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Biochemistry > Lecture 7 & 8 Signaling > Flashcards

Lecture 7 & 8 Signaling Flashcards

1
Q

Signaling through cell to cell contact

Give examples

A

Contact signaling
(antigen presentation to t cells, membrane bound signal molecule)
communication between muscle cells, through second messengers)

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2
Q

Short distance signaling between different cells

Give example

A 
Paracrine signaling
(Cytokines, low concentration,  short half life, high affinity)
(Neurotransmitters, high concentration, short half life, low affinity)
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3
Q

Short distance signaling involving the same (or same type of) cell(s)
Give example

A

Autocrine signaling

Prostaglandin

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4
Q

Long distance signaling between endocrine glands and target cells

A 
Endocrine signaling
(Long half life due to long distance to travel)
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5
Q

ACh receptors located in skeletal muscle, type of receptor?

A

Nicotinic ACh receptor

Na+/K+ channel (ion channel receptors)

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6
Q

ACh receptors located in heart muscle, type of receptor?

A

Muscarinic ACh receptor

G protein-linked receptor

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7
Q

enzyme that degrades excess ACh

A

Acetylcholine esterase

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8
Q

Autoimmune neuromuscular disease (muscle weakness, muscle fatigue) Autoantibodies against the nicotinic ACh receptors

      - inhibit ACh binding to the receptor
      - enhance the internalization and destruction of the receptor
A

Myasthenia gravis

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9
Q

How to manage Myasthenia gravis?

A

Increase ACh signaling, Since the autoantibodies attack nicotinic ACh receptors, not enough signaling is happening. Inhibiting acetylcholine esterase will increase signaling.

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10
Q

What medications help treat myasthenia gravis?

A

-stigmine drugs
pyridostigmine, neostigmine
and physostigmine, all reversible.
They inhibit ACh esterase

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11
Q 
How do organophosphates (Certain insecticides
Nerve gases (Sarin, VX)) cause death?
A

They inhibit ACh esterase causing too much

ACh to be in the synapse, too much signaling.

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12
Q

How do you treat exposure to organophosphates (Certain insecticides Nerve gases (Sarin, VX))?

A

Decrease signaling of ACh by inhibiting muscarinic ACh receptors.

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13
Q

What medication help treat exposure to organophosphates (Certain insecticides Nerve gases (Sarin, VX))?

A

Atropine, which inhibits ACh receptors.

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14
Q

Where are Type I and III nuclear receptors located and what do they bind?

A

Type I and III receptors are localized in the cytosol, they bind with steroid hormones (Cortisol, Aldosterone Progesterone, Testosterone, Estradiol)

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15
Q

An anti-inflammatory steroid drug that acts through this signaling pathway. It is ~ 30 times more efficient than the naturally occurring steroid hormone, cortisol.

A

Dexamethasone

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16
Q

Where are Type II nuclear receptors located and what do they bind?

A

Type II intracellular receptors are localized in the nucleus

They bind with Vitamin D3, retinoic acid, thyroid hormone, and fatty acids

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17
Q

These drugs activate an intranuclear fatty acid receptor (PPARγ) and increase insulin sensitivity. They are used to manage Type II diabetes.

A

Thiazolidinediones (TZDs)

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18
Q

What drugs use nitric oxide to cause vasodilation

A

nitroglycerin, nitroprusside and hydroxyurea

19
Q

G protein linked receptors that Regulate heart-rate, smooth muscle constriction, metabolism

A

Adrenergic (epinephrine, norepinephrine) receptors

20
Q

Dopamine receptor is a major pharmacological target in treatments of which diseases?

A

Schizophrenia, Parkinson’s disease, Attention deficit disorders.

21
Q

Enzyme that adds phosphate group

Enzyme that removes phosphate group

A

Kinase (requires ATP)

Phosphatase

22
Q

What type of receptors use second messengers?

A

G-protein linked receptors

23
Q

What do second messengers activate?

A

Protein kinases

24
Q

Gα subunit, stimulates adenylyl cyclase, increases cAMP

A

Gs,α

25
Q

Gα subunit, inhibits adenylyl cyclase, decreases cAMP

A

Gi/o,α

26
Q

Gα subunit, activates phospholipase Cβ, increases DAG, IP3 and Ca2+

A

Gq,α

27
Q

Gα subunit, stimulates phosphodiesterase, decreases cGMP

A

Gt,α

28
Q

Stimulatory hormones

A

Epinephrine, Glucagon, Adrenocorticotrophic hormone (ACTH)

29
Q

Inhibitory hormone

A

Prostaglandin E1 (PGE1), Adenosine

30
Q

This toxin transfers an ADP-ribose group to a stimulatory Gsα subunit (post-translational modification).

  • The adenylyl cyclase remains constantly active (lots of cAMP)
  • It causes extreme salt and water efflux from gut epithelial cells to the lumen, causing diarrhea.
A

Cholera toxin

Stimulates stimulator

31
Q

This toxin transfers an ADP-ribose group to an inhibitory Giα subunit (post-translational modification).

  • Adenylyl cyclase cannot be inhibited (lots of cAMP).
  • It leads to increased mucus secretion in airway epithelium.
A

Pertussis toxin

Inhibites inhibitor

32
Q

How does cAMP activate protein kinase A

A

Binding cAMP to the regulatory subunits dissociates the subunits of protein kinase A and activates the catalytic subunits. (The catalytic subunits then phosphorylate target proteins (using ATP).)

33
Q

α1-adrenergic receptors on smooth muscle cells mediate vasoconstriction through this mechanism.

A

Protein phospholipase Cβ

34
Q

These are used in decongestants and eye drops

A

α1-adrenergic agonists

35
Q

Role of phosphodiesterase

A

Activated by rhodopsin from phototransduction. Phosphodiesterase hydrolyzes cGMP to GMP (degrades 2nd messenger!) The fall in cGMP levels closes cGMP-gated ion channels

36
Q

How does caffeine increase heart rate?

A

Caffeine is an antagonist of the adenosine receptor and increases heart rate. (Adenosine lowers heart rate)

37
Q

Receptors used by many growth factors and insulin
-Can activate multiple intracellular signaling pathways

   - Mitogen activated protein (MAP)-kinase pathway.
   - Phospholipase Cγ (PLC γ)  pathway.
   - Phosphatidylinositol-3’-kinase (PI 3-kinase) pathway.
A

Tyrosine kinase receptors

38
Q

Glucose transporter (GLUT4) is shuttled to the plasma membrane to enhance glucose uptake by muscles and adipose tissue in this pathway

A

PI 3-kinase pathway . (PI3K)

39
Q

Pathway where transcription and translation is regulated in for genes necessary for glucose metabolism

A

MAP-Kinase pathway (MAPK)

40
Q

Pathway where excess glucose can be stored in glycogen or fatty acids (lipids)

A

Phospholipase Cγ pathway (PLCγ)

41
Q

Activating an intracellular peroxisome proliferator activated receptor (PPAR) induces the transcription of genes involved in glucose metabolism, treatment for what disease?

A

Type II diabetes

42
Q

What enzyme destroys cAMP, cGMP

A

Phosphodiesterase

43
Q

Autoantibodies stimulate TSH receptors in the thyroid gland  increased thyroid hormone production

Thyroid hormone downregulates TSH production but has no effect on autoantibodies

The negative feedback does not work  runaway thyroid gland

What disease is this?

A

Hyperthyroidism (Grave’s disease)

Biochemistry (9 decks)

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