Cell Signalling Flashcards
(26 cards)
What is signal transduction?
The conversion of one type of signal into another—for example, converting a hormonal signal into an intracellular response
What are the four types of cell signalling?
1️ Endocrine signalling → Long-distance, hormone-based signals.
2️ Paracrine signalling → Localised, short-range signals.
3️ Neuronal signalling → Fast electrical impulses targeting specific cells.
4️ Contact-dependent signalling → Physical interactions via membrane-bound
Give an example of each signalling type
Endocrine: Insulin regulating glucose uptake across the body.
Paracrine: Histamine inducing inflammation by making blood vessels leaky.
Neuronal: Acetylcholine transmitting signals at nerve-muscle junctions.
Contact-dependent: Delta signal inhibiting neighbouring cells from becoming specialised.
What are the two major classes of extracellular signal molecules?
1️ Hydrophilic molecules → Cannot cross the membrane, bind cell surface receptors.
2️ Small/hydrophobic molecules → Pass through the membrane, bind intracellular receptors.
How can the same signal induce different responses in different cell types?
Downstream signalling pathways differ in various cells, producing context-dependent effects.
What happens if a cell lacks survival signals?
The cell undergoes apoptosis (programmed cell death).
How do extracellular signals induce fast vs. slow responses?
Fast responses → Directly alter proteins in the cytoplasm (e.g., metabolism, movement).
Slow responses → Require changes in gene expression (e.g., differentiation, cell growth).
What is the function of cell-surface receptors?
Detect signals outside the cell & initiate intracellular signalling cascades.
Describe signal transduction as a relay race.
Signal is passed downstream between intracellular molecules, culminating in an effector response.
What are five key roles of intracellular signalling pathways?
Relay signals → Spread information through the cell.
Amplify signals → Allow small inputs to produce large responses.
Integrate multiple signals → Coordinate different pathways.
Distribute signals → Activate multiple effector proteins simultaneously.
Feedback regulation → Modulate responses (enhancing or inhibiting signals).
What are the two types of molecular switches?
1️ Phosphorylation-based switches → Activated/inactivated by kinases & phosphatases.
2️ GTP-binding proteins → Toggle between active (GTP-bound) and inactive (GDP-bound) states.
What are the two types of GTP-binding proteins?
Small monomeric GTPases.
Large trimeric G-proteins.
What are the three major classes of receptors?
1️ Ion-channel-coupled receptors → Allow ion flow upon ligand binding.
2️ G-protein-coupled receptors (GPCRs) → Activate G-proteins to regulate enzymes & ion channels.
3️ Enzyme-coupled receptors → Directly catalyse intracellular reactions or associate with enzymes.
What is the largest class of enzyme-coupled receptors?
Receptor Tyrosine Kinases (RTKs).
Which small monomeric GTPase is activated by RTKs?
Ras, a key regulator of downstream signalling pathways.
How does RTK activation work?
Ligand binding → Induces RTK dimerisation.
Kinase domains phosphorylate tyrosine residues.
Phosphorylated residues serve as docking sites for intracellular signalling proteins.
How does Ras activate the MAP kinase cascade?
Ras-GTP initiates a phosphorylation relay, amplifying the signal.
MAP kinase transmits signals from the plasma membrane to the nucleus, triggering gene expression changes.
What does MAP kinase stand for?
Mitogen-Activated Protein Kinase—final kinase in the Ras cascade.
How does PI 3-Kinase regulate cell survival?
RTKs recruit PI 3-Kinase, which phosphorylates PIP2 to PIP3.
PIP3 recruits Protein Kinase 1 & Akt (a serine/threonine kinase).
Activated Akt promotes survival by phosphorylating downstream targets.
What is PTEN?
A phosphatase that dephosphorylates PIP3, reversing PI3K signalling.
PTEN mutations contribute to cancer by…?
Sustaining survival signals
How are signalling pathways linked to cancer?
Mutations in RTKs, Ras, MAPK, PI3K, AKT & PTEN deregulate cell division & survival.
30% of cancers contain Ras mutations, making it a key therapeutic target.
PTEN mutations switch off negative regulation, allowing cancerous growth.
What is cancer?
Uncontrolled cell division, often caused by accumulated mutations in signalling genes
