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Foundations Test 1 > Signal Transduction > Flashcards

Signal Transduction Flashcards

1
Q

What is signal tranduction

A

Way for signal from outside to affect function via amplification

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2
Q

Flow chart of tranduction

A

Signal —– reception —- transuction —– response

Amplification from reception to transduction

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3
Q

Epinephrine binds

A

7 transmembrane domain protein known as a G-protein coupled receptor

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4
Q

G-protein coupled receptor that epinephrine binds to interacts with ____ and what does it do?

A

Heterotrimeric G protein that has 3 subunits

Will activate another enzyme

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5
Q

Epinephrine signaling pathway

A

Epinephrine binds B adrenergic receptor…G-protein phorphorylated and loses beta and gamma subunits…GTP with alpha unit binds to adenylate cyclase…adenylate cyclase converts ATP to cyclic AMP….cyclic AMP activates protein kinase A…PKA then phosphorylates serine residues on target proteins

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6
Q

Adenylate cyclase rxn

A

ATP —- cyclic AMP

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7
Q

Cyclic AMP rxn

A

Protein Kinase A ——- activate protein Kinase A

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8
Q

Protein kinase A regulated by (what mechanism)

A

Autoinhibition

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9
Q

1st part of cAMP cascade termination

A

Epinephrine dissociates…bARK phosphorylates tail of receptor…this binds B-arrestin that blocks binding of new heterotrimeric proteins

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10
Q

bARK name and function

A

Beta-adrenergic-receptor kinase

Phosphorylates receptor using ATP to allow recruitment of B-arrestin

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11
Q

B-arrestin function

A

Blocks new heterotrimeric G-proteins from binding receptor

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12
Q

Second part of cAMP termination

A

GTP associated G-protein with adenylate cyclase undergoes hydrolysis to make GDP…beta and gamma subunits return and molecule dissociates

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13
Q

What happens to cyclic AMP during termination

A

Hydrolyzed by cyclic AMP phosphodiesterase to AMP

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14
Q

Cholera enzyme rxn

A

Catalyzes ADP-ribosylkation of G-protein alpha subunit

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15
Q

Cholera mechanism of disease

A

Internal GTPase is blocked and left in on state…overproduction of cAMP and PKA leads to membrane ion transport protein phosphorylation…loss of ions and water leads to diarrhea
Intestinal

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16
Q

Pertussis rxn

A

ADP-ribosylation of the heterotrimeric subunit (which is inhibitory)

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17
Q

Pertussis mechanism of disease

A

Blocks exchange of GTP for GDP and therefore heterotrimeric subunits with GDP remain off…adenylate cyclase, once on, is never turned off
Respiratory tract

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18
Q

Enzyme-linked receptors

A

Transduce an external signal across membrane by generating intramolecular enzymatic activity

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19
Q

Cytokine receptors

A

Receptor has NO intrinsic enzymatic activity and a second protein is activated by the binding of the cytokine or signaling agent

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20
Q

Cytokine receptors often activated

A

Jak-STAT signaling

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21
Q

Insulin receptor structure

A

Dimer with two extracellular alpha for binding pocket of insulin…each B subunit contains kinase omain

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22
Q

Binding of insulin results in

A

Cross-phosphorylation and activation of the receptor

23
Q

Phosphorylated insulin receptor sites act as binding site ofor

A

IRS-1

24
Q

IRS-1 allows binding of

A

PI-3K

25
Q

PI-3K rxn

A

PIP2 —- PIP 3

26
Q

PIP3 function

A

Activates PIP 3-dependent kinase

27
Q

PIP 3-dependent kinase function

A

phophorylates and activates kinases such as AKT

28
Q

Insulin pathway

A

Receptor phosphorlates IRS…IRS binds PI3K…PI3K converts PIP2 to PIP3 via phosphorylation…PIP3 activates Pip3 dependent kinase…PIP3 dependent kinase phosphorylates AKT to activate it

29
Q

insulin structures

A

Dimer linked by 2 disulfide

30
Q

Type 1/2 diabetes onset, age, body, ketoacidosis

A

1 - sudden, any age, thin or normal, common

2 - gradual, adults, often obese, rare

31
Q

Type 1/2 diabetes autoantibodies, andogenous insulin, concordance in ID trwins, prev

A

1 - usually present, low or absent, 50%, less

2 - Absent, Normal increased or decreased , 90%, more prevalent

32
Q

Type 1 diabetes symptoms

A 
Polyuria
Polydipsia 
Polyphagia
Fatigue/weakness
Irratability
Blurred vision
Increased yeast infections
33
Q

Characteristics of T1DM

A

Hyperglycemia caused by increased gluconeogenesis and insufficient glucose absorption
Ketosis from accumulation of free fatty acids

34
Q

Underlying cause of T1DM

A

Autoimmune disorder leads to destruction of B cells in pancreas

35
Q

T2DM predominant cause

A

Obesity

36
Q

What happens in T2DM

A

Eat…food becomes glucose…pancreas secretes insulin…cells are resistant so glucose not absorbed…still feel hungry…eat again…hyperglycemic…hyperinsulinemic…eventual B cell death

37
Q

Metformin

A

Improves sensitivity of body tissues to insulin…also lowers glucose production in liver but not actual blood sugar

38
Q

Sulfonylureas

A

Increase insulin secretion

39
Q

Thiazolidinediones

A

Increase insulin sensitivity but have risks

40
Q

Adipokines

A

Cytokines secreted by adipose tissue

41
Q

Leptin function

A

Tells brain how much body fat you have (or how much energy storage you have)

42
Q

What happens to leptin after a few days of overeating?

A

Sets new baseline level as very hig h

43
Q

Leptin acts on what in brain?

A

Hypothalamus

44
Q

Insulin effect on leptin

A

Increases secretion

45
Q

Leptin effect on sinulin

A

Reduce secretion and gene expression

46
Q

How does leptin signal reach insulin

A

Directly from leptin on B cells

Via autonomic nervous system

47
Q

Leptin effect on pancres

A

Increase B cell proliferation

48
Q

Leptin signaling

A

Leptin binds to receptor, resulting in Jak-Kinases cross-phosphorylating tyrosine residues…STATs dock on tyrosines and are phosphorylated by JAK enzymes…STAT travels to nucleus to affect gene transcription

49
Q

Effect of STAT in nucleus

A

Decreased appetite and increased energy expenditure

50
Q

Leptin insensitivity

A

Leptin receptor unresponsive to STAT signaling decreases

51
Q

Results of decreased STAT signaling

A

Increased appetite
Decreased energy expenditure
Increased obesity and diabetes risk

52
Q

Repeated activation of _______ leads to leptin resistance

A

SOCS3

53
Q

Foxo1 is a product of

A

AKT - from insulin pathway

54
Q

How to leptin and insulin pathways interact in T2DM?

A

Stat5 and STAT3 normally phosphrylate Foxo1 in the nucleus which leads to B cell health…if STAT3 and STAT5 are diminished, then less FOXO1 and worse B cell health

Foundations Test 1 (15 decks)

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