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McG > Signal Transduction > Flashcards

Signal Transduction Flashcards

1
Q

What does Gs activate

A

Adenylyl Cyclase

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2
Q

what does adenylyl cyclase do and what is it activated by

A

Converts ATP to cAMP and is activated by Gs

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3
Q

what does cAMP target

A

PKA

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4
Q

what is PKA targeted by

A

cAMP

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5
Q

describe what pKA looks like

A

two regulatory subunits, two catalytic subunits

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6
Q

what do the catalytic subunits of PKA do

A

phosphorylate their targets

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7
Q

what are the targets of the catalytic subunits of PKA

A

1: Glycogen phosphorylase: activated when phosphorylated and breaks down glycogen
2: Glycogen synthase: deactivated when phosphorylated and synthesizes glycogen

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8
Q

what does Gi do

A

inhibits adenylyl cyclase

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9
Q

what does Gq do

A

activates phospholipase C-beta.

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10
Q

what is phospholipase C-Beta activated by

A

Gq

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11
Q

what is the function of phospholipase C-Beta

A

breaks down the membrane phospholipid PIP2 into IP3 and DAG

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12
Q

what does IP3 do and what does it come from

A

Comes from phospholipid PIP2 being broken down by phospholipase C-Beta. It can activate the release of calcium inside the cell which then activates PKC and many other signaling functions

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13
Q

what is PKC and what is it activated by

A

a protein kinase that is activated by calcium which is mediated by IP3

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14
Q

What does DAG do and where does it come from

A

Comes from phospholipid PIP2 being broken down by phospholipase C-Beta. Can directly activate PKC

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15
Q

what is Gt activated by

A

rhodopsin receptor

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16
Q

what does Gt do

A

activates cGMP phosphodiesterase which breaks down cGMP

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17
Q

describe cholera toxin

A

it ADP ribosylates the alpha subunit of Gs which means it can no longer catalyze GTP to GDP so adenylyl cyclase is constantly activated which means cAMP is constantly being produced so PKA is constantly activated. This causes an efflux of Cl- and water into the gut because PKA phosphorylates certain ion channels in these cells. This leads to copious watery diarrhea.

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18
Q

describe pertussis toxin

A

this enzyme ADP ribosylates the alpha subunit of Gi which prevents binding to GPCRs and thus it cannot be activated. Causes whooping cough

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19
Q

G protein ligands

A
  1. neurotransmitters (epinephrine, serotonin, dopamine)
  2. histamine
  3. sensory stimuli (light, odorants)
  4. Rx drugs
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20
Q

G protein receptors

A

proteins with 7 transmembrane domains

21
Q

receptor tyrosine kinase ligands

A
  1. platelet derived growth factor
  2. epidermal growth factor
  3. fibroblast growth factor
  4. insulin
22
Q

steps of signal transduction in RTK (receptor tyrosin kinase)

A

Receptors are single pass transmembrane proteins. Binding of ligand causes receptor to dimerize. Dimerization causes auto/trans phosphorylation and receptors become active. Phosphorylation leads to two separate events: activates the receptors catalytic function and creates sites for target protein recruitment.

23
Q

MAP kinase cascade

A
  1. RTK phosphorylated
  2. Grb2 binds to activated RTK at SH2 domain
  3. SOS bound to Grb2 at its SH3 domain
  4. SOS activates RAS because it has GEF activity (guanine exchange factor) so GDP exchanged for GTP
  5. RAS activates RAF, a ser/thr kinase that phosphorlylates MEK (a MAPKK) which then phosphorylates ERK (a MAPK)
24
Q

what kind of protein is RAS

A

a G protein

25
Q

why is RAS different from hetereotrimeric G proteins

A

can still bind GTP and GTP but doesn’t have three subunits. Active when bound to GTP and inactive when bound to GDP (this change happens with the help of GEFs, guanine exchange factors)

26
Q

what is the GEF for RAS

A

SOS

27
Q

what is a GAP

A

GTPase activating protein, accelerates the rate of GTP hydrolysis by G proteins to inactivate them

28
Q

describe the Wnt ligands

A

proteins with covalently attached fatty acid

29
Q

Describe Wnt receptors

A

look like G proteins (7 domains) but have large extracellular region at frizzled N terminus that G proteins dont have – Wnt receptors are a combination of Frizzled and LRP5/6

30
Q

what happens in Wnt pathway with no ligand

A

The APC complex (containing APC and Axin) is active and CK1 and GSK3-beta (ser/thr kinases) phosphorylate B catenin, leading to its degradation. In the nucleus, DNA binding factor TCF/LEF inhibits expression of Wnt pathway target genes

31
Q

what happens in Wnt pathway with ligand

A

Wnt binds to Fzl/LRP56 receptor causing Axin to bind to LRP5/6. Disheveled binds to Fzl and inhibits CK1/GSK3-Beta which means B catenin is no longer phosphorlylated and degraded. B catenin migrates to the nucleus where it interacts with TCF/LEF and transcriptional co-activators to activate expression of Wnt target genes

32
Q

how is the Wnt pathway regulated post translationally

A

Wnts themselves - several secreted Wnt inhibitory proteins exist including soluble frizzled-related protein and Wnt inhibitory factor 1

33
Q

what is a role of B catenin outside of the Wnt pathway

A

binds to cadherins intracellularly to tether them to actin cytoskeleton - this stabilizes cell cell junctions.

34
Q

what are some pathways of Wnt disease

A

Colo-rectal cancer. Mutations of APC cause Adenomatous Polyposis Coli because thousands of polyps are formed when B catenin is locked on. APC is a tumor supressor gene, B catenin is a proto-onco gene.

35
Q

what is the main function of wnt genes

A

proliferation of gut stem cells

36
Q

what are notch proteins

A

receptors for membrane bound ligands called delta or jagged

37
Q

when is notch signaling activated

A

when a delta or jagged expressing cell comes into direct physical contact with a notch expressing cell

38
Q

steps of signal transduction for notch

A
  1. Notch binds to ligand
  2. intracellular notch proteolytically cleaved
  3. NICD (Notch intracellular domain) migrates to nucleus where it interacts with DNA binding factor CSL
  4. CSL binds to transcriptional co-activators and turns on expression of these target genes
39
Q

what is PI3-K pathway

A

complex of regulatory subunit (p85) and catalytic subunit (p110).

40
Q

PI3-K pathway

A
  1. P85 has SH2 domain that binds to activated RTKs allowing access of P110 to PIP and PIP2
  2. PIP and PIP2 phosphorylated on 3 position of inositol ring
  3. Those on 3 position of ring activate ser/thr kinase AKt (PKB)
  4. Activated AKT phosphorylates substrates important for cell survival and inhibit programmed cell death
41
Q

what is PTEN

A

phosphatase that removes phosphate from 3 position on ring - tumor supressor, often mutated in cancer

42
Q

where are human cancer mutations often found in terms of RTKs

A

Ras, BRaf, PTEN

43
Q

cytokine receptor ligands

A

prolactin, growth hormone, interferons, erythropoeitin, etc

44
Q

why are cytokines similar and different to RTKs

A

Like RTKs, cytokines dimerize. HOWEVER - RTKs are a single polypeptide with amino terminus outside and carboxy inside, and have intrinsic tyrosine kinase activity. Cytokines DO NOT have an intrinsic tyrosine kinase activity, they need to be bound to JAK.

45
Q

pathway for cytokine receptors

A
  1. Extracellular portion binds ligand
  2. JAK complex + receptor dimerize and there is cross phosphorylation of JAK protein which leads to phosphorylation of cytokine receptor so it can bind SH2 containing proteins
  3. STAT (SH2 contianing protein) activated
  4. STAT dimerize and translocate to nucleus where they bind to DNA and activate specific genes
46
Q

what kind of receptors are used in TGF-Beta and BMP pathway?

A

Receptor Serine/Threonine Kinases

47
Q

describe receptor serine/threonine kinases

A

heterodimers of type I and type II receptors - single pass transmembrane protein

48
Q

steps of signal transduction in TGF beta/BMP pathway

A

TGF beta or BMP ligands induce type I and type II receptors to dimerize. Type II constitutively active and upon ligand dimerization, phosphorylate type I receptors. Activated type I phosphorylate SMADs which then dimerize with Co-SMADs. These enter nucleus to activate specific genes.

McG (11 decks)

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