membrane potential. This allows ion or neurotransmitters to pass through

24
Q

Explain Transduction: Enzyme-Linked receptors

A

receptors activates tyrosine kinase or serine/threonine kinase activity in the cytoplasmic domain of the receptor

hormone or growth factor binds to the extracellular domain of its specific receptor

25
Q

In enzyme linked receptors, when tyrosine kinase or serine threonine kinase is activated, what two things can occur?

A
  1. Leads to sequential phosphorylation of intracellular signaling molecules and transduction of the signal to a biological response
  2. Activation of GTP binding Ras protein

1. a domino effect of phosphorylation of substrates

THIS IS INTRINSIC KINASE ACTIVITY

26
Q

Expain enzyme linked signal transuction-Protein phosphorylation generally

sequential phosphorylation

One of the major types of molecular swithces for changing protein function during IC signaling

A
  1. You have a signal, your kinase activates, you phosphprylate with ATP, then you get output signal

Ex: insulin signaling pathway

27
Q

Expain enzyme linked signal transuction-Signaling by GTP binding regulatory protein (generally)

Exchange of GTP

One of the major types of molecular swithces for changing protein function during IC signaling

A
  1. Ras gets an input signal, but instead, GTP binding is activated so it lets go of GDP so it can bind with GTP and thats how we can get an output signal

GTPase dephosphorylase is making it inactive so it turns off the signal

28
Q

Explain activation via growth factor binding—> protein phosphorylaiton

amplification of signal

conformational and fucntional changes in a receptor tyrosine kinase during activation by growth factor binding

A
  1. There are two monomers of inactive receptor tyrosine kinase.
  2. Receptor is dimerized and hormone (EC growth factor ex:insulin) binds to it
  3. Kinase activity is stimulated and auto phosphorylates and we have active receptor tyrosine kinase
  4. Sequential phosphorylation of other substrates occur by IC signaling proteins binding.

the receptor auto phosphorylates

29
Q

Explain Insulin signaling

slide 10 of lecture

A
  1. Insulin through RAS and MAPK can lead to cellular growth
  2. Insulin thrugh Cap phosporylation can activite TC10 whihc affects lipid rafts
  3. wreg
  4. wrg

note that the different signals can work together, they are not competelty independent of one another

30
Q

Explain the role of RAS GTPase during IC signal transduction

A
  1. Growth factor binds to receptor tyrosine kinase activating it.
  2. Adapter protein binds to phosphate on the receptor and brings Ras-activating protein with it.
  3. There is inactive Ras with GDP. Ras lets go of GDP, and GTP is added to Ras, activating it. Then there is downstream activation of other pathways
31
Q

Inactive RAS is associated with

A

GDP

32
Q

Active RAS is associated with

A

GTP

33
Q

Activated RAS can activate MAP Kinase cascade. Explain this.

this is a downstream signaling patway from RAS

This is all done by tyrosine kinase receptor

A
  1. Active RAS activates MAP-KKK
  2. MAP-KKK is phosporylated by ATP and turned into MAP-KK
  3. MAP-KK is phosporylated by ATP and turned into MAP-K
  4. Then you get a change in gene expression or you get change in cytosolic or membrane protein activity.
34
Q

Does Cytokine receptors have intrinsic kinase activity?

A

NO

35
Q

Cytokine receptors are associated with what two things?

A
  • JAK: protein that is phosph. by kinase
  • STAT (signal transducers and activators of transcription): recruited by JAK to transduce the signal (AKA continue the signaling cascade)

Examples of cytokines include IL-6, NFkappaB, IFNalpha (all interleukins and interferons)

36
Q

Explain how cytokine receptors work (JAK/STAT) pathway

A
  1. JAK tyrosine kinase binds to cytokine receptor subunits
  2. Cytokine binds to receotor, turns on JAK activity and does auto phosph.
  3. Once JAK is phosph, it recruits STAT, and that gets phosph.
  4. Once STAT is phosph, it is activated and it is released from the receptor and them dimerized, and then translocates to the nucleus.
  5. STAT in the nucelus binds to the promoter of the gene and recruits other co-factors to do gene expression,
37
Q

Growth, proliferation, cell fate determination, and stem cell renewal are associated with what pathway?

A

JAK/STAT

37
Q

True or False, GPCR are the most common transduction pathway?

A

TRUE

38
Q

GPCR have how many trasmembrane domains/receptors and what does this mean?

A

It has 7 transmembrane receptors/domains meaning that it goes in and out the membrane 7 times

39
Q
  1. Insulin is associated with which pathway?
  2. Cytokines is associated with which pathway?
  3. RAS is associated with which pathway?
  4. Multiple number of ligands are associated woth which pathway?
A
  1. Sequential phosphorylation
  2. JAK/STAT
  3. GTP activating MAPK
  4. GPCR
40
Q

Explain GPCR signaling cascade

A
  1. Ligand binds to GPCR. Alpha, Beta, and Gamma G-protein gets dissociated from the GPCR.
  2. GDP is kicked off alpha subunit and GTP is bound.
  3. Beta and gamma work with opening and closing ion channels, And Alpha with the GTP activates enzymes associated with it.
  4. associated enzyme activates second messengers.
41
Q

Explain one way that associated enzyme can activated second messengers in the GPCR signaling cascade.

A
  1. Adenylyl cyclase (in the membrane) binds to your alpha w/ GTP subunit and activated cAMP through ATP.
  2. cAMP activated protein kinase A (PKA) and other proteins leading to sequential phosph

note that phosphodiesterase can break down cAMP
cAMP is a secondary messenger

42
Q

Explain one way that associated enzyme can activated second messengers in the GPCR signaling cascade.

A
  1. Phospholipase C (PLC) binds to alpha subunit w/GTP and cleaves surface lipid (DAG)
  2. DAG can activate PKC or IP3
  3. IP3 can bind and open ligand gated Ca+ channels, releasing calcium from IC stores
  4. PKC (protein kinase c) can trigger cascade of phosphorylation
43
Q

Explain GPCR with Adenylyl Cyclase

A

Inhibitory G protein (alpha I) or Stimulatory G protein (alpha s) can get activated. Which one gets activated depends on the type of ligand that binds to GPCR.

Stimulatory G protein leads to cAMP incr
Inhibitory G protein leads to cAMP decr

44
Q

Different types of alpha subunits is why different g proteins mediate distinct responses. Explain this

A

Alpha I with GTP are involved with ion channels, inhibition of cAMP, phospholipases, and phosphodiesterases

Alpha S with GTP increases cAMP
Alpha Q w/ GTP is involved with phospholipase C activating DAG
Alpha I2 w/ GTP is involved with Rho GEFs

These are major subclasses of heterotrimeric G proteins tht are activated by G by the 7 transmembrane domain GPCRs

45
Q

What are examples of second messengers>

A
  • cAMP
  • cGMP
  • DAG
  • Calcium
  • IP3
46
Q

Explain the cAMP regulated Protein Kinase A

A
  1. Activated adenylyl cyclase binds to activated alpha subunit of G protein (with GTP)
  2. ATP and cAMP allows pKA to be activated by phosp from ATP
  3. Activated pKA can enter nucleus and binds to CBP (creb-binding protein) and activates CREB (cAMP response element) by phosph.
  4. Then we get transcription, translantion, etc and synthesis of new cytosolic or membrane protein
47
Q

An ____ or _____ in signal transduction is NOT good

A

increase, decrease

48
Q

True or False, all cancers have impaired signal transduction

A

TRUE

49
Q

What is one example of a drug discovery that targets signaling pathway

A

Herceptin (Traustuzamab) blocks the receptor so growth factor can cannot bind, growth slows

50
Q

What is one example of a drug discovery that targets signaling pathway

A

Toxin conjugate: this targets celll with antibody.
1. Antibodies bind to antigens on diseases/foreign cells
2. Toxins: poisinous to cells
3. Antibody-toxin conjugate: use antibody to find target antigen and bind to lymphoma cell, this allowing toxin to kill lymphoma cell

receptor specific

radioisotope binds to antibody. Antibody binds to antigen on cell surface. Lymphoma cell is destroyed.

50
Q

About 60% of all pharmaceuticals target

A

GPCR

51
Q

What are three main points relating to drug targets: GPCRs?

A
  1. These drugs inhibit signaling pathways
  2. These drugs target cells because of receptors
  3. These drugs acts as competitive inhibitors
52
Q

Explain Signal transduction pathway: Cross Talk

A

You are promoting the same signal with 2 different types of receptors. G protein linked receptor and Receptor tyrosine kinase. You can have different amount of protein present which affects the fxn of the cell. End result is gene expression.

53
Q

A hormone binding to its receptor activates the ____ ____ which is what?

A

signaling cascade which is the amplification of the signal

54
Q

4 main points about the signaling cascade

A
  1. Hormone can bind to multiple receptors before being degraded
  2. Each receptor can activate several enzymes
  3. These enzymes produce second messengers
  4. Result in transcription of several genes, and other metabolic effects. (ex: uptake of glucose)
55
Q

Explain down regualtion

major mechanisms for the termination of receptor-dependent signal transduction

A
  1. Recpetor inactivation: The receptor gets uncoupled from the signlaing cascade
  2. Receptor internalization (temporary): The entire receptor with ligand is internalized by endosome
  3. Receptor down-regualation (permanent): The receptor with the ligand is chewed up by the lysosome.

Biochem (17 decks)

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