2nd messengers Flashcards

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1
Q

How many isoforms of Adenylyl cyclase (AC) exist?

A

9

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2
Q

All 9 form of (AC) are stimulated by?

A

Galpha(s)

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3
Q

Which form are inhibited by Galpha(i)

A

V and VI

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4
Q

Does the Gbetagamma dimer stimulate or inhibit AC?

A

Both.

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5
Q

Guanylyl cyclase make which 2nd messenger?

A

cGMP.

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6
Q

Differentiate between type 1 and type 2 guanylyl cyclase

A

type 1 is membrane bound, has a ligand binding site.

Type 2 is soluble.

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7
Q

What degrades cAMP and cGMP. Is it selective?

A

Phosphodiesterase (PDEs) degrades them into 5’ AMP and GMP, inactive.
Some PDEs degrade both cAMP and cGMP, others degrade one or the other.

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8
Q

Which sensory system uses PDEs?

A

Olfaction.

PDE2 breaks down cAMP. PDE2 is activated by cGMP.

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9
Q

Explain serotonin signaling mechanism.

A

Binds to a GPCR, which causes Galpha(s) to activate AC which in turns makes cAMP rise, until phosphodiesterase gets it all locked down and under control again.

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10
Q

Explain protein kinase A (PKA) regulation.

A

PKA is made of four subunits. two regulatory, which bind cAMP, and two catalytic. Catalytic are kept inactive until cAMP binds and allows them to disassociate from their regulatory domains.

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11
Q

Explain possible longterm and shortterm affects of PKAs.

A

PKA can activate through phosphorylation proteins in the cytosol causing a short term affect.
PKA can also activate KREB the same way, which will bind a CREB-binding protein and then activate gene transcription.

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12
Q

What does CREB stand for?

A

cAMP response element binding.

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13
Q

What is a cAMP response element?

A

It is a stretch of dna in the promoter region which activates a gene when bound to by a CAMP with cAMP binding protein.

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14
Q

How many phosphoinositides are there?

A

7 possible

PI-4-5-P2 is what makes IP3 and DAG.

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15
Q

What does IP3 do?

A

opens Endoplasmic Reticulum Calcium channels.

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16
Q

What does DAG do?

A

Activates PKC.

17
Q

What does PI3K do? What does it stand for?

A

It adds a phosphate at position three.

Phosphoinositol 3 kinase

18
Q

What are pleckstrin homology domains?

A

they are regions which bind PI(3,4,5)P3. They allow proteins to use phosphorylated phosphoinositols as a docking site.

19
Q

What is the advantage of docking sites?

A

It can bring proteins which need to phosphorylate each other into close proximity. like with BTK and PLC-gamma.

20
Q

Explain activation of B-Cells

A

Activated antigen receptor draws in PI3K.
PI3K takes PI(4,5)P2 –> PI(3,4,5)P3. Which acts as a docking site for BTK (Bruton’s tyrosine kinase) and PLC-gamma (phospholipase C gamma).
PLC gamma cuts PI(4,5)P2. into DAG and IP3. Which signal for the B-lymphocyte to proliferate.

21
Q

What happens if the PH domain of BTK is mutated.

A

BTK cannot bind to its docking site. PLCgamma is not phosphorylated doesn’t cut PI(4,5)P2 –> IP3 and DAG.
Person is immunocompromised.

22
Q

Are PI(3,4)P2 and PI(3,4,5)P2 cleaved by phospholipase C?

A

NO!!! Just PI(4,5)P2.

23
Q

If PI(3,4)P2 and PI(3,4,5)P2 are not cleaved by a phospholipase, how are they inactivated?

A

Inositol phospholipid phosphatase can take those phosphates off whenever he feels like it!

24
Q

Compare the types of PI3K

A

One is activated by receptor tyrosine kinases, it is made of a regulatory and catalytic subunit.

The other is activated by the Gbetagamma subunit. It has a different regulatory subunit an but a similar catalytic subunit.

25
Q

What other means exists to activate PI3Ks?

A

The monomeric RAS G-Protein in its active state (RAS GTP) can bind to and directly activate the catalytic subunit of PI3K.

26
Q

What task does DAG perform?

A

It activates types of PKC. DAG–> arachodonic –> prostaglandins and eicosanoids mediating inflamatory response.

27
Q

Where is phosphatidylinositol located at?

A

In the cytosolic leaflet of the PM.

28
Q

lipid kinases:

A

Add phosphates to positions on the inositol ring.

29
Q

Phopholipase C-beta is activated by what?

A

GPCRs coupled to Galpha(q/11)

30
Q

PLC beta does what?

A

cleaves PIP2 –> DAG and IP3.

31
Q

IP3 activates…

A

ER/SR ionotropic receptors for Ca2+

32
Q

What are Ca2+ ATPases used for?

A

They resequester Ca2+ into the ER/SR. They are a pump.

33
Q

How does the sperm cause a Ca2+ propagation?

A

Thought to bring its on phospholipase C into the egg.

34
Q

What about Na+ driven Ca2+ exchangers?

Ca2+ pumps?

A

They send Ca2+ out of the cell.

35
Q

What is the function of Calcium binding molecules?

A

They bind Ca2+ buffering it.

36
Q

Ca2+ spikes similar to Na channels in a …

A

… action potential. These spikes are called calcium transients.

37
Q

How where calcium transients recorded?

A

aeguorin, a Ca2+ sensitive fluorescent dye was loaded into the cell.

AVP (arginine vasopressin?) given, activates Galpha(q/11) subunit, activates phospholipase-C beta.

Ca2+ surge from PLC beta induced surge of IP3.

Low frequency Ca transients may cause a different behavior then high frequency calcium transients would cause.