Signal Dysregulation Flashcards

1
Q

What are protein kinases?

A

Enzymes that transfer phosphate groups from ATP to proteins or substrates

Switches proteins “on/off”

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2
Q

Outline the process of RTK activation

A

Ligand Binding
Recepter Dimerisation
Transphosphorylation
Signalling Cascade

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3
Q

What are some RTK dysregulation mechanisms that result in increase RTK activation

A

Mutations- Deletion of the ectodomain leaves mutated RTK constitutively activated

Overexpression leads to increased chance of ligand-independent dimerisation

Autocrine signalling from tumour cells producing their own GF ligands

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4
Q

What is the most common oncogene in humans?

A

Ras

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5
Q

How is Ras activated?

A

RTK Activation

Phosphorylation of GDP-Ras to GTP-Ras

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6
Q

What adaptor proteins link RTKs to Sos/GEF?

A

Grb2 and Shc

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7
Q

What are the 3 downsteam pathways of Ras?

A

Raf/MAPK/ERK
PI3K/Akt/PKB
Ral-GEFs

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8
Q

What is the Raf pathway responsible for?

A

Contact inhibition
Anchorage dependence
Cell shape

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9
Q

What is the most important oncological function of the Akt/PKB (PI3K) pathway?

A

Anti-apoptosis functions

Other functions:
Stimulation of proliferation
Stimulates cell size growth
Promotes angiogenesis and motility

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10
Q

How is Akt dysregulated?

A

PTEN reverse PI3K activation

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11
Q

What is the function of the Ral-GEFs pathway?

A

Anchorage independent growth and activation of Rho family proteins (motility and invasiveness)

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12
Q

How is Ras deavtivated?

A

GTPase activating proteins(GAPs)
GTPases

Note: in many cancers mutations alter the ability of GAP/GTPases to trn off Ras-GTP

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13
Q

What is dual address?

A

Proteins that normally reside in cytoplasm but move to the nucleus when activated

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14
Q

How does dysregulation of the JAK-STAT dual pathway lead to oncogenesis?

A

Mutations can create STAT3 proteins which dimerise spontaneously and act as a nuclear transcription factor.

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