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Bio 361 > Lecture 11: cell to cell communication > Flashcards

Lecture 11: cell to cell communication Flashcards

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Biology 101 flashcards
1
Q

Direct signalling uses

A

Gap junctions, which connect cells directly touching each other

  • the signal therefore passes directly from one cell to another without traversing extracellular space (stays in the cytoplasm)
  • ie. contraction of cardiac cells
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2
Q

Gap Junctions

A
  • specialized protein complexes create an aqueous pore between adjacent cells
  • can be opened or closed for regulation
  • allows rapid communication over short distances
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3
Q

Indirect signals must be:

A
  • synthesized & stored, released, transported
  • received and transduced by the receptor
  • transduced and amplified by signal transduction pathway, so target cell can generate a response
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4
Q

Chemical Messenger-problems

A
  • must be transport in aqueous solution, if messenger is not water soluble it will have trouble over long distances
  • message has to penetrate cells, so if it is not lipid soluble it cannot send its signal
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5
Q

Receptor locations

A
  1. embedded in the membrane with binding site outside the cell
  2. inside the cell
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6
Q

Ligand binding

A

-ligand or chem messenger binds to the receptor to induce change in its conformation and activates the signal transduction pathways that cause response in the cell

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7
Q

Receptor Specificity

A

-ligand binding site has a specific shape, so only some molecule fit its structure

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8
Q

agonists and atagonists

A
  • chemicals that bind to and activate receptors are agonists, the mimic natural ligands
  • antagonists bind to the receptor but block the action of the natural ligand
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9
Q

Adenosine

A

-a purine nucleoside functions for: energy transfer (atp, adp), signal transduction (cAMP), promotes healing, and as a neurotransmitter inhibits activity in the CNS*** causing sleepiness and preventing arousal after prolonged mental activity

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10
Q

Caffeine, adenosine antagonist

A
  • binds to and blocks adenosine receptors in the CNS
  • is both water and lipid soluble, can cross blood-brain barrier
  • cells respond by increasing amount of adenosine released, which is why coffee drinkers must have more to overcome increasing adenosine levels
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11
Q

Receptor Saturation

A
  • single cell expresses many molecules of a given receptor
  • the more receptors that are bound to ligand, the larger the magnitude of the response
  • saturation=all receptors are bound to ligand
  • increasing # of receptors means increased response
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12
Q

up and down regulation

A

of receptors on a target cell can change over time

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13
Q

Receptor sensitivty

A

-affinity of a receptor for a ligand

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14
Q

Dissociation constant Kd=

A

the ligand concentration at which HALF the receptors are bound to ligand

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15
Q

Affinity constant

A

Ka=1/Kd; as Ka increases, response increases

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16
Q

Inactivation of ligand signaling

A
  1. remove from ECF

2. terminate receptor activation

17
Q

Removing ligand from ECF

A
  • enzymes in liver and kidney break down hormoes, removing them from the blood (slow)
  • ligand will be destoryed at the cellular levels (fast)
18
Q

Terminating receptor activation

A

-as concentration of a hormone in the ECF decreases, bound molecules of that hormone will dissociate from their receptors

19
Q

inactivation of ligand signaling

A

-receptor down regulation, receptor sequestration, receptor inactivation, inhibitory proteins, signal protein inactivation

20
Q

Signal transduction pathways amplify signals

A

-convert conformational change of an activated receptor into an intracell response
-signald transduction pathways have multiple steps
-greater the number of steps, the greater the amp
“each activated receptor activated many substance A, which activates many B, etc)

21
Q

4 types of receptors

A
  1. intracellular
  2. ligand-gated ion channel
  3. receptor-enzyme
  4. G-protein-coupled receptor
22
Q

Intracellular receptor location

A

in cytoplasm (move to nucleus once bind to ligand) or in the nucleus, bound to DNA

  • ex: ER-a estrogen receptor, found in hypothalamus, ovary, uterus, and mammary glands
  • over-expressed in 70% of patients with breast cancer
23
Q

intracellular receptors regulate transcription

A
  • of traget genes by binding to specific DNA sequences and increasing or decreasing mRNA production
  • have 3 domains: ligand binding, DNA binding, and transactivation
  • many endocrine hormones bind to them (estrogen, testosterone, etc)
24
Q

Ligand-gated ion channels

A
  • when activated by binding ligand, the receptor changes shape, opening or closing the ion channel, allowing ions to pass and change MP
  • ie. Nicotinic ACh receptor
25
Q

Receptor enzyme

A
  • when activated the catalytic domain starts a phosphorylation cascade
  • 3 subtypes: guanylate cyclase (few), tyrosine kinase (majority in animals), serine/threonine kinase (many)
26
Q

Receptor guanylate cyclase

A
  • when activated catalyzes conversion of GTP to cGMP
  • cGMP acts as secondary messenger in signal transduction pathway
  • ie. atrial natriuretic peptides
27
Q

receptor serine threonine kinase

A
  • serine and threonine residues phosphorylated by protein, initiating a long phosphorylation cascade
  • ie. transforming growth factor beta
28
Q

receptor tyrosine kinases

A
  • phosphorylation of the receptor creates high affinity docking sites for the binding of specific intracellular signaling proteins
  • intracellular proteins bind between themselves, becoming phosphorylated and activated
  • often bind growth factors or insulin, and are involved in cell growth and proliferation
  • ie. Ras, GAPs, GNRP
29
Q

tryosine kinases and growth factor

A
  • activated Ras signals start amplification cascade/phosphorylation cascade
  • MAP-kinase phosphorylates a variety of target proteins (MAPK=mitogen activated protein kinase
  • mutation of this receptor and transduction pathway can cause cancer, due to its effect on cell growth and metabolism
30
Q

Vascular endothelial growth factor (VEGF) receptors

A
  • tryosin kinase receptors located in cell membrane of endothelial cells lining blood vessels
  • when activated by VEGF, induces cell proliferation and growth of new blood vessels (angiogenesis)
  • VEGF is produced by cells which are not receiving enough oxygen
31
Q

G-protein-coupled receptors (GPCR)

A
  • transmembrane receptors which interact with heterotrimeric G proteins
  • ligand bindings induces conformational change, causing the alpha subunit to release GDP and bind GTP
  • alpha and By subunit (aka G protein) become active and dissociate, allowing them to move through membrane to interact with ion channels or amp enzymes and initiate or mute a response
  • alpha subunit remains active until it hydrolyzes GTP, at which point it becomes inactive and reassembles with By
32
Q

speed of alpha subunit hydrolysis of GTP can be regulated

A
  • alpha subunits are slow GTPase

- RGS are proteins that control speed of a subunits’ hydrolysis of GTP, activating RGS speeds up hydrolysis

33
Q

GPCR signal transduction pathways

A
  1. a and By can stimulate ion channels to open or close, changing MP and ion concentration (ie. acetylcholine on cardiac cells)
  2. a and By subunits activate or inhibit amplifer enzymes such as adenylate cyclase, guanylate cyclase, phosphodiesterase, phospholipase
    ie. for cAMP signal trans. path. Gs activates adenylate cyclase and Gs inhibits it
    - can also regulate levels of cAMP to reg. levels of active PKA
34
Q

GPCR example: taste receptors

A
  • modified epithelial cells that release neurotransmitter onto afferent neurons
  • each receptor expresses more than one type of taste receptor protein
35
Q

G-proteins regulate activity of phosphodiesterase

A

dark: -Na+ gate channel maintained open by cGMP that bind on it
- Na+ enters the cell, contributes to resting value of Em

36
Q

G-proteins regulate Phospholipase C

A
  • phos. C breaks down PIP2 into DAG and IP3
  • DAG activates PKC, which initiates a phosphorylation cascae
  • IP3 releases Ca2+ from endoplasmic reticulum as a secondary messenger
37
Q

GPCR-Ca2+ activates calmodulin

A
  • some g-proteins open or close Ca2+ channels directly or indirectly
  • Ca2+ binds to calmodulin & binding 4Ca2+ activates calmodulin
  • activated calmodulin regulates over 100 cellular proteins
    ex: increased Ca2+activates calmodulin->activates CaM kinase II->phosphorylase tyrosine hydrolase->increase synth of catecholamines
38
Q

GPCR example: angiotensin receptor

A
  • hormone produced by liver that increases blood pressure
  • found in smooth muscles lining blood vessles and activates the subunit of G-proteins, activation phospholipase C
  • IP3 releases Ca2+ from the ER, stimulating muscle contraction=vasoconstriction
39
Q

Signal transduction pathways can interact with each other:

A
  • when bound to Ca2+, calmodulin interacts with adenylate cyclase, which produces cAMP
  • Ca2+-calmodulin can also interact with cAMP phosphodiesterase, which breaks down cAMP
  • cAMP activates PKAA, which can phosphorylate Ca2+ channels and pumps, increasing or decreasing their activity

Bio 361 (17 decks)

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