Midterm 3 Flashcards

1
Q

What are the general principles of extracellular signal to cellular response?

A
  1. Synthesis of signaling molecule
  2. Release of the signaling molecule via exocytosis
  3. Transit of signaling molecule to the target cell
  4. Binding of signaling (ligand) to a protein receptor on the target cell
  5. Binding of ligand to receptor results in a conformational change of the receptor
  6. Receptor initiates one or more intracellular pathway (cellular function, metabolism, gene expression, shape, movement)
  7. Deactivation of receptor
  8. Removal of ligand
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2
Q

What are the 4 types of intercellular signaling?

A
  • endocrine
  • paracrine
  • autocrine
  • juxtacrine
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3
Q

What are the three main classes of cell surface receptors?

A
  • G-protein coupled (GPCR)
  • Enzyme-linked
  • Ion Channel-linked
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4
Q

What are the two basic types of cell signaling? (Receptors)

A
  • cell surface receptors

- intracellular receptors

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5
Q

What are the properties of intracellular receptors?

A

-small hydrophobic signaling molecules can diffuse across the plasma membrane and bind to receptor proteins either in the cytoplasm or nucleus

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6
Q

What are the two types of intracellular receptors?

A
  • cytoplasm

- nucleus

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7
Q

What are second messengers?

A

-small substances that activate (or inactivate) specific proteins

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8
Q

What are two types of signaling pathways shown after the binding of a ligand to a receptor?

A
  • receptor binds to an effector and generates a soluble and diffusable intracellular second messenger
  • recruit proteins to their intracellular domains at the plasma membrane
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9
Q

What is a GAP?

A

GTPase-activating protein

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10
Q

What is a GEF?

A

Guanine nucleotide exchange factor

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11
Q

What are the 3 subunits of a G protein?

A
  • alpha
  • beta
  • gamma
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12
Q

What does the G protein act as when it couples with the receptor? (What part couples?

A
  • alpha subunit

- acts as a GEF

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13
Q

Where is the amino terminus of the G protein-coupled receptor located?

A

On the outside of the cell

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14
Q

What does GRK stand for?

A

G protein coupled receptor kinase

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15
Q

What is the general structure of a G protein-coupled receptor?

A
  • 7 transmembrane alpha helixes
  • ligand binding site
  • cytosol is portion that interacts with G proteins
  • GRK phosphorylation sites for receptor downregulation
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16
Q

What is a process of receptor inactivation?

A

-desensitization (block active receptors from turning on additional G proteins)

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17
Q

What is the process of desensitization?

A
  • G protein coupled receptor kinase phosphorylation a GPCR
  • Proteins called arrestins compete with G proteins to bind GPCRs

-GRK phosphorylates so that arrestin can bind and self regulate

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18
Q

What does adenylyl cyclase do?

A
  • removes two phosphates as pyrophosphate

- converts AMP to cyclic AMP (to act as second messenger)

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19
Q

What does cAMP do?

A

Activates protein kinase A

20
Q

Where does Protein kinase A phosphorylate on target proteins?

A
  • serine

- threonine

21
Q

What do kinases do?

A

Phosphorylate

22
Q

What do phosphatases do?

A

-dephosphorylate

23
Q

What does phosphorylation do?

A

-changes a proteins charge and generally leads to a conformation change which can alter ligand binding or other features of the protein resulting in an increase or decrease of its activity

24
Q

What is required to activate enzyme coupled receptors?

A

-dimerization

25
Q

What are enzyme coupled receptors?

A

-transmembrane proteins that bind ligands

26
Q

What is an RTK?

A
  • receptor tyrosine kinase

- receptor binds ligands and receptor is also tyrosine kinases

27
Q

What is autophosphorylation?

A

When the tyrosine kinase from one monomer phosphorylates the tyrosine residues on the other identical monomer

28
Q

What does Sos do? (In terms of Ras)

A

-displaces GDP for GTP on Ras activating it

29
Q

Where is Ras located?

A

It is membrane bound

30
Q

What is Src?

A

A non-receptor tyrosine kinase

A cytosolic kinase

31
Q

What are the four Src domains?

A
  • SH2
  • SH3
  • PTK (N-lobe)
  • PTK (C-lobe)
32
Q

Is every gene a proto-oncogene?

A

No, only those that can turn into a gain-of-function gene

33
Q

What is an oncogene?

A
  • when a normal gene mutates into a gain-of-function gene

- cancer gene

34
Q

What is a proto-oncogene?

A

-a normal gene

35
Q

What are v-Src and c-Src?

A

-c-Src would be considered the proto-oncogene that underwent mutations to become the oncogene (v-Src)

36
Q

What domain interacts with Grb2 and sos?

A

SH2 domain

37
Q

What is Ras?

A
  • A small GTPase that is anchored at the inner surface of the plasma membrane
  • mediates signaling by most RTKs
38
Q

What activates Ras?

A

-the binding of the GEF (SOS)

39
Q

How does Ras activate the MAP kinase signaling cascade?

A

By simply binding to RAF (MAP kinase kinase kinase)

40
Q

What is constituitively active Ras?

A

-mutated Ras protein that hydrolyzes GTP very slowly

41
Q

What do scaffold proteins do?

A

-help prevent cross-talk between parallel MAP kinase modules

42
Q

What do TGFb (transforming growth factor b) receptors do?

A

-regulates many cell functions including cell proliferation, programmed cell death, specialization and key embryonic events

43
Q

What is one thing that TGFb does?

A

-associates with receptor-regulated SMAD protein and phosphorylates it

44
Q

What is one thing about cytokine receptors?

A
  • stably associated with cytoplasmic tyrosine kinases (JAKS)

- JAKS phosphorylate STATS which migrate to the nucleus

45
Q

What is one thing Wnt does?

A

-binds to Frizzled a 7 segment transmembrane receptor (not a GPCR because doesn’t bind to G proteins)

46
Q

What is Hedgehog?

A

-a ligand

47
Q

What are TNFa and TNFa receptor

A
  • trimers

- important in the immune response