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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
**Secondary Messengers** Types / Function
work **VERY RAPIDLY**, can RISE or *fall* DRAMATICALLY, **seconds** **Ca2+** **cAMP** **DAG** **IP3**
26
Key Terms for Exam
* 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
**Structural Relationship of** **Nuclear Receptors**
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
**Adenylyl Cyclase**
**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
**Calmodulin**
ubiquitous **_Ca2+ Recepto_r** that modulates target proteins 4 Ca binding sites -\> conformational change *not an enzyme itself* **_Allosteric Regulator_** of other proteins
30
**IP3** function
**_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
**Structural Characteristics of GPCR**
_​**7**_**_-helix_** bundle structure, **seven pass / serpentine** * **EXTRAcellular domain** * binds ligand/agonist * ***TRANS*membrane Helices** * _**Intra****cellular**_**domain** * **​**cytoplasmic, interacts w/ **G-protein**
32
***Slow Response***
**_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
Draw a **diagram** of how **_negative feedback loops_** (with and without delayed responses) affect gene expression.
34
**DAG** **D**i**A**cyl**G**lycerol
***_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
**CaM-Kinases**
**_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 *Ca***2+** *levels are diminished -\>* _CaM-Kinase ramains **ACTIVE**_ = **memory device**
36
**Molecular Switches**
**Receptor Protein** Binding changes receptor activity **Intracellular Signaling Proteins** Relay info and AMPlification **Effector Proteins** Produce various Cell responses
37
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**).
38
**Ca2+** as a **Second Messenger**
**_Activates PKC_** (with **DAG**) ## Footnote *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
**Long Range Signaling Systems**
**Synaptic** (neuron --\> axon --\> NT --\> synapse --\> target cell) **Endocrine** (endocrine cell --\> bloodstream --\> target cell)
40
**Cortisol Signaling** **Type of Allosteric Regulation** **in Nuclear Receptors**
**_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
**Pertussis Toxin**
***Inhibits Exchange Factors*** * GDP* --//--\> GTP (active) * inhibits **_GEFs_*** GTP-protein will ***stay OFF***
42
**Positive Feedback Loop**
Intracellular signaling signals usually use feedback loops Ligand + Receptor = **Enzyme Product** Positive Feedback: Ligand + Receptor + **Enzyme Product** = **VERY ACTIVE ENZYME** -\> MORE Product
43
**Regulation of Nuclear Receptors**
**_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
**2 Types of Molecular Switches** in the cell
**_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
**G-Proteins**
Type of _Molecular Switch_ for _Nuclear Receptors_, 40% of all drugs work through GPCRs **_LARGE & Heterotrimeric_** GAPs - *OFF* GEFs - ON
46
**Beta-Gamma Complex Subunit** **FUNCTIONS**
**_Activates_** **_K+ Channels_** *also PLC-ish* ***Inactivates:*** ***Ca2+ Channels***
47
**Ca2+ levels in ER / Extracellular space**
**_HIGH_** maintained by **calcium pumps** **Na / Ca2+ exchange**
48
**Cholera Toxin**
***Inhibits Hydrolysis of GTP*** GTP --//--\> GDP(inactive) inhibits ***_GAPs_*** G-protein will **STAY ACTIVE** (GTP-active)
49
How **_Nuclear receptor modulator drugs_** can be effective even as **_partial agonists?_**
**_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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