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Foundations Of Medical Science > Cell Signaling > Flashcards

Cell Signaling Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What are the four major cellular junction systems?

A

Tight junctions, adherens junctions, desmosomes, gap junctions

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2
Q

Tight junction

A

Seals the gap between cells, branch network, on the apical end of cells, works to hold cell together

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3
Q

Adherens junction

A

Connects actin filament bundles to keep the cell in place, uses cadherins, alpha-catenin, and beta-catenin

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4
Q

Desmosome

A

Connects intermediate filaments from the inside of the cel to the ECM outside, acts as adhesion points

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5
Q

Gap junction

A

Allows the passage of water soluble molecules, directly connect cytoplasm of two cells, made up of connexin proteins

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6
Q

Why is the ECM important?

A

It provides a surrounding matrix in tissues, facilitates cell adhesion, anchors cells within tissue with basement “membrane” and provides the cell with a compressible, resilient environment to prevent physical damage

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7
Q

Components of the ECM

A

Collagen, fibronectin, laminin, proteoglycans, clycoseaminoglycans

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8
Q

What do integrins do?

A

Integrate the ECM to the functions of the intracellular signaling pathways

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9
Q

Growth factors

A

Bind to cell surface receptor to stimulate cell growth and/or proliferation

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10
Q

Mitogen

A

Stimulates cellular proliferation

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11
Q

Cytokine

A

Stimulates the differentiation or proliferation of immune cells

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12
Q

Chemokine

A

Attractant for motile cells through receptor mediated signaling

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13
Q

Types of receptor-mediated signaling

A

Endocrine, paracrine, autocrine

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14
Q

Endocrine

A

Signaling molecules made in specialized cells and carried to remote sites through the bloodstream (long distance signal)

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15
Q

Paracrine

A

Signaling molecules that act on nearly cells

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16
Q

Autocrine

A

Signaling molecules on one membrane that interact with adjacent receptors

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17
Q

Key steps of cell signaling

A

Signal, reception, amplification, transduction, response, feedback

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18
Q

First messenger

A

Extracellular signal that binds to start a signaling process (ligand)

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19
Q

Second messengers

A

Respond to first messenger and are released to trigger physiological changes in the cell, small molecules (NOT PROTEINS)

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20
Q

Transduction

A

The transformation of a signal into another type to ensure that energy is correctly put into the physiological change

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21
Q

Amplification

A

Signal increases in intensity over time to trigger the desired response

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22
Q

Feedback

A

Response continues until termination signal

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23
Q

Node

A

Where signaling pathways connect

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24
Q

Signal termination

A

The stopping of a signaling pathway

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25
Q

Intracellular receptor signaling

A

Carrier protein brings small, hydrophobic signaling molecule, which then diffuses across ECM into target cell, where an intracellular receptor protein takes it into the nucleus. It binds to the promoter region of a gene and activate the transcription of a new protein that alters the cell’s function

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26
Q

Membrane signaling

A

The signal binds to a TM receptor, which activates a membrane associated switch, which then activates cytoplasmic signaling pathways, and gets the desired response

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27
Q

What are the master switches of membrane receptor signaling?

A

Phosphorylation and GTP Binding

28
Q

Phosphorylation

A

Inactive protein is phosphorylated by a protein kinase to activate, then a protein phosphatase returns it to an inactive state

29
Q

GTP binding

A

Inactive G-protein is bound by GDP, GEF literally exchanges GDP for GTP, which binds to the G-protein, activating it, then an inactivator protein hydrolyzes GTP to GDP

30
Q

Small G-protein

A

Monomeric G-protein, GDP-bound is inactive, GTP-bound is active, activated by GEF, inactivated by GAP

31
Q

Large G-protein

A

Trimeric, alpha, beta and gamma subunits. Beta and gamma are regulatory subunit, the exchange of GDP for GTP by GEF triggers the release of this subunit. Coupled with 7-TM GPCR. When bound, exchange happens, alpha can activate the effector. To inactivate, hydrolysis rejoins beta gamma

32
Q

Examples of second messengers

A

Ca2+, cAMP, cGMP, IP3, DAG (NOT PROTEINS)

33
Q

Five key membrane signal transduction pathways

A

JAK-STAT, RAS-MAPK, cAMP-PKA, PI3K-AKT, IP3-PKC

34
Q

JAK-STAT purpose

A

Stimulates blood cell growth and proliferation

35
Q

JAK-STAT first messenger

A

Cytokines

36
Q

JAK-STAT receptor

A

Cytokine receptor couples to JAK

37
Q

JAK-STAT transduction events

A

Autophosphorylation of JAK proteins, then phosphorylated JAKs bind and phosphorylate STAT

38
Q

JAK-STAT target

A

Phosphorylated STAT is an active transcription factor, enters nucleus to turn on the transcription of specific cytokine response genes

39
Q

JAK-STAT second messenger

A

None

40
Q

RAS-MAPK purpose

A

Stimulate cell growth and proliferation

41
Q

RAS-MAPK first messenger

A

Growth factors

42
Q

RAS-MAPK receptors

A

Tyrosine kinase

43
Q

RAS-MAPK transduction events

A

RAS activated by GEF then activates RAF

44
Q

RAS-MAPK amplification events

A

RAF phosphorylates MEK, MEK phosphorylates ERK

45
Q

RAS-MAPK target

A

ERK phosphorylates many target proteins including transcription factors

46
Q

RAS-MAPK second messenger

A

None

47
Q

cAMP-PKA purpose

A

Stimulates transcription of genes encoding regulators of metabolic pathways

48
Q

cAMP-PKA first messenger

A

Peptide hormones

49
Q

cAMP-PKA receptor

A

7-TM receptors

50
Q

cAMP-PKA transduction events

A

Receptor activates large G-protein, which activates adenylate cyclase, stimulating cAMP production

51
Q

cAMP-PKA amplification events

A

cAMP activates PKA by stimulating the dissociation of the regulatory subunits

52
Q

cAMP-PKA target

A

PKA enters nucleus and activates transcription factors

53
Q

cAMP-PKA second messenger

A

cAMP

54
Q

PI3K-AKT purpose

A

Controls cell growth and apoptosis pathways

55
Q

PI3K-AKT first messenger

A

Selected hormones, growth factors, and cell survival ligand

56
Q

PI3K-AKT receptor

A

Receptor diners with intrinsic kinase domains or that bind intracellular kinases

57
Q

PI3K-AKT transduction events

A

Stimulation of the conversion of PIP2 to PIP3, PIP3 stimulates PDK1, which activates AKT/PKB

58
Q

PI3K-AKT target

A

Apoptosis control proteins, transcription factors, translation factors, cyclins

59
Q

PI3K-AKT second messengers

A

PIP2 and PIP3

60
Q

IP3-PKC purpose

A

Regulation of physiological processes that are mobilized by the release of calcium stores and are affected by PKC, which plays a role in modulating membrane structure events, regulating transcription, mediating immune response, cell growth and learning and memory

61
Q

IP3-PKC first messenger

A

Selected growth factors, mitogen, immune signals

62
Q

IP3-PKC receptor

A

7-TM receptor

63
Q

IP3-PKC transduction events

A

Receptor activates large G-protein which activates phospholipase C, which attacks and cleaves PI(4,5)bisphosphate to produce IP3 and DAG

64
Q

IP3-PKC amplification events

A

IP3 binds to smooth ER calcium channels and stimulates the release of Ca2+, which binds to PKC (bound to DAG) and activates PKC

65
Q

IP3-PKC target

A

PKC phosphorylates a wide variety of substrates including nuclear transcription and cytoplasmic regulatory proteins

66
Q

IP3-PKC second messengers

A

IP3, DAG, Ca2+

67
Q

How can RAS-MAPK and PI3K-AKT target cancer?

A

By chemotherapy drugs targeting specific points in the pathway to control cell growth

Foundations Of Medical Science (9 decks)

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