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C Bio > Cell Signalling III > Flashcards

Cell Signalling III Flashcards

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1
Q

PRO tyrosine kinase

A

phosphorylates target PROs at particular tyrosines

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2
Q

what is the diff b/w a RTK & GPCR?

A

GPCRs have 7 transmembrane segments

RTKs have a single transmembrane segment, but each RTK functions as a dimer so it has a total of 2

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3
Q

RTKs are involved in the regulation of what processes?

A

Growth (growth factor receptors), trigger mitosis

Cell division (defects lead to cancer)

Cell survival and death (programmed)

Cell attachments, migrations

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4
Q

what are the 2 ways RTKs dimerize?

A

1 ligand binding to both monomers (ligand causes dimerization)

each monomer binds their own ligand & the 2 monomers come together

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5
Q

what does dimerization trigger in RTKs?

A

auto-phosphorylation

the 2 monomers phosphorylate each other

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6
Q

when is insulin produced?

A

when blood glucose increases

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7
Q

where is glucose uptaken?

A

liver

muscle

fat cells

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8
Q

what effect does insulin have on BG?

A

decreases BG

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9
Q

what process is inhibited in the uptake of glucose?

A

gluconeogenesis

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10
Q

what cells make insulin?

A

beta

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11
Q

what cells make glucagon?

A

alpha

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12
Q

what does glucagon induce?

A

gluconeogenesis

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13
Q

what is unusual about the insulin receptor?

A

remains as a dimer before binding the ligand

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14
Q

structure of insulin receptor?

A

heterodimer

2 alpha chains - extracellular, ligand binding

2 beta chains - transmembrane, kinase activity (RTK)

alpha & beta are linked through disulfide bridges

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15
Q

what 2 processes occur when insulin binds to the receptor?

A

auto-phosphorylation

phosphorylation of the Insulin Receptor Substrate (IRS)

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16
Q

steps of insulin RTK

A
  1. Insulin (ligand) binds on the exterior of the cell to the alpha chains
  2. Tyrosine kinase activity Auto-phosphorylation & phosphorylation of Insulin Receptor Substrate (IRS)
  3. Other PROs bind & are activated by phosphorylated tyrosines on the RTK & IRS
  4. Stimulation of glycogen synthesis:
    a. Cell proliferation (growth factor)
    b. PRO kinase B induces movement of glucose transporters to move to the PM by vesicle movement
    i. Glucose is taken up via facilitated diffusion
    ii. Glucose is phosphorylated upon entry into the cell (maintain the gradient)
    iii. Glycogen synthesis is stimulated
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17
Q

what events occur in diabetes? & how?

A

high levels of glucose in blood

loss of glucose in urine

excessive loss of water from frequent urination

high blood pressure

BG will remain in the blood & cause the pancreas to work harder to excrete it, so it does it by urination, glucose acts as a solute in the blood & pulls water out

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18
Q

type I diabetes

A

no insulin is produced by the pancreas

auto-immune disorder where beta cells producing insulin are destroyed

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19
Q

type II diabetes

A

insulin resistance in cells that should take in glucose

beta cells are still present, but the receptors fail

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20
Q

what is the diff b/w diabetes I & II?

A

I –> no beta cells, no insulin

II –> beta cells, insulin produced

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21
Q

what causes the loss of sensitivity in diabetes?

A

Faulty receptor

Faulty intracellular signaling (downstream events fail to occur properly)

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22
Q

what is a method of restoring insulin sensitivity?

A

removal of PRO tyrosine phosphatase (PTP) through gene knockout

23
Q

what occurred in PTP gene knockout mice?

A

muscle cells remained with activated receptors where signaling is continually occurring –> glucose levels remained low

mice were fed rich diets without becoming obese

24
Q

growth factor/cytokine

A

naturally occurring substance capable of stimulating cellular growth, proliferation and cellular differentiation

25
Q

epidermal growth factor (EGF)

A

growth factor that plays an important role in the regulation of cell growth, proliferation, and differentiation by binding to its receptor EGF

26
Q

what does an EGF activate/signal to occur?

A

changes in gene expression, prepare for mitosis

transcription factors are activated, genes involved in proliferation are transcribed

27
Q

how is an EGF signal turned off?

A

EGFR is ubiquitinated

sent to lysosome for destruction or goes back to the PM

28
Q

when is Ca2+ the 1st & 2nd messenger molecule? & what does this accomplish?

A

Ca2+ induced Ca2+ release

rapid amplification & coordination

29
Q

Ca2+ induced Ca2+ release

A

Ca2+ released from internal vesicles in response to Ca2+ channels being placed on the cell surface

30
Q

what are the types of Ca2+ responses?

A

voltage dependent channels in nerves & some muslces

receptor-mediated Ca2+ channels

31
Q

how does calcium prevent polyspermy?

A

Sperm burrow in with lysosomal enzymes

Once the sperm hits the membrane, it triggers the influx of calcium event

Vesicles move the perimeter of the egg preventing entry of sperm done through Ca2+ induced Ca2+ release

32
Q

Steps of Ca2+ induced Ca2+ release

A

Ca2+ enter through voltage gated channel on PM

Ca2+ binds to ryanodine receptor on SER

Ca2+ released from the SER through the ryanodine receptor (down conc gradient)

Ca2+ bind to calmodulin when out of the SER

Activated calmodulin binds to many other effectors

Effects include:
Movement of vesicles to the perimeter of the egg to prevent polyspermy
Pumping of Ca2+ out of the cytoplasm to the SER, the vacuole & exterior of the cell (active transport)

33
Q

ryanodine receptor serves as what 2 functions?

A

receptor & channel

34
Q

Nitric oxide (NO)

A

inorganic gas, can act as an extracellular messenger & 2nd messenger

35
Q

what does NO induce the production of?

A

cGMP

activates guanylyl cyclase to make cGMP

36
Q

where is NO synthesized?

A

NO synthase within cells

37
Q

what type of hormone does NO act as?

A

paracrine & autocrine

38
Q

NO’s role in the blood

A

acetylcholine can induce NO synthase

Production of cGMP causes smooth muscle cells to relax … slows blood flow by relaxing arteries

39
Q

what is given to patients with heart probs & why?

A

nitroglycerine

produces NO to relax arteries

40
Q

how does viagra have its effect on the body?

A

viagra is a drug that inhibits cGMP phosphodiesterase to relax blood vessels

41
Q

how does the amplification of a signal work?

A

one receptor can activate several GPROs & each GPRO can activate several effector molecules

42
Q

what are the 2 kinds of coordination?

A

spatial coordination

coordination of diff responses

43
Q

spatial coordination

A

throughout the cell by diffusion of 2nd messengers (ex: cAMP, Ca2+ –> small molecules that diffuse fast)

44
Q

coordination of diff responses

A

a number of diff enzymes have to work together to accomplish metabolic pathways

(ex: cell division –> needs a lot of things prepared)

45
Q

what dies each signaling pathway provide?

A

an opportunity for cross talk b/w diff signaling pathways

46
Q

what does the cell accomplish in cross-talk?

A

integrates information from many different signaling pathways to initiate an appropriate response

47
Q

what is an ex of when cross-talk signals interfere?

A

when epinephrine induces gluceogenesis, PKA can inhibit the growth factor signaling pathway

epinephrine overrides growth factors, when there’s a stressful situation survival is more important than growth

48
Q

convergence

A

2 receptors cause the same secondary signal to be activated –> 2 pathways converge to give one unified response

Ex: glucagon & epinephrine hit 2 diff receptors but induce the same response
49
Q

divergence

A

one ligand has several effects or one signal propagates several responses

Ex: PKA turns on 3 diff PROs in gluceogenesis
50
Q

crosstalk

A

pathways interconnect

2 pathways from diff hormones give confusing messages (work together or in opposition) 

Cell receives combos of signals that can trigger diff signaling pathways
51
Q

what are exs of compartmentalization of a signal?

A

PKA is held in place by special binding PROs called AKAPs

scaffolding PROs

52
Q

how a cell responds to a signal depends on: (3)

A

number of receptors

number of other signals

type of cell (b/c different cells have different downstream signaling molecules)

53
Q

how does the cell compensate for having so many GPCRs but so little G PROs?

A

the same intracellular signaling pathway causes diff effects in diff cell types b/c the diff cells have diff downstream PROs to respond to the signal

C Bio (30 decks)

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