Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Developmental Biology > L10 - TGFbeta and FGF signalling > Flashcards

L10 - TGFbeta and FGF signalling Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

What are the three common features in signal transduction pathways?

A

Reception – ligand binds to a cell surface receptor and activates it
Transduction – receptor activation induces transduction of signal from membrane to nucleus via a cascade of secondary messenger activation
Response – a transcription factor is activated and induces transcription of specific target genes

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

What are the three sub groups of the TGFbeta protein superfamily?

A

BMP like family
GDNFs family
TGF beta like family

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

BMP like family examples

A

BMPs

GDFs

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

GDNFs family examples

A

GDNF

Neuturin

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

TGF beta like family

A

TGF-beta
Activins
Nodal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

TGFbeta signal transduction method

A
  1. Ligand binds to type 2 receptor
  2. This leads to oligomerisation bringing together the type 1 and type 2 receptor
  3. Formation of dimer results in activation of type 2 receptor
  4. Kinase activity of type 2 receptor promotes phosphorylation of type 1 receptor
    a. Promotes overall activation of receptor
  5. Downstream there are two groups of proteins
    a. SMAD 4
    b. SMAD 2 and SMAD 3
  6. SMAD 2 and SMAD 3 recruited and phosphorylated by receptor
    a. Further activated by binding of smad 4
  7. Active SMAD transcription factor complex binds to TGF beta target genes and activate their transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is BMP signalling tightly regulated?

A

You only want

  • Certain cells to respond to the signals
  • Cells to respond at certain times/locations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is BMP signalling operated through inhibition?

A

The proteins are already synthesised but their activity is controlled through extracellular inhibitors
Antagonists
- Moderate BMP signalling
- These varying levels of inhibition lead to a variety of different cell fates

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

Examples of antagonists used in BMP signalling

A

Noggin
Chordin
BMP3

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

How many RTK families are there?

A

20 each with many individual receptors – with their ligand partners

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

RTK ligand receptor complexes

A

Some ligands are specific for one receptor and vice versa

Some ligands interact with many receptors and vice versa

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

How many RTK genes have been identified in human genome?

A

58

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

Are RTK mainly monomers or polymers?

A

Monomers

Except insulin receptor

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

What are RTK extracellular and intracellular domains like?

A

Extracellular domains vary greatly – ligand binding activity
Intracellular domains have kinase activity – enzyme linked receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How many transmembrane domains do RTKs have?

A

Single transmembrane domain – 25-38 amino acids

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

How are RTKs activated?

A

The ligand has ability to dimerise and it facilitates receptor dimerization or oligomerisation

17
Q

What does cross phosphorylation of RTK receptors do?

A

Enhancers kinase activity

Opens up docking sites for the recruitment of secondary messengers

18
Q

Tools for analysis of RTK signalling exploit?

A

Dimerization

19
Q

What tools for analysis of RTK signalling can be made?

A

Using genetic engineering we can generate DNA that encodes for a normal receptor that is mutated in the kinase domain
Receptor does not have kinase activity but retains ability to bind to ligand – dominant negative form

20
Q

What does the dominant negative form of a receptor do?

A

Block subsequent activity of the dimer
Cross phosphorylation of the receptors will not occur
Useful to generate tools for loss of function studies

21
Q

How does the phosphorylated RTK receptor transduce the signal?

A

Phosphorylated tyrosine acts as docking sites for downstream signalling proteins

22
Q

What proteins bind to RTKs?

A

PI-3 kinase – inositol lipid pathway
GTPase-activating protein – RAS/MAP kinase pathway
PLC-gamma – inositol lipid pathway

23
Q

What two states does Ras have?

A

Functions as a switch with two distinct states

  • Active – bound to GTP
  • Inactive – bound to GDP
24
Q

How does Ras switch between its to states?

A

Becomes active with help from guanine nucleotide exchange factor (GEF)
Becomes inactive with help from GTPase activating proteins (GAP)

25
Q

Ras pathway - how docking leads to signal transduction?

A
  1. Activated receptor has many phosphorylated tyrosine’s acting as docking sites
  2. Binding of GRB2 and Sos (GEF) coupled receptor to inactive Ras
  3. Sos promotes dissociation of GDP from Ras
  4. GTP binds Ras and then it dissociates from Sos
26
Q

How does signal transduction downstream of RTKs occur?

A

Occurs through rapid activation, by Ras, of a series of proteins

  • All activated by phosphorylation
  • All contain kinase activity so trigger cascade of protein phosphorylation
27
Q

Signal transduction downstream of Ras method?

A

Activation of three different kinases with activates various transcription factors

  1. Raf kinase– activated by GTP activated Ras
  2. Mek kinase – activated by MAP kinase kinase kinase
  3. Map kinase - activated by dual phosphorylation of one serine and one threonine by MAP kinase kinase
    - Acts just before transcription of target genes
28
Q

How many FGF ligand members are there?

A

22

Either paracrine, intracrine or endocrine

29
Q

FGF receptors are characterised by?

A

Immunoglobulin like domains
Ligands bind to D2 and D3
Single transmembrane domain
Kinase receptor split into two domains

30
Q

How many FGF receptors are there?

A

4

Responsible for downstream events after the other 22 ligands

31
Q

What is the role of FGF8?

A

Plays a vital role during development

Patterns midbrain-hindbrain boundary

32
Q

What do FGFs form a complex with?

A

FGFs are unable to act on their own – used to help explain their specificity
FGF and its receptor form a complex with HSPGs
FGFs fist form oligomers on HSPGs

33
Q

What are heparan sulphate proteoglycans used for?

A

Important extracellular modifiers of cell-cell signalling

34
Q

HSPG protein core can be?

A

Transmembrane – fully extracellular
Tethered to membrane
Secreted

35
Q

What is HSPGs protein core associated with?

A

Associated with long chains of sugar - heparan
Each molecule of sugar can be modified – mainly by sulphation
- Modification could result in a code that creates binding site for many specific proteins

36
Q

FGF signalling pathway examples

A

GRB2 and SOS –> RAS –> RAF, MAPKK and MAPK –> FOS (oncogene) –> cell proliferation
GRB2 and GAB1 –> PI3K –> cell survival

37
Q

What are mutations in FGF receptors associated with?

A

Associated with many human disease
Pfeiffer syndrome – FGFR1
Achondroplasia – FGFR3

Developmental Biology (16 decks)

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