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Cell Biology > Cell Signaling/communication > Flashcards

Cell Signaling/communication Flashcards

1
Q

What microbe “communicates” to find a mate?

A

Yeast! They sense presence of other cells when looking for a mate

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2
Q

Is it one signal-> one action?

A

No! Cells are constantly undergoing a multitude of signals and reactions

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3
Q

What is signal transduction?

A

The whole pathway of taking a signal from outside the cell to make an internal change

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4
Q

What are the 4 “players” in signal transduction?

A

1: First Messengers/Ligands (bind to receptor- can be hydrophobic or hydrophilic)

2: Signal Transducers/receptor protein (transduces signal from outside to inside the cell)

3: Secondary Messengers (passes message to our effector proteins)

4: Effector Proteins (actually “does the work”)

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5
Q

What are three examples of effector proteins and what they could cause?

A

1: Metabolic enzyme (altered metabolism)

2: transcription regulatory protein (altered gene expression)

3: cytoskeletal protein (altered cell shape or movement)

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6
Q

Why would a cell signal not be able to be transduced?

A

If the cell doesn’t have a receptor for the signal molecule!

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7
Q

Where are receptors for hydrophilic signals found?

A

The cell surface ! (They will not cross the PM)

Ex: insulin receptors

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8
Q

Where are receptors for hydrophobic signals found?

A

Inside the cell, often inside the nucleus! (Signal will often diffuse across the plasma membrane)

Ex: testosterone and progesterone receptors

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9
Q

What are the 3 types of short-distance signaling?

A

1: Autocrine signaling: self signaling!

2: Contact dependent: two cells must be touching to be membrane-transduced from surface-surface

3: Paracrine Signaling: within the general vicinity of that cell (diffusion is over short distance)

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10
Q

What are the two types of long-distance signaling?

A

1: Synaptic (between neurons)

2: Endocrine (uses the circulatory system to go anywhere in the body, ex: hormones)

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11
Q

What’s an example of a signal that acts over a fast period of time?

A

-seconds to minutes
-altered protein function
-ex: neutrophil chasing bacteria

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12
Q

What’s an example of a signal that acts over a slow period of time?

A

-minutes to hours
-relies on altering gene expression and protein synthesis

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13
Q

Can both slow and fast pathways be activated at the same time?

A

Yes! This is most common that both occur same time

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14
Q

What are gap junctions?

A

A type of signaling, when cells are physically attached to each other and a junction allows direct contact between cytoplasm of two different cells
-allows exchange of ions and small molecules (both good and bad)

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15
Q

Why can one signal molecule have different effects on different cells?

A

The signal’s receptors activate different effector proteins! These do different pathways throughout the cell

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16
Q

What is the relationship between second messengers and phosphorylation?

A

-many second messengers activity are controlled by phosphorylation

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17
Q

What is Kinase versus Phosphatase?

A

Kinase: uses ATP to add phosphate to protein, turns it “on”’!

Phosphatase: removes phosphate, turns protein “off”!

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18
Q

What are the two ways that second messenger’s activity can be controlled?

A

1: kinase and phosphatase

2: GTP binding proteins (GAPs and GEFs)

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19
Q

Are all second messengers proteins?

A

No!

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20
Q

What are two examples of non-protein second messengers?

A

Calcium and Cyclic Adenosine MonoPhosphate (Cyclic AMP)

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21
Q

What are the three types of cell surface receptors?

A

1: ion channel- coupled receptors (ex: glucose symport)

2: G-protein-coupled receptors

3: enzyme-coupled receptors (RTKs)

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22
Q

What are Receptor Tyrosine Kinases? (RTKs)

A

-Most common type of enzyme, coupled receptors
-Usually a single pass Transmembrane protein
-kinase adds phosphate to the TYROSINE KINASE DOMAIN on inside of membrane (to send signal)

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23
Q

How are RTKs activated?

A

Dimerization!

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24
Q

How does dimerization of RTKs occur?

A

-RTKs need to be in pairs to work
-when each subunits finds a signal protein, it phosphorylates the other subunit on a TYROSINE residue

-this is called TRANS-AUTOPHOSPHORYLATION and activated the receptor

25
Q

What is trans-autophosphorylation?

A

When two RTKs swap phosphate groups with each other on their tyrosine amino acids

26
Q

What do most RTKs activate?

A

Ras!

27
Q

What is Ras?

A

A small GTPase anchored to the PM (GTP and GDP forms when activated/not)
-activation of RTK results in activation of Ras
-Ras activates the MAPK Cascade

28
Q

What is the MAPK Cascade?

A

A “Phosphorylation Cascade” where is phosphorylation is passed down
-MAP Kinase Cascade carries signal into the nucleus to change the expression of genes!

29
Q

What are the three “dominos” in the MAP Kinase Cascade?

A

1: MAP kinase kinase kinase (Raf) (activated by Ras)

2: MAP kinase kinase (Mek)

3: MAP kinase (Erk)

30
Q

Why do we need the MAPK Cascade?

A

Because Ras activation is only short-lived, we need the MAP kinase cascade to carry the signal to the nucleus!

31
Q

What two things does the MAPK Cascade cause?

A

1: Changes in protein activity

2: Changes in gene expression

32
Q

What happens when Ras is over-activated?

A

Human tumors and cancers form

-would need to target “downstream” of Ras to treat, because if overactive then regardless of inhibitors it would keep going

33
Q

What are G-protein coupled receptors? (GCPR)

A

-composed of 7 transmembrane helices
-always associated with a G-protein on the cytosolic face of the membrane
-N-term is always outside the cell (the receptor), C-term is always inside the cytosol

34
Q

What are G proteins?

A

They interact with C-term of GPCR
-trimeric: made up of three parts
-“alpha” and “Y” are lipid linked to plasma membrane, “beta” is free to move around
-the “alpha” subunit is a GTPase (GDP and GTP forms)

-A is bound to GTP/GDP and GPCR, B and Y separate when GDP-> GTP

35
Q

How does G protein Activation occur?

A

1: Signal molecule binding activates the GPCR
2: GPCR becomes a GEF and turns A-GDP to A-GTP
3: A-GTP dissociates from B and Y (but stays stuck to the membrane)
4: A-GTP binds to its target/effector and activates it (binding to the target causes A-GTP to inactive itself back to A-GDP)
5: Regulator of G-protein Signaling (RGS) is a GAP and makes sure all the As are turned back to A-GDP

36
Q

What are five ways that GPCR can prevent adaptation/desensitization of a pathway?

A

1: Receptor Sequestration: (signal pulled from outside the cell to endosome that acts like momentary jail cell)

2: Receptor Down-Regulation: (we degrade receptor + signal to stop activation of pathway)

3: Receptor Inactivation: (we inhibit the receptor of the signal)

4: Inactivation of Signaling Protein: (we inhibit intermediate)

5: Production of Inhibitory Protein: (we made an inhibitor to physically block the pathway)

37
Q

What does Arrestin do?

A

causes GPCR Desensitization!
-inhibits GPCR from interacting with G protein
-is an adaptor for Clathrin, and induced receptor-medicated endocytosis
-ONLY BINDS TO PHOSPHORYLATED GPCR, not normal functioning ones

38
Q

What does GPCR kinase do? (GRK)

A

Phosphorylated active GPCR on multiple sites, stops them from being able to send signal and tags them for endocytosis via Arrestin

39
Q

What do Second messengers do?

A

They carry the activated signal away from the membrane, and can serve to amplify the cellular response!

40
Q

What are the two main second messengers of GPCRs? (GPCRs go to activate both of these) and which pathway/effector protein does it signal?

A

1: Cyclic AMP (cAMP) signals for PKA

2: Ca2+ signals for PKC

41
Q

How do we make Cyclic AMP? (cAMP)

A

-it is derived from ATP!
- we use ADENYLYL CYCLASE to turn from ATP to cAMP
-we use CYCLIC AMP PHOSPHODIESTERASE to turn cAMP to ATP

42
Q

How is cyclic AMP activated by G-protein? What does it then do?

A

1: A-GTP activates adenylyl cyclase, which is a surface protein that turns ATP to cAMP

2: cAMP then diffuses throughout the cell and activates Protein Kinase A (PKA)

3: activated PKA then enters the nucleus and regulates the transcription of genes

43
Q

What is an example of a cellular response that is regulated by cAMP?

A

Extracellular signal molecule: Adrenaline
Target Tissue: skeletal muscle
Major response: glycogen breakdown for immediate energy

44
Q

What are some ways that Cytosolic Ca2+ is usually kept low?

A

1: Calcium is sequestered outside the cell
2:Ca2+ is sequestered inside organelles

45
Q

Why use Ca2+ instead of Na+ for cell signaling?

A

Because there’s not as much everywhere, so small changes are noticed! (Such as sand on beach example)

46
Q

What happens in the GPCR pathway when Ca2+ is the second messenger? (Practice drawing out this pathway flowchart)

A

1: G-protein is activated, which then causes B and Y subunits to activate PHOSPHOLIPASE C-B in the PM

2: PHOSPHOLIPASE C-B then converts PI(4,5)P2 into IP3 and diacylglycerol (DAG)

3: IP3 and DAG then work together to get PKC activated and attached to the PM. (DAG = is PM bound and activates PKC once it comes), (IP3= goes to ER calcium release channels and releases Ca2+ into cytosol, signaling for PKA to go to PM)

4: PKC then does a bunch of cool shit

47
Q

What is PKC?

A

Protein Kinase C (PKC)
-bound to PM when activated by Ca2+ and DAG
-does cool shit

48
Q

Positive feedback versus negative feedback?

A

Positive feedback: self promoting, continues to activates itself (ex: oxytocin in childbirth)

Negative feedback: inhibitory, pathway inhibits pathway upstream (ex: TH4 thyroid)

49
Q

What is Heparin?

A

-anticoagulant/ blood thinner
-reduces inflammation
-regulates vascular smooth muscle cell proliferation

-causes Map Kinase Phosphatase, which steals phosphates from ERK to turn it off! As a result: reduced inflammation!

50
Q

What is Angiotensin?

A

Contraction signal that transiently increases blood pressure
(Causes contracted blood vessel/vasoconstricts)

51
Q

What does cGMP do?

A

Vasodilates our blood vessels! Lets them relax more
-increases in cGMP are caused by NO (nitric oxide) and atrial natriuretic factor

52
Q

What can cause increased cGMP?

A

-NO (Nitric Oxide)
-atrial natriuretic factor
-nitroglycerin

53
Q

What are the 6 steps to relaxing the blood vessels?

A

1: Acetylcholine released, activates NO synthase (NOS)
2: NOS turns arginine into NO (nitrous oxide)
3: NO is nonpolar gas, so diffuses out of endothelial cell into outer smooth muscle cell lining
4: NO binds to guanylyl cyclase to turn it on
5: Guanylyl Cyclase now makes cyclic GMP (cGMP) using GTP
6:cGMP vasodilates and causes relaxation of outer smooth muscle cells of blood vessel

54
Q

What does PDE-5 do? (Phosphodiesterases)

A

-converts cGMP to GMP
-ergo causes tightening of smooth muscle cells!

55
Q

What does Sildenafil citrate do? (Viagra)

A

-was first made to treat high BP in kids
-blocks PDE-5, so prevent GMP from being made and ergo prevents constriction of outer smooth muscle cells
-causes vasodilation and increased blood flow

56
Q

What is the point of transautophosphorylation?

A

It happens right after dimerization of the two RTKs and GENERATES BINDING SITES FOR SIGNALING PROTEINS

57
Q

What is the order of events that happens for RTKs?

A

Ligand binds- receptor dimerization- transautophosphorylation- recruitment of other proteins to pass message along downstream

58
Q

What effector protein is used in response to adrenaline?

A

PKA!

59
Q

After ATP/GTP have been converted to cGMP/cAMP, what do they convert to bc of the phosphodiesterases?

A

AMP/GMP!
-they do not got back to ATP/GTP

Cell Biology (10 decks)

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