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Bio Chem: Term 1- Exam 1 > Term 1- Lec 7&8- Signal Transduction > Flashcards

Term 1- Lec 7&8- Signal Transduction Flashcards

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1
Q

The 4 categories of cell signaling

A

Autocrine, Paracrine, Endocrine, and Neuronal

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2
Q

Autocrine signaling

A

Short distance signaling that is meant for cells that are the same as the signaling cell. (Local distribution of ligand among cell population)

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3
Q

Paracrine signaling

A

Short distance signaling that is meant for different types of cells from the signaling cell. (Local distribution of ligand among cell population)

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4
Q

Endocrine signaling

A

Long distance signaling. Utilizes bloodstream to transport ligands long distances.

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5
Q

Contact-dependent signaling

A

Cells have a ligand attached to the surface which is mirrored by receptors on the target cells.

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6
Q

This signaling limits growth

A

Contact dependent signaling. This feature is often lost in cancer cells.

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7
Q

Type I Diabetes

A

Autoimmune. Insulin-producing (ß-pancreatic) cells are exhausted because signal is never received and the cells continue to produce the signal until they cannot anymore/told to quit forever

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8
Q

Type II Diabetes

A

Insulin is made, but target cells become less responsive. Insulin resistance.

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9
Q

Neuronal signaling

A

Specialized type of Paracrine signaling. Nerve to non-neuronal target cell. Signaling not meant for many cells and is often only delivered to one.

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10
Q

Long and short distance nerve signal travel occur where respectively?

A

Nerve signals travel long distances in axons and short distances across synapse.

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11
Q

The two phases of neuronal signaling

A
  1. Through the neuron via electric potential.

2. Signal to the target cell via neurotransmitters across synapse. (ie Acetylcholine)

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12
Q

Two mechanisms for Ligand Induced Signaling in cells

A
  1. Diffusion across the plasma membrane to activate intracellular receptors. (i.e. Steroid hormones)
  2. Binding and activation of cell surface receptors. (i.e. Insulin)
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13
Q

How do steroid hormones travel in the blood stream?

A

They require a transport protein because they are hydrophobic and not soluble.

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14
Q

What are the names of the 5 steroid hormones

A
  1. Testosterone
  2. Estradiol
  3. Progesterone
  4. Cortisol
  5. Aldosterone
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15
Q

In what type of cell and how is Nitric Oxide synthesized?

A

Arginine is acted on by Nitric Oxide Synthase (eNOS) in the endothelium to make NO

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16
Q

Why can NO only affect it’s surrounding cells?

A

It has a very short half-life, thus it cannot make it that far.

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17
Q

What is the purpose of NO?

A

To cause vasodilation

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18
Q

What are the three cell types involved in NO signaling

A

Nerve terminal, Endothelial cell, and Smooth m. (surrounding the endothelial cell of the blood vessel)

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19
Q

What is nitroglycerin’s role in vasodialtion?

A

Undergoes chemical conversion into NO, causing dialtion of the blod vessels in the heart.

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20
Q

The two types of transmembrane receptors extracellular ligands bind

A
  1. G-protein coupled receptor (GPCR)

2. Receptor tyrosine kinase (RTK)

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21
Q

Ligand binding of GPCR/RTK initiates

A

Phosphorylation cascades

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22
Q

Phosphate group transfer is what type of modification?

A

Covalent modification

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23
Q

This type of enzyme forms new phophate bonds

A

Kinases

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24
Q

This type of enzyme breaks phophate bonds

A

Phosphotases

25
Q

Kinase proteins transfer phosphates to what functional groups on which AAs?

A

The hydroxyl of Serine, Threonine, Tyrosine

26
Q

Where do kinases transfer the phosphate FROM?

A

The terminal phosphate of ATP

27
Q

The 4 targets of Kinases

A
  1. Other kinases
  2. Phosphatases
  3. Metabolic enzymes
  4. Transcription factors
28
Q

The two types of ligands that GPCR and RTK bind are:

A
  1. Encoded by genes

2. Produced through a series of enzymatic rxns

29
Q

Most growth factor bind to:

A

Receptor Tyrosine Kinase

30
Q

Molecules that activate their receptor

A

Agonists

31
Q

Molecules that interfere with receptor activation by it’s natural ligand

A

Antagonists

32
Q

Epinephrine and Glucagon both bind to what type of receptor. What do they affect?

A

GPCRs. They alter metabolism in the cell

33
Q

G∂-s

A

Activates Adenylate Cyclase

34
Q

G∂-i

A

Inhibits Adenylate Cyclase

35
Q

G∂-q

A

Activates Phospholipas C

36
Q

Adrenergic receptors

A

Bind to specific ligands to regulate metabolic processes

37
Q

The 3 main classes of adrenergic receptors

A

∂1, ∂2, and ß

38
Q

What is a ß subunits activity dependent on?

A

The G∂ proetin it is bound to.

39
Q

Cholera toxin ribosylates (adds ADP-ribose) what? What happens?

A

G∂-s. G∂-s cannot hydrolyze GTP, Adenylate cyclase remains active, cAMP continues to be produced

40
Q

Pertussis toxin ribosylates (adds ADP-ribose) what? What happens?

A

G∂-i. G∂-i cannot get rid of GDP, Adenylate cyclase activity cannot be produced, cAMP continues to be produced.

41
Q

cAMP increases the activity of

A

Protein Kinase A (PKA)

42
Q

What is the structure of PKA?

A

2 regulatory subunits and 2 catalytic subunits

43
Q

How does cAMP activate PKA?

A

cAMP binds to the regulatory subunits, which release the catalytic units

44
Q

What can PKA phosphorylate

A

It can phosphorylate the transcription factor for CREB (cAMP regulatory element binding protein) to regulate gene expression

45
Q

What enzyme deactivates cAMP, and how?

A

cAMP Phosphodiesterase. Unbinds the phosphate that makes it cyclic, turning it into low energy AMP

46
Q

The naming difference between the two types of GPCR pathways

A

G∂-s: activates Adenylate Cyclase

G∂-q: activates Phopholipase C

47
Q

What cleaves PIP2, and what is produced?

A

PIP2 is cleaved by PLC to create DAG (stays in membrane) and IP3.

48
Q

Role of Ca2+ in PLC pathway

A

Ca2+ acts as a second messenger. It is released via the IP3 signal, then it binds with PKC to activate it (PKC later connects to DAG at the membrane)

49
Q

How are cytoplasmic Ca2+ levels lowered?

A

Ca-ATPase in the ER membrane uses active transport to pump Ca2+ back intot he ER. This shuts down Ca2+ dependent signaling

50
Q

Calmodulin

A

Activated when bound to Ca2+. causes conformational changes in other proteins by “squeezing” them. Lacks enzymatic properties

51
Q

Calmodulin activates

A

CaM Kinase II.

52
Q

CaM Kinase activation cycle

A
  • Ca/Calmodulin wrap inactive CaM Kinase !! to activate it.
  • CaM Kinase II autophosphorylates
  • Once Ca levels drop, calmodulin becoves inavtive and unwraps from CaM Kinase II.
  • Phosphate attached to CaM Kinase II keeps the kinase ~50-80% active.
53
Q

General structure of RTK’s

A

Extracellular ligand binding site and Intracellular Tyrosine Kinase Domain

54
Q

Ras is what type of enzyme?

A

GTPase

55
Q

Where is Ras found in the cell?

A

Ras is anchored to the plasma membrane by a covalently attached lipid tail

56
Q

What stimulates Ras activity?

A

Guanine exchange factor (GEF) INFLUENCE (doesn’t do the work) GTP binding to Ras

57
Q

What down regulates Ras?

A

GTPase activating proteins (GAP) INFLUENCE (doesn’t do the work) the hydrolysis of GTP on Ras

58
Q

What type of protein is SOS and what recruits it to the membrane

A

SOS is a GEF. GRB2 recruits SOS so that it can activate Ras.

59
Q

Enzyme that catalyzes cAMP to AMP

A

cAMP Phosphodiesterase

Bio Chem: Term 1- Exam 1 (10 decks)

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