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2nd messengers
Uni of Notts, Signalling & Metabolic Regulation, Year 2, Topic 2
| Question | Answer |
|---|---|
| What determines whether a GPCR response is excitatory or inhibitory? | The type of Gα subunit recruited by the ligand-bound GCPR. Different ligands can activate different Gα proteins using the same receptor, altering downstream signalling |
| Why must second messengers remain at low basal levels? | Ensures signalling spikes are meaningful & detectable; contrast between basal & stimulated levels drives specificity. Sometimes a return to basal levels can be its own signal |
| What causes transient spikes in cAMP concentration? | A strong, localized activation of adenyl cyclase that temporarily overwhelms cAMP‑phosphodiesterase. After this activation, the phosphodiesterase returns concentration to base |
| AKAP & PKA regulation | AKAP (A-Kinase Anchoring Proteins) anchors PKA regulatory subunits to localised cell structure regions & other signallers. Is a scaffold protein for signalling complexes (e.g., PKA & cAMP phosphodiesterase together) |
| How does cAMP activate PKA? | cAMP binds the regulatory subunits, releasing the catalytic subunits to phosphorylate targets |
| What is CRE and why is it important? | CRE (cAMP Response Element) is a DNA sequence in a gene that binds TF CREB (CRE-Binding protein) to regulate transcription |
| How can PKA produce long‑lasting effects? | By entering the nucleus & phosphorylating CREB, altering gene transcription |
| Example of CREB‑mediated long‑term change | In olfactory neurons, CREB increases transcription of neuropilins and adhesion molecules to rewire odour pathways to olfactory receptor-specific glomeruli |
| What G protein activates phospholipase C‑β | Gαq, which becomes active when GTP binds after GPCR stimulation |
| What are the products of PIP2 cleavage by PLC‑β | DAG (membrane‑bound) and IP3 (diffusible) |
| How does IP3 increase intracellular Ca²⁺ | By binding IP3 receptors on the intracellular calcium stores (ER/SR), opening Ca²⁺ release channels |
| PKC activation | PKC activation requires both DAG and Ca²⁺, which bind cooperatively |
| Components of the Ca²⁺ signalling toolkit | Channels, pumps, exchangers, buffers, and sensors |
| Why different cell types have unique Ca²⁺ signalling patterns | Each cell expresses a unique subset of toolkit components, creating bespoke signalling systems. This makes Ca²⁺ signalling more robust: if 1 part is damaged or mutated the cell can adapt by expressing different parts |
| What triggers the initiation of a calcium wave | Local IP3‑mediated Ca²⁺ release that activates nearby ryanodine receptors via positive feedback |
| What stops a calcium wave | High local Ca²⁺ concentrations inhibit ryanodine receptors, creating a negative feedback loop |
| How do calcium waves propagate across the cell? | Receptors further from the origin open later and close later, creating a directional wave |
| What aspects of a Ca²⁺ wave encode information? | Frequency, amplitude, and duration, each activating different downstream pathways |
| What is calmodulin’s role in Ca²⁺ signalling? | Calmodulin binds Ca²⁺ and then activates target proteins such as CaM‑Kinase II |
| How does CaM‑Kinase II decode Ca²⁺ wave frequency? | Its 12‑subunit structure allows graded activation depending on how often Ca²⁺ pulses occur |
| How are Ca²⁺ levels restored after signalling? | By pumping Ca²⁺ out of the cell, buffering it, or temporarily storing it in mitochondria. This can be slowly released back into the cell for proper storage later |
| Store Operated Channels (SOCs) | Membrane protein channels which open in response to Ca²⁺ store depletion to allow in extracellular Ca²⁺ & refill stores |
Created by:
Denny12
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