Introduction to cell signalling Flashcards
Q: What are some specialized inputs into cells beyond contact/diffusible types?
A: Light, temperature, mechanical deformation (e.g., touch).
Q: What are the two main types of cellular input signals?
A:
Contact-based signals – requiring direct physical contact (e.g. integrins, gap junctions).
Diffusible signals – using soluble messengers like hormones, gases, ions.
Q: What are gap junctions and their signalling function?
A: Channels made of connexins allowing direct cytoplasmic exchange (e.g. ions, second messengers like Ca²⁺ or cAMP) between adjacent cells.
Q: What clinical issue is linked to gap junction mutations (e.g. Cx26, Cx32)?
A:
Cx26 → congenital deafness
Cx32 → Charcot-Marie-Tooth disease
Q: What is eph/ephrin signalling?
A: A bidirectional contact-dependent pathway where receptors (Eph) and ligands (ephrins) on different cells engage, triggering cytoskeletal changes and gene expression.
Q: What are integrins and how do they signal?
A: Cell surface receptors binding extracellular matrix (ECM) proteins (e.g. collagen, laminin), triggering dimerization and activating internal proteins like FAK, talin, paxillin, which influence the cytoskeleton and cellular processes.
Q: What are the main types of diffusible molecules that serve as signalling inputs?
A:
Peptide hormones (e.g. insulin, growth factors)
Lipid hormones (e.g. corticosteroids)
Gases (e.g. nitric oxide)
Ions & osmotic gradients
Metabolites like glucose
Q: What’s unique about lipid hormones compared to peptide hormones?
A: Lipids (e.g., glucocorticoids) are membrane-permeable and bind intracellular receptors, while peptides bind cell surface receptors.
Q: How does nitric oxide (NO) act as a signal?
A: Produced by nitric oxide synthase (NOS), NO diffuses to nearby smooth muscle cells → activates guanylyl cyclase → increases cGMP → promotes vasodilation
Q: Why can glucose be considered a signalling molecule in beta cells?
A: It enters cells via GLUT transporters, triggering a cascade including ATP production, Ca²⁺ influx, and insulin secretion — mimicking receptor-based cascades.
Q: What is the mechanism of GPCR signalling?
A: Ligand binds → GPCR activates G proteins (Gq, Gs, Gi, etc.) → downstream effectors activated (e.g. IP3, cAMP) → broad intracellular effects.
Q: What is the Gq protein pathway and its effect?
A: Gq activates phospholipase C → generates IP3 and DAG → IP3 releases Ca²⁺ from ER, DAG activates PKC.
Q: What is the GPCR example involving exocrine cells?
A: Receptors at the basal surface trigger IP3 production → Ca²⁺ release at apical side → secretion (e.g. digestive enzymes).
Q: How do tyrosine kinase receptors (RTKs) like insulin receptor work?
A: Ligand binds → receptor dimerization → autophosphorylation → activates PI3K → AKT → GLUT4 translocation & gene transcription.
Q: How is contact signalling involved in cancer progression?
A: Disruption of cadherins and connexins facilitates epithelial-mesenchymal transition (EMT) → allows tumour invasion and metastasis.
Q: What is insulin resistance and why is it puzzling?
A: A condition in type 2 diabetes where cells fail to respond to insulin. It may involve receptor desensitization, impaired AKT signalling, and GLUT4 translocation, but exact mechanisms remain unclear.
