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cell signalling Flashcards

1
Q

signal transduction

A

conversion of information from one physical/chemical form to another
(to pass on signal from signal molec to receiving cell)

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2
Q

agonist

A

any ligand/signal that activates a receptor

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3
Q

antagonist

A

ligand that blocks actions of agonist

–> competitive binding to receptor

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4
Q

desensitization

A

INactivation of receptor
(prepare for reception of new signal)
go to “clean slate”

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5
Q

cross-talk

A

interaction between signaling pathways

intermediates and products of pathways can affect behavior of other pathways

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6
Q

1st major illumination of (existence of) signalling pathways

A

studying retroviruses
– found that Rous sarcoma virus transmission could cause tumors (–> discovered basic signalling molecs bc studied the viruses)

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7
Q

proto-oncogene

A

normal cellular gene, NOT (yet) oncogenic.
= responsible for some part of cell proliferation/growth
(can become oncogenic if mutated)

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8
Q

oncoprotein

A

the actual protein (encoded by an oncogene) responsible for cancerous cell growth and proliferation

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9
Q

specificity

A

signaling molec must fit (and be specific/unique) to the binding site on its complimentary receptor

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10
Q

major features of signal transduction systems (6)

A
  1. specificity (high)
  2. affinity (high)
  3. sensitivity (high)
  4. amplification
  5. integration(must exist)
  6. desensitization/adaptation (must exist)
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11
Q

specificity determined by…

A
  • complementarity between signal and receptor
  • tissue/cell-specific receptor distribution
  • tissue/cell-specific intracellular response system (vary in distribution)
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12
Q

Integration characteristic(s)

A

applies uniform response throughout environment

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13
Q

signal types

A
  1. hydrophilic (proteins, polypeptides, AA derivatives – epinephrine and norepinephrine)
  2. hydrophobic (cholesterol and fatty acid derivatives)
  3. both (dissolved gases – NO, CO)
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14
Q

characteristics of hydrophilic signal molecs

A
  • can be stored
  • short half-life
  • receptors on plasma membrane
  • indirect mechanisms
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15
Q

paracrine system

A

LOCAL signaling (w/in tissue/body region),
releases signal molecs to the extracellular space.
- lower affinity at receptors
ie: immune (cytokines), development

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16
Q

autocrine system

A

specialized paracrine signaling,
release local mediators, bind to same (own) cell type.

receptor type and proximity => specificity

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17
Q

7 steps in signalling

A
  1. synthesize signal
  2. release signal
  3. transport to target cell
  4. bind to receptor
  5. cell response
  6. remove signal (from receptor)
  7. terminate response
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18
Q

orphan receptors (type II)

A

non-steroid nuclear receptors, originally did not have known ligands! (now many do)

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19
Q

Selective Receptor Modulators (SRMs)

A

type of drug, = lab-engineered NR ligands,
are tissue-selective receptor agonist or antagonists.
*can also be MIXED (agonist and antagonist for different tissues at once)
ie: tamoxifen or raloxifene (for breast cancer)

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20
Q

mechanism of differential tissue-selectivity for SRMs

A

the NR changes conformation depending on which SRM binds,
–> diff. co-regulatory proteins bind to the NR

  • ligand differences depend on small changes to sequence in “P-Box”
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21
Q

P-Box

A

the site at which the sequences of different SRMs vary most.

change p-box ==> change tissue-binding characteristics

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22
Q

DNA-binding mechanism for NRs

A

NRs bind to HREs (hormone response elements) on DNA
via Zinc fingers,
(type I: palindromes; type 2: direct repeats)
*few DNA seqs bind NRs, BUT most that DO encode transcription factors, so can influence more genes!

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23
Q

Hormone Response Element (HRE)

A

a sequence of DNA which binds NRs,

  • palindrome (inverted repeat) for type I NRs
  • direct repeat for type II NRs

*NOT unique across tissues/genes, get specificity elsewhere

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24
Q

PPAR alpha

A

NR in liver, binds fibrates;
regulates FA oxidation, lowers serum lipid levels;
(increase lipid oxidation, lower circulating triglycerides)

  • dyslipidemia
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25
Q

PPAR delta (aka: delta-beta)

A

NR in adipocytes and other tissues,
has NO specific endogenous ligands;
increases FA oxidation, VLDL uptake, and Energy Expenditure;

  • Dyslipidemia and obesity
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26
Q

PPAR Gamma

A

NR mostly in adipose tissue (also mm, macrophages)
binds glitazones (also FAs and eicosanoids);
increases adipogenesis (NEEDed for making white fat!),
lowers blood glucose levels, increases insulin sensitivity!
- preDM, obesity, metabolic syndrome

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27
Q

LXR

A 
NR in liver, binds oxysterols; 
promotes secretion of cholesterol by
- inhibit SREBP
- increase bile acid synth by promoting gene for Cyp7a enzyme
*atherosclerosis, dyslipidemia
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28
Q

FXR

A

NR in liver and intestine, binds bile acids;
promotes bile acid re-absorption (from ileum) by…
- increase # bile acid transporters in ileum
- inhibit gene for Cyp7a enzyme (bile synthesizer)
*high cholesterol and dyslipidemia

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29
Q

RXR (alpha, beta and gamma)

A

NR present throughout body,
binds 9-cis-retinoic acid.
*requires heterodimeric partner
– f(x) and associated diseases depend on which heterodimeric partner *accutane targets this NR!

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30
Q

Mechanism for NR type I

A
  1. hormone (ligand) crosses plasma membrane
  2. binds to NR/HSP complex, freeing HSP (chaperone)
  3. NR/ligand enters nucleus, binds DNA
  4. recruit co-activator
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31
Q

Mechanism for type II NRs

A
  1. hormone (ligand) enters nucleus (through nuclear pore)
  2. binds to NR on DNA
    (NR = RXR-heterodimer)
  3. NR complex swaps out co-repressor for co-activator
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32
Q

NO (nitric oxide) synthesis

A

substrate: argenine
product: citrulline and NO
3 NO synthases:
- Neuronal Constitutive NOS (nNOS)
- Endothelial constitutive NOS (eNOS): in smooth mm.
- Induced NOS (iNOS): in macrophages

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33
Q

NO as signal molec

A

gas, free radical, VERY short half life,
does NOT bind classically.
regulates:
-relaxation of smooth muscle (vascular) tone
-immunological f(x) (antimicrobial)

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34
Q

destructive characteristics of NO

A

free radical,
binds to any cell structures and interrupts cellular processes
–> kills the cell and neighbor cells

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35
Q

intracrine signalling

A

signalling both withIN and between cells,

only example: NO

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36
Q

medical use of nitroglycerin

A

used to treat angina

- releases 3 NOs

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37
Q

endothelial releasing factor

A

= Nitric Oxide

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38
Q

4 types of binding domains (for modular proteins)

A 
PH = pleckstrin homology domain
PTB = phosphotyrosine-binding domain
SH2 = Src homology 2 domain
SH3 = Src homology 3 domain
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39
Q

2 examples of GPCR effectors (G-protein coupled receptors)

A
  1. adenylyl cyclase

2. phosphoinositide cascade

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40
Q

structure of a GPCR

A

7 transmembrane domains,

  • effector molec (IN membrane)
  • g-protein (cytoplasmic side of membrane) –> “trimeric complex” (alpha, beta, gamma), *alpha separates from beta/gamma to f(x)
  • receptor w/ NH2 tail (on extracellular side of membrane)
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41
Q

response of receptor depends on…

A

strength, duration and timing of signal

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42
Q

hydrophobic signaling molecs

A

proteins, polypeptides, AA derivatives (NE/Epinephrine)
stored in secreting cells, long half life,
direct mech, intracellular Rs
mostly type II NRs

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43
Q

hydrophilic signaling molecs

A

cholesterol and fatty acid derivatives, (steroids)
NOT stored, short half life,
INdirect mech, plasma membrane Rs
mostly type I NRs

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44
Q

“Both” hydrophilic and hydrophobic signal molecs

A

gases NO and CO2.

covalently bind to the receptor (guanylyl cyclase R)

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45
Q

7 steps of cell signaling

A
  1. Synthesize ligand, 2. Release signal (ligand)
  2. Transport to receptor, 4. Bind to Receptor
  3. Response
  4. Remove ligand, 7. Terminate response
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46
Q

when cell does not receive the appropriate signals

A

induces apoptosis
(cell suicide)
bc can’t continue growth, cell cycle, etc. w/o signals!

47
Q

types of pathway desensitization

A
  1. Receptor sequestration
  2. Down-Regulation of Receptor (internalize and degrade R)
  3. receptor INactivation
  4. INactivate 2nd messengers (downstream)
  5. make INhibitory protein for 2nd messengers
48
Q

3 parts to a cell receptor

A

(= protein)

  1. extracellular domain
  2. transmembrane domain
  3. intracellular domain
    * each receptor has >1 functional domain!
49
Q

type I NR characteristics

A

(steroid TFs – ligands = steroid derivs),
form homodimers, bind to palindromes.
LOW concentration in blood
(–> high affinity, R has high specificity)

50
Q

Type I NR major ligands

A

= steroids (cholesterol derivatives).

  • progesterone
  • estrogen, estradiol; tamoxifen/raloxifene
  • androgen (testosterone)/DHEA
  • aldosterone (mineralcorticoids)
  • cortisol (glucocorticoid)
51
Q

Type II NR major ligands

A

(proteins and polypeptides)

  • PPAR alpha and gamma
  • Xeonbiotic receptor (PXR, CAR-beta)
  • bile acid receptor (FXR)
  • oxysterol receptor (LXR)
52
Q

NR type II characteristics

A

(“dimeric orphan receptors”)
form heterodimers w/ RXR,
bind direct repeats.
high concentration in blood (“promiscuous”)
–> low receptor specificity and affinity

53
Q

AF1 domain of nuclear receptor

A

activator factor 1,
activated by signal in ABnormal state
(ie: cancer cells)
* at N end of protein

54
Q

AF-2 domain in nuclear receptors

A

activator function 2,
activated by ligand binding in normal/healthy cells.
*near Carboxyl end of the protein, part of ligand binding domain

55
Q

DNA binding Domain (“DBD”) of nuclear receptors

A 
in middle of receptor protein, 
binds DNA (HRE site if type I) when R = activated.
56
Q

best target in NR pathway for cancer treatment

A

Co-regulators!
- inhibit co-activators
or stimulate co-repressors.
–> help w/ tissue-targeting, minimizing side effects

57
Q

Ligand Binding Domain (LBD)

A

site on NR where ligand binds to activate the protein.
- nearer C end,
contains AF-2 domain

58
Q

Examples of Cytokine Receptors (ligands)

A
  1. Growth hormone
  2. erythropoeitin
  3. prolactin
  4. Leptin
  5. Interferon (alpha/beta/gamma)
59
Q

Cytokine Receptors (tyrosine kinase receptors)

A

NOT enzymes, = receptors for cytokine ligands

families: Src, JAK, STAT

60
Q

mTOR

A

serine/threonine kinase,
promotes cell growth and protein synthesis.
activated by AKT

61
Q

receptor tyrosine kinase (RTK) mechanism

A
  1. INactive: in membrane as monomer
  2. ligand binds, Rs dimerize (except Insulin R = already dimerized)
  3. activate intracellular tyr. kinase domain
    3.tyrosine kinases cross-P (auto-P) the opposite receptor
  4. increase kinase f(x)/make docking station for signal molecs.
  5. more phosphorylation–> activate downstream pathways
    (Src, PI, PI3-K, MapK)
62
Q

Receptor Tyrosine Kinases (RTKs)

A

cell signal receptors,
set of 2 Rs on 2 intracellular proteins w/ tyrosine kinases.
Activate when ligands bind –> auto-phosphorylate and dimerize.
ligands: EGF, FGF, insulin (growth factors!)
pathways activated: Src, Phospholipase C, MAP kinase, PI-3K

63
Q

Phospholipase C cascade

A 
initiated by RTK, 
activates Phosphoinositide (PI) pathway (w/ GPCRs)
--> increase cytosolic Ca2+ levels 
(boost signaling w/ Ca2+)
** directly makes DAG and Ins-1,4,5-P3
64
Q

Src pathway

A

= cytosolic tyrosine kinase enzyme,
starts of signal cascade to increase cell motility, decrease adhesion (regulate cell f(x)).
activated by RTKs and Cytokine Receptors

65
Q

Ras proteins

A

a GTPase signal molec;
activated by RTKs (= freed from plasma membrane),
relay cell proliferation signals to MAP kinase cascade.
* + reg: GEFs
- reg: GAPs

66
Q

“GAP” protein (GTPase activating protein)

A

INactivate Ras signal molec.
(increases rate of hydrolysis of GTP on Ras)
* Binds directly to the RTK,
(helps return Ras to inactive when RTK is inactive).

67
Q

“GEF” (guanine exchange factor)

A

increase Ras function;
–> promotes exchange of GDP and uptake of GTP to Ras
(when active, increase rate of f(x))

68
Q

MAP kinase cascade (mitogen activated kinase)

A
  • a serine/threonine kinase cascade, longer lived than RTKs*
    1. Ras activates Raf-1 (MAP kinase kinase kinase)
    2. Raf-1 activates Mek (MAP kinase kinase)
    3. activate MAPK * by dual +P of tyrosine and threonine
  • -> activate more… –> promote cell proliferation
  • ** activates Myc, Jun, Fos Tfs!***
69
Q

Insulin Receptor Substrate (“IRS”)

A

Insulin-specific receptor that binds to RTK (when RTK = activated),
=> docking station for mTOR, AkT, and MAPK

70
Q

mitogens

A

cell signaling moles,
induce cell proliferation
ie: Growth Factors, estrogen

71
Q

cytokine receptors (tyrosine kinase-coupled receptors)

A

ligands: growth factors, prolactin, erythropoietin, cytokines (interferon-gamma)
R is NOT enxyme, relies on tyrosine kinases from cytoplasm to phosphorylate the R and start cascade (Srcs/JAKs)
Activate: STATs (transcription factors)

72
Q

Cytokine

A

a signaling molec that binds to tyrosine kinase-coupled receptors (aka cytokine Rs)
- promotes hematopoeitic differentiation and protection against viral infection (interferons)

73
Q

Cytokine receptor mechanism

A
  1. cytokine binds to 2 Rs –> dimerize
  2. R-bound JAKs (= tyr. kinases) cross-phosphorylate the each other
  3. JAKs phosphorylate the R
  4. STATs bind to R
  5. STATs = phosphorylated by JAKs
  6. STATs dimerize, release, go to nucleus to upregulate gene transcription (hematopoiesis, immune function–> Myc/Fos)
74
Q

STAT

A

family of signal proteins activated by cytokine R/JAK complex.
dimerize when tyrosines = phosphorylated,
go to nucleus to upregulated gene transcription of
- hematopoiesis - mammary gland dvpt
- immune F(x) Myc/Fos

75
Q

pathways activated by cytokine receptors

A 
- STAT
and same as RTKs...
- INS 	- MapK
- Src 	- Phospholipase C (gamma)
- PI-3K
76
Q

Epo

A

signal molec, activates EpoR (a cytokine R)
promotes red blood cell formation
* often used for blood doping*

77
Q

SHP phosphatase

A

protein that INactivates JAKs

if def., will have extra EpoR activity –> extra high RBCs

78
Q

ANPs (Atrial Natiuretic Peptides)

A 
signal hormones released by heart, 
bind to guanylyl cyclase Rs (NPRs). 
promote smooth muscle relaxation in blood vessels
--> vasodilation. 
*also: BNP (brain), CNP (cardiac)
79
Q

receptor guanylyl cyclase (aka NPR – natiuretic protein R)

A

Receptor for ANPs, (“A” for ANP/BNP; “B” for CNP)
has cytoplasmic guanylyl cyclase enzyme to make cGMP.
cGMP activates PKG (protein kinase G)
–> cascade, ie: to inactivate IP3 –> sm. muscle relaxation

80
Q

Maroteax dysplasia

A

a type of short-limbed dwarfism caused by mutations in NPR-B

Natiuretic Protein Receptor B

81
Q

TGF-beta receptor lignds

A

TGFbetas, BMPs (bone morphogenetic proteins), anti-mullerian hormones, inhibins, activins.
paracrine signaling (held in ECM until released locally)
complex, may homo- OR hetero-dimerize

82
Q

BMPs

A

Bone morphogenic proteins,

ligand for TGF-beta Rs

83
Q

TGF-Beta Receptor

A

aka: serine/threonine kinase receptor
w/ activation by ligands, phosphorylate SMADs,
SMADs go to nucleus to alter gene transcription.
Regulate: cell prolif/death, immune response, homeostasis
** inhibits cell prolif., = tumor suppressor! ***

84
Q

TGF-beta R mechanism

A
  1. ligand binds to TGF-Beta RII, activates
  2. Receptor II activates and dimerize w/ receptor I
  3. serine/threonine kinase of RI phosphorylates SMAD
  4. activated SMAD goes to nucleus as TF
    (inhibit cell prolif, prevent tumors)
85
Q

Canonical Wnt Pathway

A

signaling pathway in cell to regulate cell adhesion;
* regulates beta-catenin proteolysis (ubiquitination).
Also activates: Phospholipase C and Dsh pathways.
ligand: Wnt; Receptors: Frizzled and LRP
*INactive –> beta-catenin degradation.

86
Q

INactive (basal state) Wnt Pathway

A

Receptors not dimerized, no “disheveled” released.

  • -> beta-catenin = sequestered in cytosolic degradation complex, where phosphorylated (marked for Ubiquitination and degradation).
  • —> Groucho corepressor inhibits Wnt target genes (ie: Myc)**
87
Q

Beta-catenin Degradation Complex

A 
in cytosol, 
contains 4 proteins:
- GSK3, CK1 = ser/thr kinases 
(+P to B-cat. to mark for ubiquitination and degradation)
- axin, APC = scaffold proteins
88
Q

Groucho

A

corepressor for Wnt genes,
binds to LEF1/TCF when Wnt pathway = inactive
to inhibit Wnt target genes (ie: myc)

89
Q

Mech of Wnt pathway activation (and f(x))

A
  1. Wnt binds to Frizzled R –> cluster Frizzled and LRP Rs
  2. activate (phosphorylate) Disheveled protein
  3. recruit degradation complex to receptors
    —> Wnt free to go to nucleus to promote target genes (ie: Myc)
    (promote cell proliferation, etc)
90
Q

“APC” (Adenomatous Polyposis Coli)

A

familial colon cancer from mutation in APC,
causes formation of MANY polyps in colon, appears in early adult.

–> no Wnt degradation, so excessive cell proliferation!

91
Q

PTEN

A

regulatory lipid phosphatase, dephosphorylates PIP3.
–> blocks enzymatic activity (no AKT activation)
= tumor suppressor

92
Q

PI-3K (phosphoInositol-3-kinase)

A

Enzyme activated by RTKs,
PIP2 –(add P at 3 position)–> PIP3
–> PIP3 recruits AKT for phosphorylation by PDK1

** PIP3 –(PTEN)–> PIP2

93
Q

AKT

A

signal enzyme downstream of RTK,
recruited to membrane by PIP3, activated (+P) by PDK1.
** +P to many more downstream proteins (starts cascade)

(aka: protein kinase B)

94
Q

PDK1

A 
enzyme, part of RTK/PIP3 signal pathway/complex. 
activates AKT (+P) after recruited by PIP3
95
Q

downstream molecs phosphorylated by AKT

A

activated: MDM2, mTOR, NF-kB

INactivated: BAD

96
Q

mTOR

A

ser/thr kinase complex, activated by phosphorylation from AKT.
promotes cell growth, glycolysis/glucose transport, and protein synthesis (= oncoprotein)
inhibits p53
* stimulated by growth factors, inhibited by Rapamycin

97
Q

BAD

A

regulatory enzyme inhibited by AKT,
active: sequesters Bcl2 –> so promote apoptosis
(Bcl2 blocks apoptosis)

if: active AKT –> INactive BAD –> active bc12 –> NO apoptosis

98
Q

function of g-protein alpha subunit

A

= GTPase,
hydrolizes G-protein to turn signal off
(desensitizes)

99
Q

G-protein in GPCRs (f(x))

A

transduces signal from receptor to effector.
w/ GTP bound: ON
w/ GDP bound: OFF

*alpha subunit INactivates the signal (swaps GDP for GTP)

100
Q

isoprenoid unit

A

cholesterol derivative,

anchors G-protein to cytosolic side of plasma membrane

101
Q

characteristics of second messengers

A
  1. short half life (seconds)

2. high affinity for target

102
Q

GRK (g-protein receptor kinase)

A

desensitizes GPCR,
phosphorylates receptor so Arrestin (inhib. molec) will bind.

aka: beta-ARK (beta adrenergic receptor kinase)

103
Q

cAMP phosphodiesterase

A

converts cAMP to 5’-AMP,
= inactivates cAMP

(cAMP made/activated by adenylyl cyclase)

104
Q

AC (adenylyl cyclase) pathway

A

AC –(activate)–> cAMP,

2 cAMP –(activate)–> PKA –> (phosphorylate target proteins or cAMP Response Element “CREBP”)

105
Q

CREBP

A

cAMP Response Element Binding Protein,
a transcription factor
binds CBP (CREB binding protein), which is activated by PKA
(part of GalphaS pathway, w/ Adenylyl cyclase)

106
Q

mech. of pertussis toxin

A

binds and blocks Galpha-i

–> overactive AC –> too much PKA

107
Q

mech. of cholera toxin

A

blocks f(x) of g-protein alpha subunit

  • -> no deactivation of Gsalpha
  • -> overactive AC –> too much PKA
108
Q

protein kinase C

A

family of ser/thr kinases,
used in signaling cascades to phosphorylate target molecs.
(activated by DAG&Ca2+ from GPCRS, cGMP from NPRs)
promote cell proliferation

109
Q

DAG (diacylglycerol) in signaling

A
  1. w/Ca2+, activated PKC
  2. precursor for eicosanoids and prostaglandins

(made from PIP2 in PI pathway)

110
Q

PI (phosphoInositide pathway)

A 
activated by GPCRs, **ligs: Ach, NE, Epinephrine, Ghrelin**
1. PLC-beta (phospholipase C) --> PIP2
2. PIP2 --> IP3 and DAG
3. IP3 --> activate Ca2+ channel
    DAG (+Ca) --> PKC
111
Q

major cellular proteins that bind Ca2+

A
  1. PKC (phosphokinase C)

2. calmodulin (“CaM”)

112
Q

enzymes that bind CaM (calmodulin)

A
  1. eNOS/nNOS
  2. PKC
  3. phosphorylase kinase (regulates glycogen phosphorylase)
113
Q

major (relevant) GPCR ligands

A
  1. Ghrelin (activates PI and AC pathways at same time!)
  2. MSH-alpha (POMC neurotransmitter)
  3. GLP-1
  4. external signals (light/sound/pressure)
    more: Ach, glucagon, CCK, LH, prostaglandins…

SMP (8 decks)

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