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Nervous system > Cell-cell communication > Flashcards

Cell-cell communication Flashcards

1
Q

What are the 4 main classes of receptor?

A

Endocrine, paracrine, synaptic, contact dependent

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2
Q

What is contact dependent signalling?

A

Two cells in close proximity
Proteins on cell surface interact with eachother
Direct contact between cells
e.g. Gap junctions

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3
Q

Where are gap junctions found?

A

Both of coupled cells or cellular compartments

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4
Q

What is a homotypic connexon?

A

12 same connexins

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5
Q

What is a heterolytic connexon?

A

More than 1 connexin used

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6
Q

What is a homomeric connexon?

A

All 6 proteins are same connexin

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7
Q

What is a connexon?

A

6 connexins

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8
Q

Characteristics of Dextran based dye

A

Can’t pass through gap junctions

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9
Q

Characteristics of Lucifer yellow dye

A

Pass through gap junction into surrounding cells

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10
Q

What does GJA1 do?

A

Codes for Cx43, formation of craniometaphyseal dysplasia

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11
Q

What does GJA3 do?

A

Codes for Cx46, formation of cataracts

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12
Q

What does GJA5 do?

A

Codes for Cx40, formation of AF

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13
Q

What does GJB1 do?

A

Codes for Cx32, formation of Charcot-Marie-Tooth syndrome

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14
Q

Which connexions are expressed by atrial tissue?

A

Cx40 and Cx43

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15
Q

What is AF?

A

Channels contain mutated connexins/ decreased number of connexins with decreased channel activity
Channels form on lateral membrane
Heterogenous or decreased expression of connexins

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16
Q

What does Charcot-Marie-Tooth syndrome affect?

A

Peripheral nerves

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17
Q

Symptoms of Charcot-Marie-Tooth syndrome

A

Gait problems, numbness in lower limbs, reflexes lost at ankles and knees

18
Q

Most common form of CMT

A

X-linked form - CMT1X

19
Q

What is CMT1X caused by?

A

> 400 mutations in GJB1 gene that encodes gap junction protein Cx32
Fails to form functional channels
Decrease in conduction of AP

20
Q

Why does CMT lead to muscle atrophy?

A

In peripheral nerves, it decreases the conduction velocity of APs

21
Q

How to identify LQTS

A

Abnormal Qt interval on ECG

22
Q

Why does LQTS occur?

A

Decrease in depolarising cardiac membrane currents or increase in depolarising cardiac currents late in cardiac cycle

23
Q

Why might delayed depolarisation occur?

A

Reductions in either rapidly or slowly activating delayed repolarizing cardiac potassium current

24
Q

What causes prolonged depolarisation?

A

Persistent inwards leak of sodium

25
Q

What is cardiac dysfunction?

A

Mutations in heart Na+ and K+ channels lead to cardiac channelopathy called LQTS

26
Q

What is LQTS1 caused by?

A

Loss of function in KCNQ1 which codes for slow K channel

27
Q

What is LQTS2 caused by?

A

Loss of function in KCNH2 which codes for rapid K channel

28
Q

What is LQTS3 caused by?

A

Gain of SCN5A gene which encodes for sodium channel, causing failed inactivation of channel

29
Q

What is a missense mutation?

A

Nucleotide change means different codon and different amino acid

30
Q

How is SQTS formed?

A

Missense mutations cause increase of function of KCNH2 in SQTS1, KCNQ1 in SQTS2 and KCNJ2 in SQTS3

31
Q

What is Ras?

A

Monomeric GTP-binding protein

32
Q

How is RAs activated?

A
  • Most RTKs activate Ras - a monomeric GTP-binding protein (GTP-ase)
  • RTKs linked to enzymes - the enzyme is a kinase which phosphorylate molecules
  • Tyrosine kinases add phosphate to tyrosine
  • Ligand binds to receptor - often receptor is dimer and sometimes tetramer
  • Binding of ligand stabilizes dimer, receptors phosphorylate each other and this allows adaptor molecules to bind which determine downstream signaling
  • Adaptor molecules recruit Ras guanine exchange factor (GEF) to catalyze conversion of Ras from inactive GDP bound form to active GTP bound form
  • This then signals to other molecules
  • Most RTKs activate Ras signaling molecule
33
Q

What is Herceptin used to treat?

A

Breast cancer - increased signalling downstream of RTLK

34
Q

How is EGFR treated?

A

Tyrosine kinase inhibitors

35
Q

What cancer is EGFR linked to?

A

Colorectal cancer

36
Q

What cancer is ERBB2 linked to?

A

Breast cancer

37
Q

How are GPCRs activated?

A
  • Absence of ligand when GPCR is inactive - GPCR = G-protein coupled receptors
  • GPCRs bind to G proteins which are a trimeric protein, alpha, beta and gamma subunits
  • G protein bind GDP when GPCR is inactive but binds GTP when active, also causes trimeric protein to split (alpha and beta/gamma subunits) and two signals
  • Alpha, beta/gamma unit and G-protein all exert signals
  • G protein hydrolyses GTP to GDP to inactivate GPCR
38
Q

How are GPCRs inactivated?

A
  • G protein hydrolyses GTP to GDP to inactivate GPCR
  • E.g. target protein is adenyl cyclase
  • ATP -(adenyl cyclase)→ cAMP -(cAMP phosphodiesterase)→ 5’AMP
  • Alpha subunit hydrolyses GDP to GDP and then reassembles with beta/gamma subunits
39
Q

Symptoms of cholera

A

Severe water loss, vomiting and muscle cramps

40
Q

What microorganism causes cholera?

A

Vibrio cholera

41
Q

How does cholera cause water loss?

A
  • Cholera toxin binds to enterocytes (epithelial cells in GIT) and the toxin enters the cell by endocytosis
  • Toxin formed form A and beta units (B assists body entry)
  • The A subunit stimulates fluid secretion by activating cAMP formation
  • A subunit activates Gsa
  • A subunit catalyses transfer of ADP ribose from NAD to arginine group on alpha subunit of G-alpha-S sub molecules
  • ADP ribosylation inhibits the ability of G-alpha-S to hydrolyse GTP and inactivate the molecule - this means that G protein is ‘locked’ in active position and this maintains a persistent activation of adenylate cyclase and formation of cAMP which in turn activates protein kinase A (PKA)
  • G protein is in GTP-bound form
  • Stimulates adenylate cyclase
  • cAMP produced activates PKA
  • CFTR is phosphorylated and activated
  • Efflux of Cl- ions (and sodium ions and water)
  • Due to charge across membrane, sodium ions pass out of cell and water is lost due to change in osmotic gradient
42
Q

What does defective GPCR signalling result in?

A
  • Decrease in production of G proteins: pseudohypoparathyroidism (genetic loss of G(s) protein a subunits results in no response to parathyroid hormone)
  • Decreased signal initiation: whooping cough (pertussis)(a bacteria toxin adds ADP-ribose to the receptor-binding C-terminal tail of G(i) protein alpha subunits, causing reduced responsiveness of G proteins to receptor activation
  • Increased signal initiation: essential hypertension - mutations in G protein beta subunits
  • Defective signal termination

Nervous system (24 decks)

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