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Pharm 1 - SP19 > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

_ channels
plasma membrane or organelle, signal by opening ion gates, drugs can affect synaptic transmission at different loci, liberation of Ca++ stores will have profound effect on cells

A

ligand activated ion channels

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2
Q

_ receptors
adenylate cyclase and the pleotrophic effects of PKA; Phospholipase A2 and the liberation of arachidonic acid; phospholipase Cbeta and signaling by IP3 and DAG

receptor desensitization

A

G protein coupled receptors
G protein cycle

Galpha effectors - adenylate cyclase

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3
Q

_ receptors
receptor dimerization, phosphorylation, docking of effectors MAP kinase cascade-transcription factor activation, JAK-STAT pathway

A

tyrosine kinase receptors

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4
Q 
_ receptors 
mechanism of action: class one and class 2 nuclear receptors
A

ligand activated nuclear receptors

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5
Q

hormonal activation of liver phosphorylase is mediated by _, a second messenger, the hormone is the first messenger

A

cAMP

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6
Q

phosphorylase is regulated by phosphorylation by _ enzymes

A

kinase enzymes

kinase cascade

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7
Q

about 40% of all drugs are directed agonists or antagonist of one or another _ receptor

A

g protein coupled receptor

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8
Q

_ receptors
signaling in excitable cells , important in concept of pain
multisubunit proteins

produce graded potential (effects are local)

depolarizing - let in Na+(usually not particularly selective), examples?

hyperpolarizing - let in Cl- making harder to reach the AP, examples?

A

ligand-activated ion channels - plasma memrane edition

excitable cells like skeletal muscle

depolarizing - Ach, serotonin, glutamate

hyperpolarizing - glycine, GABA

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9
Q

activating and inhibiting ligand activated plasma membrane ion channels is the basis of synaptic transmission of _

A

nerve impulses

plenty of drugs targeted here

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10
Q

some drugs might mimic or block the actions of neurotransmitters to affect synaptic transmission

some drugs might block the channel to affect the synpatic transmission

Sometimes enzymes inactivate NT and sometimes receptors on the presynatpic reuptake

Never want the postsnapatic to get NT after shit has already happened

some drugs might affect NT metabolism

which kind of receptor

A

lingand activated channel plasma membrane

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11
Q

_ receptor

IP3-mediated Ca++ release from the ER

inositol 1,3,5 bis-phosphate
this receptor mediated Ca++ release from the ER internal store “puffs” of Ca++ alters cell physiology

A

ligand-activated ion channel organelle edition

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12
Q

_ receptor

single polypeptide 7 transmembrane alpha helices

800 functional genes encode this receptors

400 in your nose

too many ligands to mention

A

G protein coupled receptors

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13
Q

agonists bind to the GPCR’s alterr the proteins confirmation, leading to the activation of a _ g protein

  1. Ligand bound GPCR stimulates _ exchange
  2. the causes the complex to fall apart into two pieces _ and _
  3. the _ has an intrinsic GTPase activity. Eventually the GTP is hydrolyzed to GDP and Pi. RGS proteins accelerate this process
  4. After _ hydrolysis the complex reassembles
A

trimeric G protein
3 subunits alpha, beta, gamma

  1. GDP-GTP exchange
  2. Galpha and GbetaGgamma
  3. Galpha
  4. after GTP hydrolysis the complex reassembles

Beta and gamma together can affect shit and then alpha by itself

The signaling system is designed to shut itself off. Doesn’t keep signally on and on - it shuts up by itself

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14
Q

The G protein cycle

major - the liberated G_protein

minor - the liberated G_ protein

bind to and activate proteins in the cell

A

major - the liberated Galpha protein

minor - the liberated GbetaGgamma protein
plays a role in signaling, but not as important

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15
Q

the G protein cycle

major - the liberated Galpha protein

effects _ to take ATP and converts to cAMP

A

adenylate cyclase

Galpha > ATP >adenylate cyclase> cAMP + PPi

cAMP - protein kinase A - phosphorylation of a large number of proteins producing a large number of biological effects

protein kinase - catalytic tetramer

cAMP goes up - regulatory subunit

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16
Q

G protein receptors

phosphorylation of transcription factors by PKA and other protein kinases can lead to changes in _

A

in gene expression in cell

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17
Q

PKA mediated activation of glycogenolysis (mobilization of glcuose) in the liver is an example of what kind of receptor

A

g protein coupled receptors

18
Q

major effectors of Galpha’s

signaling molecules are embedded within phospholipids in the membrane, and G protein coupled receptors liberate them by activating _

A

phospholipases

phospholipase A2, C, D

19
Q

which phospholipase in the G protein receptor cycle liberates arachidonic acid

A

phospholipase A2

20
Q

arachidonic acid is the source of _ signaling molecules

A

Eicosinoids

prostaglandins - important signaling molecules and mediators of pain and inflammation

21
Q

major effectors of Galpha’s - phospholipase Cbeta

products of PLCbeta mediated hydrolysis are _ and _ both are important signaling molecules (minor) that liberates calcium from the sarcoplasm reticulum

A

DAG (diacyl glycerol) and IP3 (3,4,5, triphosphate

cleavage of PIP2 by phospholipase C yields DAG and IP3
PIP2 - phosphatidylinositol 4,5 bis phosphate - minor phospholipid in membrane

22
Q

G protien

PIP2 - phosphatidylinositol 4,5 bis phosphate - minor phospholipid in membrane serves as the substrate for _
phosphatidyl identifies it as a phospholipid

A

phospholipase C

23
Q

PIP2 cleaves phospholipase C into DAG and IP3

which product causes transient increase in [Ca++] increases binding of Ca++ to calmodulin, altering the structure of the Ca/Calmodulin complex

the complex is able to interact and activate numerous effector proteins

A

IP3

2 examples are
1. Calcium/calmodulin dependent protein kinase

  1. nitric oxide synthase
    (NO-> guanylate cyclase -> GTP-> cGMP
24
Q

PIP2 cleaves phospholipase C into DAG and IP3

which product actiavtes protein kinase c (PKC)

A

DAG

Ca++ dependent

most isoforms of PKC regulated bu DAG (DAG allows the enzyme to bind Ca tighter) therefore, the enzyme can function at lower Ca concentrations

25
Q

how does the G protein receptor turn off

A

the trimeric G protein gets turned on, but it shuts itself off

the receptor gets turned off by a process called desensitization

phosphorylation by GRK(recruited by GbetaGgamma)

  1. binding by a Beta-arrestin
  2. formation of clathrin-coated pit
  3. endocytosis
26
Q

the G protein coupled receptor after it has by desenitized/endocytosed it has one of two fates what are they

A
  1. recycling
  2. degradation

sometimes drugs are administered chronically, this can lead to loss of responsiveness to the drug and results that would seem paradoxical if one failed to consider desensitization

27
Q

Signalign by receptor tyrosine kinases (RYK’s)

_ - critical
Doing the most important stuff inside cells - chemokines and cell signals and behavior

Binding of the ligand to the receptor leads to dimerization of the receptors - stuff does the most important things inside cells

A

Phospho tyrosine

accounts for 0.5% of the phosphorylated protein in cells

growth factors, differentiation factors, cytokines

28
Q

RYK’s - receptor tyrosine kinases

  1. receptors either contain an intrinsic or extrinisic tyrosine kinase enzyme
  2. binding of ligand leads to _ of the receptor
  3. some receptors form homodimers, some receptors form heterodimers, and some receptors do both
  4. dimerzation leads to _ of receptors
  5. tyrosine phosphorylation of receptors leads to _ of signaling molecules
  6. the positioning of proteins near the _leads to different cascades of signaling
A

dimerization

most important things like chemokines, growth factors, cytokines

  1. leads to transphosphorylation of receptors

The receptors are phosphorylated - this is why they exist - important because leads to docking of signaling molecules

  1. phosphorylation leads to docking of signaling molecules
  2. proteins near the memrbane leads to different cascades

Ras

Grab 2 - docking site

Pattern of gene expression/regulation changed by tyrosine kinases

29
Q

receptor tyrosine kinase example of signaling cascade

  1. binding of ligand(cytokine) leads to phosphorylation of receptor by _ kinase
  2. this leads to binding of _ protein (one of 6) to the phosphorylated receptor
  3. these leads to phosphorylation of STAT protein by Jak kinase
  4. this leads to dimerization of STAT protein
  5. this leads to translocation of STAT dimer to _ and transcriptional activation of panels of genes
A
  1. JAX kinase
  2. STAT protein
  3. to nucleus

_____________
STAT brings it to membrane so it can interact with tyrosine kinase

When 2 or more STAT do this - it has 2 parts

SH2 domain - docking

Dimerization affects interfureons

30
Q

STAT-Jax RYK’s example

STAT monomers contain both an _ domain and a _ that can be phosphorylated

A

contain both a SH2 domain- docking

and a tyrosine that can be phosphorylated

To form an active protein to regulate gene expression

31
Q

_ proteins mediate the profound biological responses to cytokines

A

STAT

receptor tyrosine kinases

32
Q

receptors for steroid hormones (glucocorticoids, mineralcorticoids, testosterone, estrogens, progesterone) and other molecules such as Vitamin D, retinoic acid, thyroid hormone

A

nuclear hormone receptors

33
Q

nuclear receptors are characterized as either class 1 or class 2

_ nuclear receptors exist as a complex with heat shock proteins in the absence of a ligand

ligand binding induces the compelx to fall apart, from a homodimer and bind to its specific DNA response element

once bound to its specific response element it binds coavtivaotrs to stimulate _

A

class 1

cofactors to stimulate transcription

Glucocortacoids - steroids - estrogens -

Intracellular receptors - HSP proteins form multi-protein complex

Cortisol comes in thru diffusion - bind and the shit falls a part

What exist on target genes - have a particular DNA sequence that is able to bind the receptor 2 molecules of glucocortico

Leads to activation complex

These receptors are themselves the thing
Bends then moves and becomes a part of the new DNA

Cofactors - lysine positive charge - dna negative charge - histone DNA interaction is basically electrostatic

If we want transcription to take place we have to loosen up the “bond” so we add HISTONE to lessen the negative charge -

34
Q 
in the nuclear receptors which class 
There is an activation complex being made in class _
A

class 1

35
Q

class _ nuclear receptors activate target genes

ligand enters cell and binds to receptor

ligand receptor complex binds to specific DNA sequences on target gene

and expression of the target gene increases

they form 2

A

class 1

36
Q

class _ nuclear receptors

binds to target DNA at its specific response element in the absence of ligand

binds corepressors in the absence of ligand and represses transcription

form homo and heterodimers

ligand binding produces a switch from binding corepressors to binding coactivators

A

class 2

In the absence of ligand - they don’t exist as dimer or two they sit right on DNA

Binding to target genes even in absence of ligand -
They bind corepressors
Takes actyl groups off the histones and making the electrostatic bond stronger
Inhibiting transcription of target genes

37
Q

class 1 or 2 nuclear receptor ligands

thyroid hormone, retinoic acid, vitamin D

A

class 2

38
Q

class 1 or 2 nuclear receptor ligands

glucocorticoids, progesterone, estrogens, androgens

A

class 1

39
Q

which receptor

plasma membrane or organelle, signal by opening ion gates, drugs can affect synaptic transmission at different loci, liberation of Ca++ stores will have profound effect on cells

A

ligand activated ion channels

40
Q

which receptor

Adenylate cyclase and the pleotrophic effects of PKA

phospholipase A2 and the liberation of arachidonic acid

phospholopase Cbeta and signaling by IP3 and DAG

receptor desensitization

A

G protein coupled receptors

41
Q

which receptor

receptor dimerization, phosphorylation, docking of effectors

MAP kinase cascade-transcription factor activation, JAK-STAT pathway

A

signaling by tyrosine kinase receptors

42
Q

which receptors

mechanism of action - class 1 and class 2 nuclear receptors

A

ligand activated nuclear receptors

Pharm 1 - SP19 (26 decks)

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