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BMIS 430 > Chamberlain > Flashcards

Chamberlain Flashcards

1
Q

how do cells transduce messages through the plasma membrane

A

Receptors

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2
Q

what are the 5 types of signaling

A

endocrine
paracrine
juxtacrine
intracrine
autocrine

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3
Q

Explain endocrine signalling
What is the signalling molecule for endocrine signalling?

A

sent via circulation,, targets receptors on cell in distant tissues, signalling molecules are hormones
ex: sex hormones

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4
Q

Explain Paracrine signalling

A

local signalling targets receptors on neighbouring cells, highly common
ex: Fibroblast growth factor family, insulin-like growth factor family

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5
Q

T/F normal cells synthesize their ligands in paracrine signalling

A

false

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6
Q

Explain juxtacrine signalling

A

receptor and target are embedded in plasma membrane, local signalling, cell-cell contact, GAP and tight junctions
ex: Notch, cadherins

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7
Q

Explain intracrine signalling

A

signalling within a cell, signal and receptor are in the cell
ex: some hormones, some GFs

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8
Q

explain Autocrine signalling

A

signalling via a single cell, express both receptor and target, common in cancer
ex: interleukin-1 and 2

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9
Q

Which signalling is common in cancers?

A

Autocrine, cancer can synthesize their own ligands

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10
Q

What are signals that cells sense

A

Food, integrin/cell junction signalling, hormone signalling, growth factor signalling

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11
Q

what links cells to ECM

A

integrins

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12
Q

why is integrin signalling important

A

protects cells from anoikis

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13
Q

what is anoikis

A

apoptosis due to loss of cell attachment

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14
Q

what is talin

A

recruits cell signalling components in integrin signalling, connected to beta subunit

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15
Q

what does talin recruit

A

recruits phosphorylated FAK which binds Grb2 which binds Sos, which allows Ras to go from GDP to GTP

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16
Q

what is the talin pathway that you should know? (slide 28)

A

Talin–> FAK –> Grb2 –> Sos –> Ras-GDP –> Raf –> MEK –> Erk

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17
Q

why are integrins important in cancer

A

provide mechanisms to protect against anoikis such as survival signalling (endosomes, ECM free signalling)

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18
Q

describe the general pathway of growth factors

A

Growth factor ligand –> receptors –> adaptors and enzymes –> signalling cascades –> transcription factors –> effect

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19
Q

What are growth factor

A

small peptides that interact with specific receptors, many secreted as inactive precursors, tie cells within a tissue together into a single community

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20
Q

What are mitogens? what are some examples? how are they different during cancer?

A

induce a cell to proliferation, VEGF, PDGF, EGF, always active during cancer usually only activated during ccell damage

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21
Q

what are the 3 groups of structures of growth factors

A

Single protein, homodimers, heterodimers

22
Q

What are some of the different types of receptors?

A

G-protein coupled receptors, Nuclear receptors, Notch receptors, Patched receptor (hedgehog). receptor tyrosine kinase

23
Q

what is the largest and most diverse group of membrane receptors in eukaryotes

A

G-protein coupled receptors

24
Q

What are the six main classes of G-protein coupled receptors

A

A (rhodopsin-like)
B (secreting receptor family)
C (Metabotropic glutamate/pheromone)
D (Fungal mating pheromone receptors)
E (Cyclic AMP receptors)
F (Frizzled/Smoothened) *

25
Q

describe canonical Wnt signalling

A

Wnt binds to Frizzled which then binds to Dishevelled. This then activates and binds to the axin complex. The complex is pulled apart leaving axin still bound to Dishevelled and LRP. Beta-catenin gets released from inactive GSK-3B, Wtx, and Apc. this results in beta-catenin promoting proliferation and stem cell state. Beta-catenin will go into the nucleus and activate transcription factors

26
Q

Describe Non-canonical Wnt signalling

A

When frizzled binds to Wnt, it binds to an inactive G-protein (alpha, beta, gamma subunits), the inactive G-protein separates into alpha and beta-gamma subunits which are then activated. the alpha subunit replaces GDP for GTP and promotes PDE which inhibits cGMP. The beta-gamma subunit promotes PLC-B which cuts lipids in half, and ultimately increase PKC and calcium to activate cell signalling

27
Q

What do nuclear receptors bind to

A

Steroid sex hormones, retinoids, vitamin D, small hydrophobic molecules,, bind to hormone repsonse elements

28
Q

Which receptor is important in breast cancer?

A

Nuclear receptors

29
Q

Describe Notch interactions with delta

A

when Delta and Notch interact, it signals for delta to be endocytosed and breaks apart the complex

30
Q

Explain hedgehog signalling

A

If Hedgehog binds to patched, Gli is not cleaved and genes are induced and transcribed
If hedgehog does not bind to patched, Gli is cleaved and becomes a repressor of transcription

31
Q

What are receptor tyrosine kinases, what are the 3 major domains

A

Extracellular domain, transmembrane domain, intracellular domain

32
Q

what is transphosphorylation

A

receptor phosphorylates its binding partner

33
Q

what are the combinations of homo and heterodimers

A

1-1
1-2: 2 ERBB2 doesn’t bind ligand
3-3: uses up ligand but doesn’t phosphorylate partner, doesn’t activate ligand
3-2: 2 doesn’t bind ligand, 3 doesn’t phosphorylate partner
4-4: normal
4-2: 2 doesn’t bind ligand

34
Q

T/F there are multiple binding sites on EGF receptor

A

True

35
Q

how do receptors act in a cancer cell

A

they’re either mutated affecting structure or overexpressed but they’re constitutively active

36
Q

how do growth factors become deregulated

A

they become truncated which emit signals even in the absence of ligands

37
Q

which receptor would fusion not work with?

A

insulin because its already a dimer

38
Q

What are the two types of genes created from signalling cascades

A

immediate early genes, delayed early genes

39
Q

T/F There are more tyrosine kinases than Serine/Threonine kinases

A

False, 90 tyrosine kinases, 429 serine/threonine kinases

40
Q

what was the first tyrosine kinase discovered

A

Src

41
Q

What’s the difference between v-Src and C-Src.

A

v-Src for viral Src. C-Src was the normal, cellular Src

42
Q

study Src mech of action slide 66

A
43
Q

What are the types of protein domains and what is one example for each

A

Modified peptide: SH2 bind to p-Tyr
Peptide: PDZ binds to carboxylic acid
Domain/Domain: PDZ binds PDZ
Phospholipid: C1 binds DAG
Nucleic Acid: PUM binds RNA

44
Q

explain the yeast two hybrid system

A

Bait and prey are constructed from a proteome library. The library is screened for potential interactions between the bait and prey. If the interaction occurs then transcription will occur and from the results, you can see which receptors were important

45
Q

what is the important MAPK signalling pathway

A

creates ERK1/2

46
Q

what’s the important PI3K/ AKT signalling pathway

A

AKT –> mTORC1

47
Q

What is the Akt/PKB pathway? what are the 4 effects

A

phosphorylation activates the Akt/PKB which then affects 4 molecules
Inhibits GSK-3B which inhibits proliferation
Promotes HIF-1a which promotes angiogenesis
inhibits bad which inhibits apoptosis
inhibits TSC2 which inhibits protein synthesis

48
Q

will you ever see PIKC3A and PTEN mutations in the same cell

A

no usually one or the other

49
Q

How mutated is p85a in cancer

A

not highly mutated

50
Q

what are the two pathways of Ras activation

A

Tyrosine kinase binds to Grb2 which binds its SH3 domains to Sos which switches Ras from the inactive form to the active form
Tyrosine kinase binds Shc which binds to Grb2 which binds its SH3 domains to Sos which witches Ras on

51
Q

explain the regulation of Ras

A

GTP hydrolysis and Ras inactivation induced by GAP
Ras activation triggered by GEF(Sos)

52
Q

how is the mutant Ras signaling different from normal

A

loses the ability to alter between active/inactive states, GAPA doesn’t affect the mutant Ras

BMIS 430 (7 decks)

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