CBG.10 Flashcards

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1
Q

What are the 4 main types of signalling pathways?

A

Autocrine
Paracrine
Endocrine
Juxtacrine

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2
Q

explain how autocrine pathway works, giving an example?

A

autocrine is self stimulation, so it is short distance. for example interleukin 2 from a stimulated T cell causes the T cell to proliferate monoclonally

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3
Q

What is the paracrine pathway?

A

paracrine is signalling between local cells, for example neuronal signalling, and many growth factors

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4
Q

explain the endocrine pathway

A

the endocrine pathway is signalling between distant cells, for example insulin signalling via the blood in mammals, or gibberellin via xylem in plants

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5
Q

explain the juxtacrine pathway

A

juxtacrine pathway is direct contact between cells, often via membrane bound ligands, for example Th cell stimulation of B cells, also gap junctions and plasmodesmata are other good examples.

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6
Q

what three different effects can acetyl choline have on different cells?

A

heart muscle cells- decreases the contraction rate of the heart muscle
salivary glands - causes secretion of enzymes
skeletal muscle cells - causes contractions

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7
Q

what are the five main classes of cell signalling recptors?

A
  • nuclear receptors
  • G protein coupled receptors
  • enxyme coupled receptors
  • ligand gated ion channels
  • adhesion receptors
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8
Q

give an example of a ligand gated ion channel

A

Nicotinic ACh recptor is a ligand gated Na+ channel

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9
Q

where can you find Nicotininc ACh receptor Na+ channels?

A

musculoskeltal junctions

CNS synapses

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10
Q

what are the agonists and antagonists for the Nicotininc ACh receptor Na+ channel?

A

Nicotine is the agonist - it opens the channels

Curare is the antagnoist - it blocks the channels, i.e paralysis

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11
Q

what are nuclear receptors?

A

They are ligand modulated gene regulatory proteins, which bind hydrophobic signalling molecules

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12
Q

Give three examples of hydrophobic signalling molecules for nuclear recptors

A

Oestrogen - a sex steroid hormone
Retinoic acid - vitamin A acid, also a morphogen
Thyroxine - human growth hormone

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13
Q

once nuclear receptors have bound to their ligand hormones what are they able to do?

A

Nuclear receptors are then able to bind to DNA

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14
Q

How are steroid receptors antagonists used in medicine?

A

They are used for chemotherapy for treatment of breast cancer. Most breast cancer cells require oestrogen to divide, the steroid recptor antogonist tamoxifen blocks oestrogen receptors, therefore stopping cell division and proliferation.

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15
Q

what is tamoxifen used for in drug treatment?

A

it is used to treat breast cancer as it is able to block oestrogen recptors. Most breast cancer cells require oestrogen to divide.

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16
Q

when a G protein is bound to GTP is it in its active or weak form?

A

active

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17
Q

when a G protein is bound to GDP is it in its active or weak form?

A

weak

18
Q

what are G proteins?

A

weak GTPases, which are time delayed biological switches

19
Q

what does GAP stand for?

A

GTPase activating protein

20
Q

what is the function of GAP?

A

it increases the GTPase activity of a G protein

21
Q

what does GEF stand for?

A

guanine nucleotide exchange factor

22
Q

what does GPCR stand for?

A

G-protein coupled receptors

23
Q

what is the function of GPCRs?

A

they act as ligand modulated GEFs, for example for adrenaline

24
Q

what are GPCRs?

A

they are proteins which are G-coupled receptors,

which have 7 ubiquitous transmebrane receptors

25
Q

How do GPCR amplify their signal?

A

they act through secondary messengers such as cAMP and IP3/DAG

26
Q

What happens when adrenaline binds to a G coupled receptor?

A

It results in a chain of events - firstly it causes the ADP bound to the alpha subunit of the G coupled receptor to convert to ATP
The alpha ATP complex dissasosiates from the GPCR and binds to adenylate cyclase
Adenylate cyclase converts ATP to cAMP
cAMP binds to AK - PKA complex
PKA dissasosiates from the complex
PKA phosphorylates CREB, a TF
CREB passes through a nuclear pore into the nucelolus and induce transcription

27
Q

what is the function of adenylate cyclase?

A

converts ATP to cAMP

28
Q

what are three characteristics of the cAMP signalling system?

A

Amplification
Sharp response
Short duration

29
Q

how is cAMP removed from the cell?

A

cAMP allows PKA release, PKA activates phosphodiesterase which rapidly removes cAMP

30
Q

how many cAMP are needed to release PKA?

A

4

31
Q

what is amplification?

A

small signal leading to a much larger signalling cascade

32
Q

can protein kinases act as a biological switch?

A

yes. phosphorylation by protein kinases acts as a biological switch, activating proteins, e.g tyrosine or serine/threonine

33
Q

Receptor tyrosine kinases

A

receptor tyrosine kinases are single pass enzyme coupled transmebrane receptors

34
Q

what are the characteristics of the extracellular receptor domain of RTK

A

cysteine rich or globulin like

35
Q

give 2 examples of ligands which act on RTK

A

epidermal growth factor

insulin

36
Q

once a ligand has bound to a RTK what happens next?

A

the RTK dimerise and then acts through phosphorylation cascades

37
Q

which transcription factor is activated/phosphorylated as a result of epidermal growth factor binding to EGF RTK?

A

Myc

38
Q

what does Myc bind to?

A

enhancer box sequence

39
Q

what does a mutation in Ras likely result in?

A

cancer

40
Q

what is the cause of neurofibromatosis?

A

Ras-GAP mutation

41
Q

which membrane bound receptor is involved in most growth factor cascades?

A

Receptor tyrosine kinases