Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BMIS 430 > Chamberlain > Flashcards

Chamberlain Flashcards

(52 cards)

Start Studying
1
Q

how do cells transduce messages through the plasma membrane

A

Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 5 types of signaling

A

endocrine
paracrine
juxtacrine
intracrine
autocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F normal cells synthesize their ligands in paracrine signalling

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain intracrine signalling

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

explain Autocrine signalling

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which signalling is common in cancers?

A

Autocrine, cancer can synthesize their own ligands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are signals that cells sense

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what links cells to ECM

A

integrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why is integrin signalling important

A

protects cells from anoikis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is anoikis

A

apoptosis due to loss of cell attachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is talin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why are integrins important in cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the general pathway of growth factors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the 3 groups of structures of growth factors

Study These Flashcards
A

Single protein, homodimers, heterodimers

22
Q

What are some of the different types of receptors?

Study These Flashcards
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

Study These Flashcards
A

G-protein coupled receptors

24
Q

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

Study These Flashcards
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
describe canonical Wnt signalling
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
Describe Non-canonical Wnt signalling
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
What do nuclear receptors bind to
Steroid sex hormones, retinoids, vitamin D, small hydrophobic molecules,, bind to hormone repsonse elements
28
Which receptor is important in breast cancer?
Nuclear receptors
29
Describe Notch interactions with delta
when Delta and Notch interact, it signals for delta to be endocytosed and breaks apart the complex
30
Explain hedgehog signalling
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
What are receptor tyrosine kinases, what are the 3 major domains
Extracellular domain, transmembrane domain, intracellular domain
32
what is transphosphorylation
receptor phosphorylates its binding partner
33
what are the combinations of homo and heterodimers
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
T/F there are multiple binding sites on EGF receptor
True
35
how do receptors act in a cancer cell
they're either mutated affecting structure or overexpressed but they're constitutively active
36
how do growth factors become deregulated
they become truncated which emit signals even in the absence of ligands
37
which receptor would fusion not work with?
insulin because its already a dimer
38
What are the two types of genes created from signalling cascades
immediate early genes, delayed early genes
39
T/F There are more tyrosine kinases than Serine/Threonine kinases
False, 90 tyrosine kinases, 429 serine/threonine kinases
40
what was the first tyrosine kinase discovered
Src
41
What's the difference between v-Src and C-Src.
v-Src for viral Src. C-Src was the normal, cellular Src
42
study Src mech of action slide 66
43
What are the types of protein domains and what is one example for each
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
explain the yeast two hybrid system
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
what is the important MAPK signalling pathway
creates ERK1/2
46
what's the important PI3K/ AKT signalling pathway
AKT --> mTORC1
47
What is the Akt/PKB pathway? what are the 4 effects
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
will you ever see PIKC3A and PTEN mutations in the same cell
no usually one or the other
49
How mutated is p85a in cancer
not highly mutated
50
what are the two pathways of Ras activation
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
explain the regulation of Ras
GTP hydrolysis and Ras inactivation induced by GAP Ras activation triggered by GEF(Sos)
52
how is the mutant Ras signaling different from normal
loses the ability to alter between active/inactive states, GAPA doesn't affect the mutant Ras

BMIS 430 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions