Cell Signaling and Signal Transduction- Exam 1 Flashcards

1
Q

Cell theory

A
  1. living organisms are made of cells
  2. cells are the building blocks of life
  3. all existing cells come from pre-existing cells
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2
Q

Signal input for cells

A

physical environment and other cells

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3
Q

Signal output from cells

A

extracellular matrix and signals to other cells

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4
Q

What do signal transduction pathways do?

A

regulate transcription factor and other cytosolic metabolic pathways directly

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5
Q

Types of signaling

A
  1. direct

2. indirect

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6
Q

Direct signaling

A

signals pass through gap junctions which are made of six connexin proteins, this way small molecules can pass through without crossing plasms membranes. Example: calcium in glial cells

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7
Q

Autocrine signaling

A

the target cell is also the secreting cell

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8
Q

paracrine signaling

A

Signal released from a cell has an effect on neighboring cells.

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9
Q

hormonal signaling

A

a type of long-distance signaling where an endocrine excretes hormones in a blood vessel to travel to a target cell

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10
Q

synaptic signaling

A

a nerve cell releases neurotransmitter molecules into a synapse, stimulating the target cell

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11
Q

On and off

A

Phosphorylation ( on Ser. Thr. Tyr): kinases, phosphatases

G-proteins: GTP binding (activation), GTP hydrolysis (inactivation), arrestins (bind to G-protein)

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12
Q

Three stages of cell signaling

A
  1. Reception
  2. Transduction
  3. Response
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13
Q

Reception

A
  1. cytoplasmic receptors

2. transmembrane receptors

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14
Q

cytoplasmic receptors

A

signal molecules are hydrophobic and can permeate the plasma membrane, ideal for steroids such as estrogen, testosterone, and cortisol

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15
Q

transmembrane receptors

A

transmembrane proteins with extracellular binding domains that have large hydrophilic ligand binding to them and they do NOT cross the plasma membrane

  1. GPCRs
  2. Enzyme-linked receptors
  3. ligand-gated ion channels
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16
Q

GPCRs

A
  • very common
  • a frequent target for drug design (because it has amplification properties?)
  • seven transmembrane helices
  • three subunits: alpha, beta, gamma
  • termination: initially GTP hydrolysis, then GRK/arrestins
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17
Q

Enzyme-linked receptors

A
  • receptor tyrosine kinase
  • only one TM segment
  • ligand binding=dimerization\
  • trans-autophosphorylation on tyrosine residues( what does this mean bruh?)
  • termination by receptor internalization
  • ligand-mediated(ligand dimer), receptor-mediated(receptor dimer)
18
Q

ligand-gated ion channels

A

-IP3 and Ryanodine receptor (in neuro bio lecture)

19
Q

Transduction

A

Second messengers (example: cyclic AMP)

-the first messenger is the extracellular ligand, the second messenger is its intracellular surrogate

20
Q

Caffeine

A

Caffeine inhibits cAMP phosphodiesterase

21
Q

glucose example

A

glucose: released from liver cells, regulated by glucagon and/or epinephrine

GPCR
effector protein: adenylyl cyclase
protein kinase A
cytoplasmic and nuclear responses

22
Q

calcium example

A

calcium allows for buffering and hotspots and waves (e.g. glial cells)

larger concentration outside, in mitochondria, and in ER than in cytosol so when calcium is pumped into those regions an ATP powered pump is required.

23
Q

activation of calcium fluxes example

A
GPCRs or RTKs
effector protein: phospholipase C
Protein kinase C
second messengers:
calcium, IP3, DAG
24
Q

PIP2, DAG, IP3

A
PIP2= phosphatidyl inositol phosphate
DAG= diacylgylcerol
IP3= inositol triphosphate
25
Q

calmodulin example

A

in addition to protein kinase C, sometimes calcium uses CaM to affect the downstream activity of enzymes

CaM undergoes a conformational change by binding to four calcium ions

26
Q

calcium-induced calcium release in animals

A

what happens in brain glial cells

calcium ions can be used to release more calcium ions from the endoplasmic reticulum including from the sarcoplasmic reticulum of muscle cells

27
Q

CICR in plants

A

when too much water is released, the hormone abscisic acid is released, this triggers the influx of calcium ions into the vacuole which causes an outflux of the calcium ions from the vacuole which then causes water to follow out of the vacuole leading to a lower turgor pressure causing the guard cells to close the pore thereby inhibiting the loss of water

28
Q

amplification

A

cascade/amplification fo cAMP or PKA is when one ligand molecule triggers the production of infinitely more molecules downstream causing a much larger response

example: one molecule of epinephrine or glucagon can lead to the production fo 100,000 molecules of glucagon

29
Q

example of amplification

A
RTK
Ras/MAPk pathway
Ras: a single subunit G-protein
Ras stimulates cell division
Ras is mutated in about 30% of cancers such that it cannot hydrolyze GTP to GDP which leads to continuous cell division leading to cancer due to lack of cell division termination
30
Q

blood vessel dilation

A
  1. ACh receptor
  2. Calcium flux activates nitric oxide synthase
  3. nitric oxide synthase produces nitric oxide
    nitric oxide activates guanylyl cyclase which leads to the production of cGMP
  4. cGMP leads to the relaxation of blood vessels causing the blood to flow
31
Q

Viagra

A

Viagra inhibits cGMP phosphodiesterase

32
Q

Response

A

cytoplasmic and nuclear responses

33
Q

CRE and CREB

A
CRE= cAMP response element
CREB= CRE binding element
34
Q

CREB activation in the liver

A

leads to the transcription and translation of genes involved in gluconeogenesis

35
Q

specificity of responses

A

divergence: one molecule leads to two responses
crosstalk: respond to different signals and interact

example of crosstalk: PKA activates CREB phosphorylation but inhibits MAPk pathway that can also modulate CREB phosphorylation

36
Q

termination of cAMP

A

cAMP phosphodiesterase

37
Q

termination of cGMP

A

cGMP phosphodiesterase

38
Q

termination of protein-p

A

phosphatase

39
Q

termination of calcium ions

A

reuptake back into the endoplasmic reticulum or sarcoplasmic reticulum in the case of muscle cells

40
Q

cholera

A

toxin modifies G protein so that it cannot hydrolyze GTP leading to an inability to terminate the transduction pathway leading to constant high levels of cAMP which means that the patient experiences acute diarrhea, dehydration, and vomiting