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BioMedChem M2 > 11/12 - Signal Transduction Pathways > Flashcards

11/12 - Signal Transduction Pathways Flashcards

1
Q

Adaptation / Desensitation

+ examples

A

How cells ADJUST their SENSITIVITY to a signal

Receptor Sequestration

Receptor down-regulation (lysosome)

Receptor inactivation

inactivation of signaling protein

Production of inhibitory protein

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2
Q

Ca2+ Levels in the CYTO

A

LOW

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3
Q

INTRAceullular Receptors

Ligand / Types

A

Ligand = Small hydrophobic signal molecule

typically carried by a carrier protein

Biggest barrier is the cell membrane

Examples (2):

Cytoplasmic Receptor

Nuclear Receptors

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4
Q

Extraceullular Receptors

Ligand / Types

A

Cell-Surface Receptors

Typically signaled by a HydroPHILIC Signal molecule (ligand)

Examples (3)

GPCR

Enzyme-Coupled

Ligand Gated

Voltage Gated Ion Channels

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5
Q

Alpha Subunit Functions

A

Activates & *Inhibits* -

Adenylyl Cyclase

Just Activates

Ca2+ Channels & PLC-beta

(phospholipase-C-beta)

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6
Q

Which G-Protein Subunits are Anchored to the Plasma membrane?

and how?

A

ALPHA & GAMMA

by LIPID TAILS

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7
Q

GAPs

A

= GTPase ACTIVATING proteins, BUT (opposite)

TURN OFF G-protein

GTP (active) -> GDP (inactive) monomeric GTPase

inhibited by cholera toxin

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8
Q

Examples of Steroid Hormones

A

derivatives of Cholesterol, Main ligand for Nuclear receptors

Sex hormones = Estradiol / Testosterone

Adrenal Glands = Cortisol

Thyroid Hormones = Thyroxine

Vitamin D3 / Retinoic Acid

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9
Q

Sketch a generic

signal transduction pathway

that includes receptor, intracellular signaling proteins, and effector proteins.

A
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10
Q

Nuclear Receptor’s Respond to what?

(ligands)

A

some i_ntracellular signals_

Mainly Steroid Hormones, (all derivatives of cholesterol)

All hydrophobic & small, so that they can cross the membrane to reach intracellular receptors

Can NOT be carried by themselves in BLOOD, need a

Carrier Protein!

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11
Q

Draw a diagram of how

POSITIVE feedback loops

(with and without delayed responses) affect gene expression.

A
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12
Q

Negative Feedback Loop

A

Intracellular signaling signals usually use feedback loops

Could have either short or Long delay

Signal Kinase => Ligand + receptor = enzyme product

Enzyme product -> HIGHLY ACTIVE phosphotase (off)

signals to INHIBIT the enzyme

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13
Q

CREB

A

CRE-Binding Protein

is PHOSPHORYLATED by PKA in the nucleus

(PKA = cAMP-Dependent Protein Kinase)

CREB binds with CBP onto –> CRE for TRANSLATION

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14
Q

4 Ways to Control Protein Activity

A
  1. Protein Synthesized
    1. ​no protein -> active protein
  2. Protein PHOSphorylated
    1. ​inactive protein -> active P-protein
  3. Protein DE-Phosphorylated
    1. ​inactive P-protein -> active protein
  4. Ligand Binding = Nuclear Binding
    1. ​inactive protein -> nuclear membrane -> active protein
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15
Q

Arrestin

A

Protein found in every cell type in the body that:

DESENSITIZES GPC-receptor

= negative feedback!

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16
Q

Local Signaling Systems

A

Contact-Dependent

(signaling cell -> membrane bound signal to target cell)

Paracrine

(Signaling cell -> local mediator -> target cell)

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17
Q

How are signals detected?

Types of Extracellular Receptors

+

Intracellular Receptors

A

Integral-membrane Receptors

GPCR

Enzme-Coupled Receptors

Ligand Gated + Voltage Gated Ion Channels

Cytoplasmic + Nuclear Receptors

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18
Q

GEFs

A

= Guanine nucleotide EXCHANGE factors

turn ON G-proteins

  • GDP(inactive) ->* GTP (active) monomeric GTPase
  • inhibited by pertussis toxin*
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19
Q

PLC-Beta & Phospholipid Signaling

action

A

G-Protein EFFECTORS

G-Protein (alpha subunit) -> inositol phospholipid signaling ->

ACTIVE PLC-Beta

converts

PIP2 -> IP3 + DAG

(second messengers)

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20
Q

PKA Functions / Activation

A

cAMP-dependent Protein Kinase A

  • Activated by a rise in cAMP
  • 2 Functions:
    • Quick Response (immediate)
      • phosphorylation of Ser/Tyr
    • ​Long-Lasting
      • Translocation to NUCLEUS
      • phosphorylaition of transcription FACTOR
        • CREB + CBP
  • Ex. adrenergic receptor signaling
21
Q

Fast Response

A

< seconds - minutes

Signal -> Altered Protein FUNCTION -> response

Usually have factors already present in the cell:

Molecular switches / Second messengers / Relocalization

22
Q

PKA Vs PKC

A

PKA = Activated by cAMP

PKC** = Activated by **DAG** + **Ca2+

Ca2+ is released by IP3 binding to Ca Channels

23
Q

Structural Characteristics of G-protein

A

After binding, interacted with intracellular domain of GPCR

(3) TRImeric G-protein
* can be ATTACHED to the GPCR, or NOT*

  • Alpha - lipid tail anchor to membrane
    • GDP bound when inactive
  • Beta
  • Gamma - lipid tail anchor to membrane
24
Q

4 functional domains of an

INACTIVE Nuclear Receptor

A

“COOL LTD”

  1. COOH
    1. binds inhibitory protein
  2. Ligand Binding Domain
  3. DNA-Binding Domain
  4. Transcription-Activating Domain
    1. H2N-tail
25
Q

Secondary Messengers

Types / Function

A

work VERY RAPIDLY,

can RISE or fall DRAMATICALLY, seconds

Ca2+

cAMP

DAG

IP3

26
Q

Key Terms for Exam

A
  • Nuclear Receptors
  • Cytoplasmic Molecular Switches
  • Large, Heterotrimeric GTPases
    • G-Proteins
  • Modulation of Membrane bound enzymes and ion channels
    • AC - adenylyl cyclase
    • PLC - phospholipase C
  • Secondary messengers:
    • cAMP / Ca2+ / IP3 / DAG (diacyglycerol)
  • Response Enzymes:
    • PKA / PKC / CaM - Kinase
27
Q

Structural Relationship of

Nuclear Receptors

A

All are structurally related, located in cyto** or **nucleus

Usually bound to inhibitory complexes =

ALWAYS Inactive

or

ALWAYS ACTIVE

= Are active until ligand binds

28
Q

Adenylyl Cyclase

A

EFFECTOR: Membrane protein regulated by

G-proteins (both activated/inactivated by alpha-subunit)

& Ca2+(not a second messenger in this instance)

RELEASES 2nd messenger –> cAMP

29
Q

Calmodulin

A

ubiquitous _Ca2+ Recepto_r that modulates target proteins

4 Ca binding sites -> conformational change

not an enzyme itself

Allosteric Regulator of other proteins

30
Q

IP3

function

A

WATER SOLUBLE 2nd messenger

made along with DAG from PLC-B breakdown of PIP2

Binds gated Ca2+ Channels

releases the Ca2+ from ER lumen

helps Activates PKC w/ DAG

31
Q

Structural Characteristics of GPCR

A

​7-helix bundle structure, seven pass / serpentine

  • EXTRAcellular domain
    • binds ligand/agonist
  • TRANSmembrane Helices
  • Intracellulardomain
    • ​cytoplasmic, interacts w/ G-protein
32
Q

Slow Response

A

Min - Hours

Signal -> nucleus -> Transcription / Translation

-> Altered Protein SYNTHESIS -> response

Synthesis of new factors may involve:

chromatin remodeling / T+T

Post-translational modification / relocalization also

33
Q

Draw a diagram of how

negative feedback loops

(with and without delayed responses) affect gene expression.

A
34
Q

DAG

DiAcylGlycerol

A

LIPID ANCHORED 2nd messenger

made along w/ IP3 from PLC-B breakdown of PIP2

ACTIVATES PKC w/ Ca2+

Ca2+ is from IP3’s binding to Ca2+ channels on ER lumen

PKC –> phosphorylates Proteins

cleaved INTO arachidonic acid

35
Q

CaM-Kinases

A

Ca2+ / Calmodulin-dependent protein kinases

mediate many of the Ca2+ signals in cells

RISE in Ca2+ -> ACTIVE calmodulin -> binds to Cam-Kinase

POSITIVE FEEDBACK = autophosphorylates ITSELF

Ca2+ levels are diminished -> CaM-Kinase ramains ACTIVE

= memory device

36
Q

Molecular Switches

A

Receptor Protein

Binding changes receptor activity

Intracellular Signaling Proteins

Relay info and AMPlification

Effector Proteins

Produce various Cell responses

37
Q

Draw a diagram of how

G proteins cycle between active and inactive states;

describe the general class of enzymes that regulate this process (GAPs and GEFs).

A
38
Q

Ca2+ as a Second Messenger

A

Activates PKC (with DAG)

acts on CaM Kinase + Calmodulin

Role in:

embryonic developent / muscle contraction / secretion

  • function NOT as 2nd messenger:*
  • along w/ G-protein (alpha) regulates adenylyl cyclases’s*
  • release of cAMP (another 2nd messenger)*
39
Q

Long Range Signaling Systems

A

Synaptic

(neuron –> axon –> NT –> synapse –> target cell)

Endocrine

(endocrine cell –> bloodstream –> target cell)

40
Q

Cortisol Signaling

Type of Allosteric Regulation

in Nuclear Receptors

A

CORTISOL signaling

Cortisol (steroid hormone) crosses plasma membrane

binds to intracellular receptor –>

expose Nuclear localization signal –> ACTIVE receptor

EFFECTOR = Hormone-Receptor complex

does not have any RELAY or amplification

41
Q

Pertussis Toxin

A

Inhibits Exchange Factors

  • GDP* –//–> GTP (active)
  • inhibits GEFs*

GTP-protein will stay OFF

42
Q

Positive Feedback Loop

A

Intracellular signaling signals usually use feedback loops

Ligand + Receptor = Enzyme Product

Positive Feedback:

Ligand + Receptor + Enzyme Product

= VERY ACTIVE ENZYME -> MORE Product

43
Q

Regulation of Nuclear Receptors

A

ALLOSTERIC regulation/activation

Ex. cortisol signaling

Ligand binding -> allosteric binding

-> inhibitory domain** (COOH) **dissociates –>

receptor is now ACTIVE –> binds to receptor binding element

Transcription of target gene

44
Q

2 Types of Molecular Switches

in the cell

A

Phosphorylation

(O-K) ON - Kinase, adds phosphate to protein

(OfP) OFF - Phosphotase = hydrolyzes phosphate

GTP-Binding

no specific on or off

Large / hetero trimeric = G-Proteins

small monomeric = GTPases

45
Q

G-Proteins

A

Type of Molecular Switch for Nuclear Receptors,

40% of all drugs work through GPCRs

LARGE & Heterotrimeric

GAPs - OFF

GEFs - ON

46
Q

Beta-Gamma Complex Subunit

FUNCTIONS

A

Activates

K+ Channels

also PLC-ish

Inactivates:

Ca2+ Channels

47
Q

Ca2+ levels in ER / Extracellular space

A

HIGH

maintained by calcium pumps

Na / Ca2+ exchange

48
Q

Cholera Toxin

A

Inhibits Hydrolysis of GTP

GTP –//–> GDP(inactive)

inhibits GAPs

G-protein will STAY ACTIVE (GTP-active)

49
Q

How Nuclear receptor modulator drugs can be effective even as partial agonists?

A

TAMOXIFEN = SERM (selective ER modulator)

  • Partial Agonist action:
    • ​can also target / bind to other tissues
      • ​not just the Estrogen receptor in the breast but also ovaries etc.
  • Main Action:
    • ​crosses membrane –> estrogen receptor
      • inhibits growth of cancer cells

BioMedChem M2 (8 decks)

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